Transcript CORONARY ARTERY DISEASE

CORONARY ARTERY
DISEASE/MI
By Henri Godbold MD
Med Peds
Noon Conference 9/21/2006
ETIOLOGY
• Manifestation of atheroma with preserved
caliber of lumen
• Rupture of the plaque’s fibrous cap
causing a thrombosis
• The clot overwhelms the endogenous
fibrinolytic mechanism may propagate and
lead to occlusion
CLINICAL MANEFESTATIONS
• Transient ischemic cardiac events if
prolonged can lead to necrosis and
scarring with or without MI
• Patients can present with cardiomegaly
and heart failure secondary to ischemia of
damage left ventricle
ANGINA
• Chest pain caused by mismatch of myocardial
O2 supply & demand
• Classified as:
– Stable (usually from concentric plaque)
• Usually 2º atherosclerotic obstruction
– Unstable (usually from an ulcerated, ruptured
plaque)-nidus for platelet aggregation
• New onset or increased frequency
Only about 20% of pts. with ischemic ST
changes have classic angina
ANGINA TREATMENT
• Modify risk factors & correct aggravating factors
(anemia, HTN, drug abuse, non-compliance)
• Emphasize meds. known to prolong survival
post-MI
• ASA also should be standard therapy
• CCRB and nitrates may be useful for symptoms
• Careful with combining meds. with similar effects
(ie. Beta blockers, and verapamil)
ASSOCIATED SYMPTOMS
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Dyspnea
Diaphoresis
Dizziness
Syncope
Palpations
Deep breathing pain
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Nausea and vomiting
Edema
Orthropnea
Paroxysmal nocturnal
dyspnea
• Positional pain
CARDIAC RISK FACTORS
Absolute
- FH
- smoking
- DM
- HTN
- Hyperlipidemia
(LDL> 130, HDL<35)
- AGE
(men>45,Female>55)
Relative
• Obesity
• sedentary life
• stress
• postmenopausal state
OTHER
• Hx CVA and PVD
disease
ROLE OF INFLAMATION AS A
RISK FACTOR
• Vascular injury
• Lipid peroxidation: along with the effects
of HTN, DM, and smoking amplify the
harmful effects of oxidized LDL cholesterol
• Chronic inflammation promoting
athersclerotic plaque which rupture and
thrombose in vessels
CIRCULATING MEDIATOR
Inflammatory process:
• Acute phase reactants
• Cell adhesion molecules
• Inflammatory Markers–
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C-reactive protein (CRP)
IL-6
serum amylase A
TNF alpha
selectins
macrophage inhibitor cytokines 1
CD40 ligands
Characteristic of CRP
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High sensitivity
Assay well standardized
Widely available
Strong predictor of future myocardial
infarctions and stroke
• High plasma concentration are associated
with a 1.5-to-7 fold increase in the relative
risk of symptomatic atherosclerosis
Role of homocysteine in risk
stratification
• Statistically significant but modest
increase in risk of CAD events
• Folic acid can reduce serum elevation
• Neither prospective or randomized trails
show reduction in elevation reduces CHD
risk
• Routine measurement are not warranted
MANAGEMENT APPROACH
• Goals are reduce coronary morbidity and
mortality via:
• Primary prevention: reducing risk of first
event
• Secondary prevention: reducing risk of
event in person with established
disease
• Correct reversible risk factors: smoking,
hypertension, uncontrolled DM, obesity,
stress, life style modification
• Risk Stratification (Table 27.4)
CAD Risk Association with Lipoprotein
Cholesterol Abnormalities
Lipoprotein Levels (mg/dl)
cholesterol
LDL
HDL
VLDL
<130
130-159
>160
>65(chol/HDL ratio >4.5)
Estimated
CHD Risk
low
moderate
high
low
<35(chol/HDL ratio <4.5)
Mod-high
50-100(or fasting TG 250-500) low
>100(or fasting TG >500)
? high
DIAGNOSIS
• First step: estimate pretest probability
base on know CV risk factor(age, gender)
and symptoms) Is as follows:
• Low(<10%):
- Asymtomatic men and women of all
ages
- Women younger than 50 yrs or order
with typical angina
• Intermediate (10%-90%):
– Men of all ages with atypical angina
