Slide 1

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 2

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 3

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 4

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 5

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 6

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 7

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 8

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 9

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 10

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 11

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 12

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 13

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 14

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 15

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 16

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 17

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 18

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 19

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 20

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 21

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 22

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 23

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 24

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 25

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 26

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 27

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 28

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 29

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 30

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 31

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 32

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 33

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 34

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 35

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 36

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 37

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 38

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 39

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 40

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 41

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 42

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 43

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 44

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 45

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 46

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 47

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 48

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 49

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU


Slide 50

Ischemic Heart
Disease
BY

Ragab Abdelsalam.(MD)
Prof. of cardiology

* Clinical

Presentations :

The clinical presentation of
ischemic heart disease usually
depends on the underlying
mechanism.

• Presentation & Mechanism
1-Stable Angina

exertion .
2- Unstable Angina:

-Transient myocardial
- ischemia on

- Prolonged ischemia.
-Plaque fissuring >
minimal myocardial damage.
3-Prinzmetal (variant) angina: Coronary spasm.
4- Acute Myocardial Infarction: Coronary
artery occlusion with tissue necrosis .

5- Silen Ischemia: Asymptomatic episodes
of ST – segment depression, due to
reversible abnormalities of myocardial
metabolism, and usually occurs with
autonomic dysfunction (as in DM) diabetes
mellitus .

6- Syndrome – X:Typical >>Anginal pain with
positive exercise test and normal coronary
Angiorgaphy
7-Heart Failure: > Loss of contractile function,
Aneurysm,Fibrosis,Ischemic cardiomyopthy.
8-Conduction defects: >> Edema & Necrosis,
Fibrosis.
9-Arrhythmia
>> Electrical Instability
10-Sudden death: Any of the above plus
ventricular arrhythmias.

Angina Pectoris
Definition:

It is a clinical syndrome of a
distinctive chest pain due to
temporarily insufficient myocardial
blood supply

* Types:
A) It is either :
1- Stable
2- Unstable

• b) Clinical background :
• Post – infarction Angina.
• Post – PTCA Angina.
• Post CABG Angina

c) Specific Forms :
- Prinzmetal’s Angina (Spastic).
- Post – Prandial.
- 2nd – wind Angina.
- Cocaine intoxication.

Etiology:
*Pathogenesis of pains :
Hypoxia >> Decrease blood flow >>
accumulation of metabolites (Lactic acid,
pyruvic, histamine ….) stimulate the never
endings via upper 4 thoracic segments to the
>> Brain>>>>>pain.

*Risk

Factors:

Major
• Hypertension.
personality .
• Diabetes mellitus.
(Sedentary) life.
• Dyslipidemia.
• Family History.
Smoking
•

Minor
- Type A
- Inactive
- Stress.
- Male Sex.
- Age
- Obesity

• *Precipitating Factors:
•
•
•
•
•
•

Heavily exersion.
Emotion.
Cold.
Digestion (Heavy meals).
Tachycardia.
Smoking.

*Clinical

data:

A- Pain: The typical Anginal pains.
> Character: Strangling, heaviness. Chocking,
dull, ache, & sense of (anger animi).
> Site: Retrosternal.
> Degree: Mild or moderately severe but rarely
of intense or crushing as in AMI.
> Radiation: From left retrosternal to left
shoulder, left arm, little finger, Jaw, back &
sometimes to epigasterium & right. Shoulder.
> Effort: It is exertional chest pain.

B - Autonomic effects: sweating, irritability,
diaphoresis

C - Physical Examination
Hands  > Nicotine stains
Pulse & Blood pressure
Eyes: (arcus , xanthelasma.)

Heart: There may be
Aortic stenosis , or HOCM or S4 & S3, MR.
Or normal findings.

Other systems >> Comorbidity

* Investigation:
A Basic Investigations :

Electrocardiogram (ECG).
Exercise ECG – Treadmill or
Bicycle.

B) Specialized Investigations :

> Radionuclide Perfusion Imaging.
> Stress Echocardiography.
> Coronary Angiography.

C- Other Imaging Techniques :
> Magnetic Resonance Imaging (MRI).
> Ultrafast computed Tomography
(UCT).
> Posterior Emission Tomography
(PET).
> Colour Kinesis.
> Contrast Echocardiography

* Summary Of Treatment
> Initial:

Sublingual nitrate.
Sublingual crushed 75 mg
Aspirin

Then:
> Risk Stratification 
> Control risk factors 

Drugs:
> B. Blocker. e.g. Atenolol
> Calcium channel blockers e.g.
deltiazem .
> Long – acting nitrates. e.g.
nitroglycerin
> Aspirin. Acetylsalsylic acid 75 mg
> Metabolic agents as trimetazidine.

• *Revascularization

:

–PTCA (Percutaneous
Transluminal coronary
angioplasty).
–CABG (Coronary Artery

Bypass Grafting).

