Transcript دكتر سجادي

Diagnostic approach of
valvular myocardial and
pericardial disease
Amirreza Sajjadieh
Interventional Cardiologist
1392/11/13
Myocardial and Pericardial Diseases
Outlines:
• Introducation
• Myocardial diseases:
1. - Myocarditis
2. - Cardiomyopathy : 4 major types :
1. Dilated.
2. Hypertrophic.
3. Restrictive.
4. Arrhythmogenic right venticular.
• Pericardial diseas:
1. acute pericarditis
2. pericardial effusion and cardiac tamponade
3. constrictive pericarditis.
MYOCARDIAL DISEASES
Introduction Of Myocardial Diseases:
• Although the myocardium is involved in most types of heart
disease, the term myocarditis and cardiomyopathy are usually
reserved for conditions that primerly affect the heart muscle.
• So we are discussing today Myocardial diseases that is not due to
ischaemic, valvular or hypertensive heart disease or a known
infiltrative, metabolic/toxic or neuromuscular disorder
Myocardial diseases may be caused by:
1. an acute or chronic
inflammatory pathology
(myocarditis)
2. idiopathic myocardial disease
(cardiomyopathy).
Myocarditis
•
•
1.
2.
3.
4.
Acute inflammation of the myocardium.
It has many causes:
Idiopathic
Infective
Viral: Coxsackievirus, adenovirus, CMV, echovirus, influenza, polio, hepatitis, HIV.
Parasitic: Trypanosoma cruzi, Toxoplasma gondii (a cause of myocarditis in the newborn or
immunocompromised)
5. Bacterial: Streptococcus (most commonly rheumatic carditis), diphtheria (toxin-mediated
heart block common)
Cont.causes:
• Spirochaetal: Lyme disease (heart block common),leptospirosis.
• Fungal.
• Rickettsial.
• Toxic.
• Drugs: Causing hypersensitivity reactions, e.g. methyldopa,
penicillin, sulphonamides, antituberculous,modafinil.
• Radiation: May cause myocarditis but pericarditis more common.
• Autoimmune: An autoimmune form with autoactivated T cells and
organ specific antibodies may occur.
Pathology:
• In the acute phase myocarditic hearts are flabby with
focal haemorrhages; in chronic cases they are enlarged
and hypertrophied.
• Histologically an inflammatory infiltrate is present.
• lymphocytes predominating in viral causes.
• Polymorphonuclear cells in bacterial causes.
• eosinophils in allergic and hypersensitivity causes.
Clinical features:
• Myocarditis may be an acute or chronic
process.
• its clinical presentations range from:
an asymptomatic state associated with limited
and focal inflammation.
 fatigue, palpitations, chest pain, dyspnoea
and fulminant congestive cardiac failure due
to diffuse myocardial involvement.
Physical examination:
• includes soft heart sounds.
• a prominent third sound.
• often a tachycardia.
• A pericardial friction rub may be heard.
Investigations:
■ Chest X-ray may show some cardiac enlargement.
■ ECG demonstrates ST- and T wave abnormalities and arrhythmias.
■ Cardiac enzymes are elevated.
■ Viral antibody titres may be increased. However, since enteroviral
infection is common in the general population, the diagnosis
depends on the demonstration of acutely rising titres.
■ Endomyocardial biopsy may show acute inflammation but false
negatives are common by conventional criteria. Biopsy is of limited
value outside specialized units.
■ Viral RNA can be measured from biopsy material using polymerase
chain reaction (PCR). Specific diagnosis requires demonstration of
active viral replication within myocardial tissue.
CARDIOMYOPATHY
• Cardiomyopathies are a group of diseases of the myocardium
that affect the mechanical or electrical function of the heart.
• They are not secondary to coronary artery diseases,
hypertension, or congenital, valvular or pericardial
abnormalities.
• They are frequently genetic and may produce inappropriate
ventricular hypertrophy or dilatation and can be primarily a
cardiac disorder or part of a multi-system disease.
Four main types:
1. Dilated.
2. Hypertrophic.
3. Restrictive.
4. Arrhythmogenic right venticular.
1. Dilated cardiomyopathy (DCM):
• is characterized by dilatation of the ventricular chambers
and systolic dysfunction with preserved wall thickness.
• In about 25% of the patients it is a familial disease.