– Women 50yrs or older with atypical angina
– Women 30-59yrs with typical angina
• High (>90%):
– Men 40yrs or older with typical angina
– Women 60yrs or older with typical angina
TESTING MODALITIES
Cardiac Stress Testing:
• Preferred approach to assessing CAD in patients with suspected or
known disease
• Goal to induce myocardial ischemia by increasing myocardial
oxygen demand
• Indicated for the diagnosis of myocardial ischemia
• Indicated for ECG abnormalities WPW, >1mm resting ST
depression, LBBB
• After cardiac catherization to identify if ischemia is present in the
distribution of the coronary lesion identified
Exercise Stress Test
• Preferred to pharmacologic stress
• Provides data on exercise capacity and
hemodynamic response to exercise
• Patients with normal baseline ECG, ischemia
can be detected using ECG monitoring
• Patient with abnormal baseline ECG, who
undergo pharmacologic or exercise stress
testing, either echocardiographic or radionuclide
imaging is needed to detect ischemia
Stress Echo
• Detects provoked regional ventricular wall
motion abnormality
• Uses myocardial perfusion imaging:
– Sestambi(Cardiolite) radionuclide tracer,
decrease uptake represent the area of
ischemia measure by scintigraphy
– Vasodilator agents: Adenosine, Persantine
and dobutamine
Postitron Emission
Tomography(PET)
• More specific and sensitive than
conventional nuclear imaging
• Can combine high resolution CT imaging
of anatomy and function for noninvasive
assessment of coronary disease
Coronary Angiography
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Invasive
Pretest probability of disease is high
Stress test is positive
Symptomatic presentation despite a
negative stress test
• Diagnosis and therapy can be preformed
simultaneosly (i.e. percutaneous
revascularization)
Indication Revascularization in
Patient with Chronic Stable Angina
CABG is recommended for
• Left main coronary artery stenosis
• 3-vessel CAD(greatest survival benefit with EF
<50%)
• 2-vessel CAD and proximal LAD stenosis with
LV EF <50% or ischemia on noninvasive testing
• 1-2 vessel CAD w/o prox LAD stenosis who
survived sudden cardiac death or sustain VT
• Percutaneous Coronary Intervention (PCI)
is recommended for
– Nondiabetics w/ 2-vessel CAD
– Proximal LAD stenosis
– Normal LV function w/ anatomy amenable to
PCI
• Either CABG or PCI recommended
– 1 or 2 vessel CAD w/o prox LAD stenosis and
high risk criteria on noninvasive testing
– Prior CABG or PCI w/ recurrent stenosis and
a large area of ischemia or high risk criteria
on noninvasive testing
– Symptoms refractory to medical therapy with
an acceptable risk of revascularization
TREATMENT
• Vigorous lifestyle modification- low fat and
cholesterol diet; regular exercise; and
smoking cessation
• Aspirin- antiplatelet
• Statin- lipid-lowering
• Beta blocker and CCB- reducing
myocardial oxygen consumption
• ACE inhibitor-especially patients w/ DM
and /or left ventricle systolic dysfunction
• Nitrates: reduce angina by peripheral
venodilation and coronary artery dilation
– To avoid tolerance need atleast 8hrs daily free
period
– Do not use in patients receiving
phosphodiesterase type 5 inhibitors(
sildenafil, vardenafil, tadalafil) lead to life
threatening hypotension
Hyperlipidemia Drugs
HMG-CoA reductase inhibitor (Statins)
• First line
• Inhibits intracellular cholesterol and increase
clearence LDL
• Starting dose 10-20mg/d w/ max dose 80mg/d
• Adverse effects hepatocellular dysfunction and
myositis
• Monitor transaminases intially then f/u
measurements 6 month and 1 year
Bile Acid Sequestrants
• Interrupt enterohepatic circulation in the
gut
• Highly effective used in combination in
those high risk patients
• Side effects constipation, bloating,
heartburn and nausea
Ezetimibe
• Block absorption from the gut
• Inhibits cholesterol transport by interfering
with specific transporters proteins and