Acute Coronary Syndromes
* These syndromes represent a dynamic
spectrum of a similar disease process,
being part of a continuum
* Each syndrome is associated with specific
strategies in prognosis and management

* The three major syndromes
are
1-Unstable angina.
2- Non – ST elevation
3-myocardial infraction.

*Pathophysiology:
>. All of the coronary syndromes are initiated by
the same event:

>> Rupture of an unstable plaque leads to
Coronary artery occlusion:

> Intermittent occlusion 
Unstable Angina
> Complete occlusion AMI

The 3 “I” S of coronary
artery events, means:
> Ischemia.
>Injury.
> Infraction.

• Ischemia :
Occurs with a mismatch between blood flow
and oxygen need by a section of the
heart .>>> Pain

Rapidly reversed by :
> Reducing O2 – need.
> Increasing O2 supply.

Injury:
Total occlusion >> more prolonged
ischemia >> damage >> Hyperacute
symptoms of a classic AMI.
> Occurs within 20-40 min.
> Cardiac dysfunction.
> Conduction of impulses may be altered.

Pain is severe but serum markers
are not yet released .

Infraction
actual death of the injured
myocardial cells.
Necrosed cells >> loss of cell wall integrity
>> release of intracellular components
such as :
- Myoglobin.
- Creatine phosphokinase (CPK).
- Troponins.
** These enzymes are measured as serum
markers of infarction.

* Electrocardiogram (ECG)
• a-Ischemia:
•

- < 20 min.
- Peaked T – waves.
- Inverted T – waves.
- Depressed ST – segment.

b) (20 – 40 min)
>> ST

– segment elevation.

c) Infraction:
.

.

- >1-2 hours
- Abnormal Q – waves.
 2 mm wide or
 25 % height of R – wave, in that lead

*Clinical

data :

• 1) Symptoms:
– Chest pain:

• Typical chest pain, severe, but
prolonged & sense of impending death.
(Angor Animi.(
– Nausea, vomiting, sweating, dizziness,
extreme weakness and dyspnea.
– Symptoms of complications.

• Silent – painless myocardial infarction

Symptoms of complications.
> As , dyspnea PND , irritability , palpitation
– Silent – painless myocardial infarction:

•
•

In diabetics.
In elderly.

* Signs :
•
•
•
•
•
•

Anxious patient.
Signs of cardiogenic shock if present:
Cold sweats.
Peripheral cyanosis.
Hypotension, thready pulse.
Oligurea.

> Pulse: Arrhythmias may be detected.
> Low grade fever

** Auscultation:
> First heart sound may be make.
> Pulmonary component of S2 may be
accentuated.
> Third heart sound.
> Pericardial friction rub if pericarditis occurs

> Murmur of mitral regurgitation or VSD if
complications occur.
> Moist rales may be heard at the base of
the lungs.

** However, auscultation may reveal no
abnormality.

Investigation :
- Electrocardiogram (ECG).
-ECG monitoring.
-Cardiac enzymes:
> Troponins.
> Myoglobin.
> SGOT.
> LDH.
> CPK – isoforms.
- Echocardiography.
- Radionoclide scintigraphy.
- Cardiac catheterization.

Complications of AMI
A) Early :
- Arrhythmias.
- Acute heart failure.
- Cardiogenic shock.
- Acute mitral regurgitation.
- Ventricular septal rupture or free wall rupture.
- Acute pericarditis.
- Mural thrombosis.
- Sudden death.

B) Late :
- Dressler’s syndrome >> fever, joint
pain, pleurisy & pericarditis.
>> has a dramatic response to
indomethacin or corticosteroids.

- Myocardial Aneurysm and thrombus.
- Chronic heart failure
- ischemic cardiomyopathy.

Assessment and
treatments of (ACS)
I- Initial Assessment :
- Rapid, but detailed History.
- Vital signs & physical examination.
- 12 – lead ECG & serial ECG.
- X – ray on chest.
- Enzymatic Assessment.

2- Initial General Treatment :
** Memory aid “ MONA”
M >>
O >>
N >>
A >>

Morphine = pain killer 2-4mg / 5-10 min.
Oxygen : 4L / min.
Nitroglycerin : SL or I.V.
Aspirin : 160 – 325 mg (Chew).

3- Specific Treatment :
> Reperfusion therapy : only for
patients with S-T segment elevation or
new LBBB.

>Thrombolytic agents: (door – to –
needle time < 30 min).

> Primary PTCA: (door – to – dilation
time < 60 min

Conjunctive therapy:
combined with thrombolytic
agents :
- Aspirin.
- Heparin.

Adjunctive therapies:
Agents given instead of or in addition to
thrombolytic agents :
-

- IV nitroglycerin.
- B-Blockers.
- ACE – inhibitors especially in:
• Large infarction.
• Heart failure.
• Hypertension.

THANK YOU