• Sporadic DCM can be caused by multiple conditions:
■ myocarditis – Coxsackie, adenoviruses, erythroviruses,
HIV, bacteria, fungae, mycobacteria, parasitic (Chagas’
disease)
■ toxins – alcohol, chemotherapy, metals (cobalt, lead,
mercury, arsenic)
■ autoimmune.
■ endocrine.
■ neuromuscular.
Clinical features:
•
•
•
•
•
•
DCM can present with:
heart failure.
cardiac arrhythmias.
conduction defects.
thromboembolism.
sudden death.
• Increasingly, evaluation of relatives of DCM patients is
allowing identification of early asymptomatic disease, prior
to the onset of these complications.
• Clinical evaluation should include a family history and
construction of a pedigree where appropriate.
Investigations:
• ■ Chest X-ray demonstrates generalized cardiac enlargement.
• ■ ECG may demonstrate diffuse non-specific ST segment and T
wave changes. Sinus tachycardia, conduction abnormalities and
arrhythmias are also seen.
• ■ Echocardiogram reveals dilatation of the left and/or right
ventricle with poor global contraction function.
• ■ Cardiac MR may demonstrate other aetiologies of left
ventricular dysfunction (e.g. previous myocardial infarction) or
demonstrate abnormal myocardial fibrosis. Cardiac MR is also
useful for identifying myocardial thrombus .
• ■ Coronary angiography should be performed to exclude coronary
artery disease in all individuals at risk (generally patients > 40 years
or younger if symptoms or risk factors are present).
• ■ Biopsy is generally not indicated outside specialist care.
2. Hypertrophic cardiomyopathy
(HCM)
• It is characterized by marked vantricular hypertrophy in the
absence of an alternate cause (e.g. aortic stenosis or
hypertension).
• Usually with disproportionate involvment of the
interventricular septum.
• The hypertrophic non-compliant vantricles impair diastolic
filling, so that stroke volume is reduced.
• Most cases are familial, autosomal dominant and caused by
mutation in genes coding for proteins that regulate
conraction, e.g troponin and B-myosin.
Clinical features:
Symptoms:
• ■ many are asymptomatic and are detected through family screening of an
affected individual or following a routine ECG examination.
• ■ chest pain, dyspnoea, syncope or pre-syncope (typically with exertion),
cardiac arrhythmias and sudden death are seen.
• ■ sudden death occurs at any age but the highest rates (up to 6% per
annum) occur in adolescents or young adults.
■ dyspnoea occurs due to impaired relaxation of the heart muscle or the
left ventricular outflow tract obstruction that occurs in some patients.
■ If a patient develops atrial fibrillation there is often a rapid
deterioration in clinical status due to the loss of atrial contraction and the
tachycardia – resulting in elevated left atrial pressure and acute
pulmonary oedema.
Signs:
• ■ double apical pulsation (forceful atrial
contraction producing a fourth heart sound).
• jerky carotid pulse because of rapid ejection
and sudden obstruction to left ventricular
outflow during systole
• ■ ejection systolic murmur due to left
ventricular outflow obstruction late in systole.
• ■ pan-systolic murmur due to mitra
regurgitation.
• ■ fourth heart sound (if not in AF).
Investigations:
• ■ ECG abnormalities of HCM include left ventricular hypertrophy,
ST and T wave changes, and abnormal Q waves especially in the
infero-lateral leads.
• ■ Echocardiography is usually diagnostic and in classical HCM
there is asymmetric left ventricular hypertrophy (involving the
septum more than the posterior wall), systolic anterior motion of
the mitral valve, and a vigorously contracting ventricle.
• ■ Cardiac MR can detect both the hypertrophy but also abnormal
myocardial fibrosis.
• ■Genetic analysis, where available, may confirm the diagnosis and
provide prognostic information for the patient and relatives.
Treatment:
• The management of HCM includes treatment of symptoms and the
prevention of sudden cardiac death in the patient and relatives.
• Risk factors for sudden death:
• ■ massive left ventricular hypertrophy (> 30 mm on
echocardiography).
• ■ family history of sudden cardiac death (< 50 years old).
• ■ non-sustained ventricular tachycardia on 24-hour Holter
monitoring.
• ■ prior unexplained syncope.
• ■ abnormal blood pressure response on exercise (flat or
hypotensive response).