dose not interfering w/ other drugs and fatsoluble vitamins
• Lowers LDL by 15 to 20%; If use with
statin, provides additional 15% reduction
Niacin( B-complex vitamin)
• Inhibits mobilization of free FA from fat
cells to the liver
• Raises HDL 15% to 35%
• Lowers triglycerides 20% to 50% and
LDLs 5% to 25%
• Side affects flushing, pruritis, PUD,
hyperglycemia, rashes
Fibrates(Gemfibrozil and Fenofibrate)
• Not first-line
• Decreases VLDL synthesis enhancing
clearance
• Raises HDL cholesterol
• Well tolerated except in combo w/ statins
possible rhabdomyolysis
Nonprescriptions dietary
Supplements
Omega-3 Fish Oils
– Decreases VLDL, and platelet inhibition
Antioxidant vitamins
– Capable of increasing LDL resistance to oxidative changes and
reduce the risk of arterial wall injury
Garlic, Fiber, and Red yeast extract
Treatment Thresholds
Recommendation of NCEP Panel
• High risk or CAD plus multiple risk factor
• LDL cholesterol threshold 100mg/dl, treatment
goal <70mg/d
• Moderately high risk(no CAD, multiple risk
factor and 10 yr CAD risk 10%-20%)
• LDL cholesterol threshold 130mg/dl, treatment
goal <100mg/dl
• Moderate risk with 2 or more CAD risk
Factors (10yr risk probability is <10%)
– LDL cholesterol cut off 160mg/dl
• Fewer than 2 CAD risk factors
– LDL cholesterol >190mg/dl require drug rx
– Optional rx for levels between 160-190mg/dl
• Isolated low HDL cholesterol
– Treatment with statin seems to lower CAD
morbidity
– Even though the strong inverse relationship
between HDL levels and CHD risk, there is
no data showing that raising HDL alone
significantly reduces CAD mortality
• Primary Prevention
– NECP target LDL Cholesterol <130mg/dl,
ATPIII optimal level <100mg/dl and target of
less than 100mg/dl for person with moderate
high CAD risk
• Secondary Prevention
– LDL cholesterol < 100mg/dl with an optimal
goal of <70mg/dl for very high risk patients
ACUTE MYOCARDIAL
INFARCTION(AMI)
Overview
• 15% are asymptomatic
• Women more likely to have silent infarcts
• Differential diagnosis of prolonged chest
pain: AMI, aortic dissection, pericarditis,
esophageal problems, biliary tree,
pneumothorax, pulmonary embolism,
pleurisy, chest wall problems, and
psychogenic
• Arrhythmias in the first 48 hrs are due to
ischemia
• MR due to papillary muscle dysfuntion is seen
with inferior wall MIs
• VSD is seen with anterior and inferior MIs
• Inferior MIs are associated with more stable
arrhythmias
• Anterior MIs can result with poorer prognosis
associated with Mobitz II and BBBs
• Both anterior and inferior MIs can result in septal
wall rupture
Acute Coronary Syndrome (ACS)
NSTEMI(non Q wave MI)/UA: episodic
cessation of coronary blood flow or
vasospasms(prinzmetal’s) or drug
induce, like cocaine
• NSTEMI: Detectable release of biological
markers(Tnp I, T, MB isoenzymes) hours
after the onset of ischemic chest pain
•
Unstable angina(UA): no detectable
markers released
• STEMI(Q wave MI)
– most often by occlusive thrombus
– Rule out other life-threatening conditions (i.e. aortic
dissection, PE, tension pneumothorax, esophageal
rupture, perforated ulcer)
– Risk stratification-TIMI risk score
– ID higher risk patients for adverse event particularly
with anterior wall MIs
– Cardiac marker helpful but do not delay
implementation of reperfusion therapy, if not
contraindicated
TIMI RISK SCORE PATIENTS
WITH DIAGNOSIS STEMI
• Prognostic variables
Age >75 yrs
Age 65-75yrs
DM, HTN, or angina
• PE
SBP <100mm Hg
HR > 100/min
Killip class II-IV
wt < 67kg (150 lb)
Points
3
2
1
3
2
2
1
• Prognostic Variables
Points
Presentation
Ant. ST elevation or LBBB
1
Time to reperfusion > 4 hrs
1
Risk score = total points (0-14) correlates
30-day mortality rate (%) with 0 risk=0.8%, 5
risk=12%, and >8 risk=36%
Myocardial Infarction
Marker
Initial
elevation
Myoglobin 1-4 hrs.
Peak
elevation
6-7 hrs.
Return to
normal
24 hrs.
Troponin I 3-12 hrs.
24 hrs.
7-10 days
CKMB
3-12 hrs.
20 hrs.