• patients with two or more risk factors should be
assessed for implantable cardioverter- defibrillator
(ICD).
• In patients in whom the risk is less, amiodarone is an
appropriate alternative.
• Chest pain and dyspnoea are treated with B-blockers
and verapamil.
• Family members should be screened for evidence for
evidence of disease by ECG and echocardiography.
Restrictive cardiomyopathy
• In this rare condition, ventricular filling is
impaired because the ventricles are 'stiff' .
• This leads to  high atrial pressures with
atrial hypertrophy  dilatation  later atrial
fibrillation.
Restrictive cardiomyopathy
Aetiology:
1. Amyloidosis is the most common cause of
restrictive cardiomyopathy in the UK.
2. other forms of infiltration (e.g. glycogen
storage diseases), idiopathic perimyocyte
fibrosis .
Restrictive cardiomyopathy
Clinical features :
1. Dyspnoea.
2. fatigue .
3. embolic symptoms are the presenting features.
NB : Restriction to ventricular filling (especially
right) results in persistently elevated venous
pressures, consequent hepatic enlargement,
ascites, and dependent oedema.
Restrictive cardiomyopathy
1.
Investigations:
Chest X-ray: may show pulmonary venous congestion. The heart can be
normal or show cardiomegaly and/or atrial enlargement.
2.
ECG usually has low-voltage and ST segment and T wave abnormalities.
3.
Echocardiogram shows symmetrical myocardial thickening and often a
normal systolic ejection fraction, but impaired ventricular filling.
4.
Cardiac catheterization and haemodynamic studies help distinction from
constrictive pericarditis.
5.
Endomyocardial biopsy in contrast with other cardiomyopathies is often
useful in this condition and may permit a specific diagnosis such as
amyloidosis to be made.
PERICARDIAL DISEASES
Pericardial disease
The pericardium acts as a protective covering for the
heart.
It consists of two separate layers, the inner visceral
pericardium and the outer parietal pericardium.
The visceral pericardium reflects back upon it self at the level
of the great vessels to join the parietal pericardium, thus
forming a sac.
The pericardial sac contains up to 50 mLof pericardial fluid in the
normal heart, although this is a potential space for fluid to collect.
The pericardium serves to lubricate the surface of the heart,
prevents deformation and dislocation of the heart and acts as a
barrier to the spread of infection.
Presentations of pericardial disease
include:
• acute pericarditis.
• a pericardial effusion and cardiac
tamponade
• constrictive pericarditis.
1-acute pericarditis
• This refers to inflammation of the
pericardium. Classically, fibrinous material is
deposited into the pericardial space and
pericardial effusion often occurs.
• Acute pericarditis has numerous aetiologies
Most commonly in the UK, it is due to viral
infection and myocardial infarction, although
in many
• cases the cause is unknown.
Type
• Viral pericarditis: The most common viral causes are
Coxsackie B virus and echovirus. Viral pericarditis is
usually painful but has a short time course and rarely
long-term effects.
• Post-myocardial infarction pericarditis: occurs in about 20%
of patients in the first few days following MI.. It may be
difficult to differentiate this pain from recurrent angina when
it occurs early (day 1-2 post- infarct) but a good history of the
pain and serial ECG monitoring is helpful.
• Pericarditis may also occur later on in the recovery phase after
infarction.
• Uraemic pericarditis: is due to irritation of the
pericardium by accumulating toxins. It can occur in 610% of patients with advanced renal failure if dialysis is
delayed.
• Bacterial pericarditis :may rarely occur with septicaemia or
pneumonia or it may stem from an early postoperative
infection after thoracic surgery or trauma or may complicate
endocarditis.
• Staphylococcus aureus is a frequent cause of purulent
pericarditis in HIV patients. This form of pericarditis,
especially staphylococcal, is fulminant and often fatal.
• Other endemic infectious pericarditis includes:
mycoplasmosis and Lyme pericarditis which are often
effusive and require pericardial drainage. The diagnosis
is based on serological tests of pericardial fluid and
identification of organisms in pericardial or myocardial
biopsies.
• Tuberculous pericarditis: usually presents with
chronic low-grade fever, parti cularly in the evening,
associated with features of acute pericarditis,
dyspnoea, malaise, night sweats and weight loss.
• Fungal pericarditis: is a common complication of
endemic fungal infections, such as histoplasmosis
and coccidioidomycosis but may be also caused by
Candida albicans, especially in
immunocompromised patients, drug addicts or
after cardiac surgery.
• Malignant pericarditis. :Carcinoma of the
bronchus,
• carcinoma of the breast and Hodgkin's
lymphoma are the most common causes of
malignant pericarditis. Leukaemia and
malignant melanoma are also associated with
pericarditis.
etiology
• Infectious pericarditis
Viral (Coxsackievirus, echovirus, mumps, herpes, HIV)
Bacterial (staphylococcus, streptococcus,
pneumococcus, meningococcus, Haemophilu influenzae, mycoplasmosis,
borreliosis, Chlamydia)
Tuberculous
Fungal (histoplasmosis, coccidioidomycosis, Candida)
• II. Post-myocardial infarction pericarditis
Acute myocardial infarction (early)
Dressler's syndrome (late)
• III. Malignant pericarditis
Primary tumours of the heart (mesothelioma) Metastatic
pericarditis (breast and lung carcinoma, lymphoma,
leukaemia, melanoma)
• IV. Uraemic pericarditis
• V. Myxoedematous pericarditis
• VI. Chylopericardium
• VII. Autoimmune pericarditis
Collagen-vascular (rheumatoid arthritis, rheumatic fever,
systemic lupus erythematosus, scleroderma)
Drug-induced (procainamide, hydralazine, isoniazid,
doxorubicin, cyclophosphamides)
• VIII. Post-radiation pericarditis
• IX. Post-surgical pericarditis
Postpericardiotomy syndrome
• X. Post-traumatic pericarditis
• XI. Familial and idiopathic pericarditis
Clinical features
• Pericardial inflammation produces sharp central
chest
• pain exacerbated by movement, respiration and
lyingdown. It is typically relieved by sitting forward.
• It may be referred to the neck or shoulders.
• The main differential diagnoses are angina
• and pleurisy.
The classical clinical sign is
• a pericardial friction rub occurring in three phases corresponding to atrial
systole, ventricular systole and ventricular diastole. It may also be heard as
a biphasic 'to and fro' rub.
• The rub is heard best with the diaphragm of the stethoscope at the lower
left sternal edge at the end of expiration with the patient
leaning forward.
• There is usually a fever, leucocytosis or lymphocytosis when pericarditis is
due to viral or bacterial infection, rheumatic fever or myocardial
infarction.
• Large pericardial effusion can compress adjacent bronchi and lung tissue
and may cause dyspnoea.
•
•
Investigations
• ECG is diagnostic. There is concave-upwards (saddle-shaped)
ST elevation .These changes evolve over time, with resolution of the ST elevation,
T wave flattening/inversion and finally T wave normalization.
• The early ECG changes must be differentiated from ST
• elevation found in myocardial infarction .
•
Sinus tachycardia may result from fever or haemodynamic
• embarrassment, and rhythm and conduction
• abnormalities may be present if myocardium is involved.
•
Cardiac enzymes should be assayed as they may be
• elevated if there is associated myocarditis
•
Chest X ray, echocardiograms and radionucleotide
• scans are of little value in un complicated acute
• pericarditis.
ECGs associated with pericarditis.
(a) Acute pericarditis. Note the raised ST segment, concave
upwards (arrow),
(b) Chronic phase of pericarditis :associated with a pericardial effusion. Note the T
wave flattening and inversion and the alternation of the QRS
amplitude (QRS alternans).
(c) The same patient after evacuation of the pericardial fluid. Note that the QRS
voltage has increased and the T waves have returned to normal.
2-Pericardial effusion and cardiac
tamponade
• A pericardial effusion is a collection of fluid
within the potential space of the serous
pericardial sac as in the figure
• commonly accompanying an episode of acute
pericarditis.
• When a large volume collects in this space,
ventricular filling is compromised leading to
embarrassment of the circulation. This is
known as cardiac tamponade.
Chest X-ray showing a pericardial effusion,
the heart appears globular.
Chest X-ray showing a peric ardial
calcification (arrow).
Valvular Heart Disease
Types
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•
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•
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Mitral Stenosis
Mitral Regurgitation
Mitral Valve Prolapse
Aortic Stenosis
Aortic regurgitation
Tricuspid valve is affected infrequently
– Tricuspid stenosis – causes Rt HF
– Tricuspid regurgitation –causes venous overload
Rheumatic Heart Disease
• Inflammatory process that may affect the
myocardium, pericardium and or endocardium
• Usually results in distortion and scarring of the
valves
Rheumatic Heart Disease, cont.
• Subjective symptoms
– Prior history of
rheumatic fever
– General malaise
– Pain – may or may not
be present
• Objective symptoms
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–
–
–
Temperature
Murmurs
Dyspnea
polyarthritis
Rheumatic Heart Disease
• Diagnosis
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H/P
WBC and ESR
C-reactive protein
Cardiac enzymes
EKG
Chest x-ray
Echo
Cardiac cath
Cardiac output
Rheumatic Heart Disease
• Nursing Care
– Vital signs
– Rest and quiet environment
– Give antibiotics, digitalis, and diuretics
– Provide adequate nutrition
– Monitor I/O
– Explain treatment and home care
Mitral Stenosis
•
•
•
•
•
•
•
•
Usually results from rheumatic carditis
Is a thickening by fibrosis or calcification
Can be caused by tumors, calcium and thrombus
Valve leaflets fuse and become stiff and the cordae tendineae
contract
These narrows the opening and prevents normal blood flow
from the LA to the LV
LA pressure increases, left atrium dilates, PAP increases, and
the RV hypertrophies
Pulmonary congestion and right sided heart failure occurs
Followed by decreased preload and CO decreases
Mitral Stenosis, cont.
• Mild – asymptomatic
• With progression – dyspnea, orthopneas, dry cough,
hemoptysis, and pulmonary edema may appear as
hypertension and congestion progresses
• Right sided heart failure symptoms occur later
• S/S
– Pulse may be normal to A-Fib
– Apical diastolic murmur is heard
Mitral Regurgitation
• Primarily caused by rheumatic heart disease, but may be
caused by papillary muscle rupture form congenital, infective
endocarditis or ischemic heart disease
• Abnormality prevents the valve from closing
• Blood flows back into the right atrium during systole
• During diastole the regurg output flows into the LV with the
normal blood flow and increases the volume into the LV
• Progression is slowly – fatigue, chronic weakness, dyspnea,
anxiety, palpitations
• May have A-fib and changes of LV failure
• May develop right sided failure as well
Mitral Valve Prolapse
• Cause is variable and may be associated with
congenital defects
• More common in women
• Valvular leaflets enlarge and prolapse into the LA
during systole
• Most are asymptomatic
• Some may report chest pain, palpitations or exercise
intolerance
• May have dizziness, syncope and palpitations
associated with dysrhythmias
• May have audible click and murmur
Aortic Stenosis
• Valve becomes stiff and fibrotic, impeding blood flow with LV contraction
• Results in LV hypertrophy, increased O2 demands, and pulmonary
congestion
• Causes – rheumatic fever, congenital, arthrosclerosis
• Atherosclerosis and calcification is primary cause in the elderly
• Complications – right sided heart failure, pulmonary edema, and A-fib
• S/S – Early: dyspnea, angina, syncope
Late: marked fatigue, debilitation, and
peripheral cyanosis, crescendodecrescendo murmur is
heard
Aortic Regurgitation
• Aortic valve leaflets do not close properly during diastole
• The valve ring that attaches to the leaflets may be dilated, loose, or
deformed
• The ventricle dilates to accommodate the ^ blood volume and
hypertrophies
• Causes: infective endocarditis, congenital, hypertension, Marfan’s
• May remain asymptomatic for years
• Develop dyspnea, orthopnea, palpitations, ,and angina
• May have ^ systolic pressure with bounding pulse
• Have a high pitch, blowing, decrescendo diastolic murmur
Assessment for Valve Dysfunction
• Subjective symptoms
– Fatigue
– Weakness
– General malaise
– Dyspnea on exertion
– Dizziness
– Chest pain or discomfort
– Weight gain
– Prior history of rheumatic heart disease
Assessment, cont.
• Objective symptoms
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Orthopnea
Dyspnea, rales
Pink-tinged sputum
Murmurs
Palpitations
Cyanosis, capillary refill
Edema
Dysrhythmias
Restlessness
Diagnosis
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•
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•
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History and physical findings
EKG
Chest x-ray
Cardiac cath
Echocardiogram
Anatomy
Acquired Heart Disease
Small Heart
RADIOGRAPHIC FEATURES OF AORTIC STENOSIS
•
•
•
•
•
Enlargement of the ascending aorta
due to poststenotic dilatation
Mild or no cardiomegaly in
compensated stage
Substantial cardiomegaly occurs
only after myocardial failure has
ensued
No pulmonary venous hypertension
or pulmonary edema is seen during
most of the course of this disease
Calcification of aortic valve may be
discernible on radiograph but is
more readily shown on CT
RADIOGRAPHIC FEATURES OF ARTERIAL
HYPERTENSION
•
•
•
Enlargement of the thoracic aorta—
ascending, arch, and descending
aorta
Mild or no cardiomegaly until the
onset of myocardial failure
No pulmonary edema or pulmonary
venous hypertension until the
occurrence of diastolic dysfunction
due to severe left ventricular
hypertrophy or myocardial failure
RADIOGRAPHIC FEATURES OF MITRAL STENOSES
•
•
•
•
•
•
Pulmonary venous hypertension or edema
is present
Pulmonary edema may be observed
intermittently
Mild cardiomegaly is seen in isolated mitral
stenoses
Enlargement of the left atrium is
characteristic
Enlargement of the left atrial appendage is
frequent and suggests a rheumatic etiology
Right ventricular enlargement indicates
some degree of pulmonary arterial
hypertension or associated tricuspid
regurgitation.
RADIOGRAPHIC FEATURES OF MITRAL STENOSES
•
•
•
Enlargement of the pulmonary arterial
segment is indicative of associated
pulmonary arterial hypertension
Right ventricular enlargement in the
absence of prominence of the main
pulmonary artery suggests associated
tricuspid regurgitation. The right
atrium is also enlarged with tricuspid
regurgitation
The ascending aorta and aortic arch are
usually inconspicuous in isolated mitral
stenosis. Even slight enlargement of
the thoracic aorta raises the question
of associated aortic valve disease
RADIOGRAPHIC FEATURES OF HYPERTROPHIC
CARDIOMYOPATHY
•
•
•
•
•
Normal in most patients
Mild cardiomegaly and pulmonary
venous hypertension in a minority
of patients
Left atrial enlargement can be
caused by associated mitral
insufficiency or reduced left
ventricular compliance
In the obstructive form (subaortic
stenosis), ascending aortic
enlargement is infrequent
Left ventricular enlargement may
occur in end-stage disease
RADIOGRAPHIC FEATURES OF RESTRICTIVE
CARDIOMYOPATHY
•
•
•
•
•
•
Pulmonary venous hypertension is
typical
Pulmonary edema may occur
intermittently
Normal heart size or mild
cardiomegaly in most patients
Left atrial enlargement
Left atrial appendage is typically
not enlarged
Moderate to severe cardiomegaly
can ensue in end-stage disease
RADIOGRAPHIC FEATURES OF ACUTE MYOCARDIAL
INFARCTION
•
•
•
•
Normal chest x-ray in about 50%
of first acute infarctions
Normal heart size with
pulmonary venous hypertension
or pulmonary edema in about
50% of first acute infarctions
Cardiomegaly is usually
indicative of acute infarction in a
patient with history of previous
infarctions
Cardiomegaly may be indicative
of ischemic cardiomyopathy
RADIOGRAPHIC FEATURES OF ACUTE MYOCARDIAL
INFARCTION
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•
•
•
Signs of complication of acute
myocardial infarction
Intractable pulmonary edema
may occur with papillary muscle
rupture (mitral regurgitation) or
ventricular septal rupture (left to
right shunt).
Enlarged cardiac silhouette may
be caused by pericardial
effusion.
Abnormal cardiac contour may
be a sign of true (bulge of the
anterolateral or apical regions)
or false (bulge of the posterior
or diaphragmatic regions)
aneurysms
RADIOGRAPHIC FEATURES OF CONSTRICTIVE
PERICARDITIS
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•
•
•
•
Pulmonary venous hypertension
Normal heart size or mild
cardiomegaly
Left atrial enlargement may be
discernible
Flattened cardiac contours are
pathognomonic but infrequently
observed
Calcification of the cardiac margin,
especially the atrioventricular and
interventricular grooves
Acquired Heart Disease
Large Heart
RADIOGRAPHIC FEATURES OF AORTIC
REGURGITATION
•
•
•
•
Absence of pulmonary venous
hypertension or pulmonary edema
until late in the course of this lesion
Moderate to severe cardiomegaly
Left ventricular enlargement
Enlargement of ascending aorta and
aortic arch
RADIOGRAPHIC FEATURES OF MITRAL
REGURGITATION
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•
•
•
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Variable degree of pulmonary
venous hypertensive or pulmonary
edema (less severe than with mitral
stenosis)
Moderate to severe cardiomegaly
Left ventricular enlargement
Left atrial enlargement
Enlargement of left atrial
appendage
RADIOGRAPHIC FEATURES OF TRICUSPID
REGURGITATION
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•
•
•
•
No pulmonary venous hypertension
or pulmonary edema (isolated
tricuspid regurgitation)
Pulmonary venous hypertension or
edema indicates associated mitral
valve disease
Moderate to severe cardiomegaly
Right ventricular enlargement
Right atrial enlargement
RADIOGRAPHIC FEATURES OF CONGESTIVE (DILATED)
CARDIOMYOPATHY
•
•
•
•
Pulmonary venous hypertension or
pulmonary edema may be but is
not invariably present
Moderate to severe cardiomegaly
Left ventricular enlargement
Left atrial enlargement is
infrequently evident but can be
caused by mitral regurgitation
caused by left ventricular
enlargement
Congestive Heart Failure
Cardiomegaly, increased pulmonary vascular
markings, fluid in the horizontal fissure
CHF
What do the arrows
indicate?
Kerley B Lines
Short (1 -2 cm)
white lines at the
lung bases,
perpendicular to the
pleural surface
representing
distended
interlobular septa
RADIOGRAPHIC FEATURES OF PERICARDIAL
EFFUSION
•
•
•
•
No pulmonary venous hypertension
or pulmonary edema
Moderate to severe enlargement of
cardiac silhouette
Associated pleural effusion is not
uncommon
Specific features, such as “fat pad”
and/or “variable density” signs, are
infrequently evident
ENLARGEMENT OF MAIN PULMONARY ARTERY
•
Etiology
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Pulmonary arterial hypertension
Excess pulmonary blood flow (left to
right shunts, chronic high output states)
Valvular pulmonic stenosis
Pulmonary regurgitation
Congenital absent pulmonary valve
(aneurysmal pulmonary artery)
Absence of left pericardium
Aneurysm of pulmonary artery
Idiopathic dilatation of pulmonary
artery
Cardiac Calcification
•
Ascending aortic calcification
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Mitral annular calcification
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Dense C-shaped calcification in the region of the mitral valve.
It may be a causative factor of mitral regurgitation.
It is frequently observed in apparently normal elderly patients.
Aortic annular calcification
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•
Most frequently observed on the right anterolateral margin of the ascending aorta in elderly
individuals, especially in the presence of aortic valve disease.
In the past, it was considered to be a characteristic of syphilitic aortitis.
A circular calcification in the region of the aortic valve.
Extension of this calcification into the region of the conducting system can produce complete heart
failure.
Valvular calcification (aortic and mitral).
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Calcification of the aortic valve of sufficient density and extent to be visualized on the radiograph is
nearly always associated with hemodynamically important aortic stenosis (gradient more than 50
mm Hg).
Cardiac Calcification
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Coronary arterial calcification
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Left ventricular mural calcification
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Most frequently located in the anterolateral or apical regions of the left ventricle and marks the site
of a transmural MI or aneurysm.
Pericardial calcification
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Coronary arterial calcification is frequently observed by fluoroscopy or CT.
It must be both dense and extensive to be recognized on the thoracic radiograph.
Indicative of constrictive pericarditis.
Located usually in the interventricular or atrioventricular grooves of the heart.
Unusual sites
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Intracardiac tumor (left atrial myxoma),
Pericardial tumor (dermoid), or
Healed granulomas (myocardial tuberculoma).
An extremely rare process of the left ventricle, Loeffler's eosinophilic fibroplasia, can cause
calcification of the left ventricular wall.
Cardiac Calcification
Cardiac CT Angiography
Cardiac CT Angiography
Coronary CT angiography
Coronary CT angiography