2-3 days
CKMB
isoform
LDH
2-6 hrs.
18 hrs.
2 days
10 hrs.
1-2 days
10-14 days
• ST elevation: Q-wave(transmural infarct) or Non
Q wave subendocardial infarct)MI
– Not frequently seen
– Earlist changes is hyperacute or peaked T waves
– ST segment elevation in leads corresponding to
involved region of myocardial damage
– Initially J point elevation and concave ST segments
- Over time ST segments becomes convex
or rounded upwards
- ST segment indistinguishable from T waves
- QRS-T complex resemble a monophasic
action potential
- Initial Q waves develop several hrs to days
and the loss of R wave amplitude
Abnormal Q wave criteria:
• Q waves in leads V1 to V3 or a Q wave
greater than or equal 30 msec in leads I,
II, aVL, aVF, or V4 to V6
• Must be present in two contiguous leads
and a depth greater than or equal 1mm
• Overtime Ist 2 wks or several hrs after the
event R wave amplitude is markly reduced
• Q waves deepen
Overtime, several hrs or weeks after the
event
– R wave amplitude is markedly reduced
– Q-wave deepens
– T waves become inverted
Management of UA and NSTEMI
STEMI/New LBBB
STEMI or New LBBB
Give ASA, beta blockers,
nitrates prn, GP IIb/IIIa, UHF
or LMWH & monitor rhythm
Fibrinolytic therapy
if not contraindicated
and if PCI not
immediately available
**PCI within
12 hrs. of CP
Onset and within 90
Minutes of arrival to ED
PCI
STEMI/New LBBB
• Consider emergent reperfusion (fibrinolytics
or PCI) in ALL pts. that present with STEMI
or new LBBB within 12 hrs. of onset of
symptoms and who are < age 75
• Fibrinolytics
– LBBB benefits most
anterior>inferior (amt. of myocardium saved)
– NSTEMI (not much myocardium lost), the risks of
fibrinolytics outweighs the benefits
– So, ONLY give fibrinolytics to STEMI or NEW
LBBB or RBBB
Actually shown to increase mortality in NSTEMI
Medical Therapy for ACS STEMI
• Fibrionolytic (reteplase, tenectaplase)
– Indications: PCI unavailable
– timing: <6-12 hrs
– CI: ICB, chronic severe HTN, elderly
• Glycoproteins IIb/IIIa inhibitors: (Abciximab)
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Indications: All ACS
timing: on decision to go to cath lab
CI: CABG, coagulopathy, renal failure
Typically not given to those with UA/NSTEMI unless
PCI is anticipated
– Give along with ASA & heparin in those that PCI is
likily
Contraindication to fibrinolytics
– Absolute
• Previous hemorrhagic stroke at ANY time; other CV events within one year
• Intracranial neoplasm
• Active internal bleeding
• Suspected aortic dissection
– Relative
• Persistent BP>180/110
• Remote CVA (>1year)
• INR>2-3; bleeding problem
• Recent (2-4 wks) major trauma
• Non-compressible vascular puncture
• Previous exposure to streptokinase/antistreplase
• Pregnancy
• Active peptic ulcer
• Chronic HTN
• Narcotic analgesics: (Morphine)
– Indications: Severe pain
– Timing: Presentation
– CI: Respiratory depression
• Antithrombotics: (Heparin, LMWH)
– Indications: ALL ACS (except those who will receive
streptokinase)
– Timing: Presentation
– CI: thrombocytopenia, drug allergy
– Heparin is required if using t-PA, r-PA, or TNK
– LMWH is better in pts. with NSTEMI
• Nitrates: sublingual, oral, IV
– Indications: Angina
– Timing: Presentation
– CI: Hypotension
• Beta-Blockers
– Indications: Active ischemic symptoms and
prophylaxis
– Timing: On admission in CCU or ED
– CI: CHF, bradycardia, asthma
• Antiplatlets agents:(Clopidogrel, ASA)
– Indication: antiplatlet unless CI
– Timing: On decision to go to the cath lab
– CI: Upcoming CABG Sx, coagulopathy
• ACE inhibitors:
– Indication: CHF,ant wall infarct, EF < 40%,
pulmonary congestion, increase BP
– Timing: On admission
– CI: hyperkalemia, RF, hypotension
• Statins:
– Indications: CAD
– Timing: On admission
– CI: Myopathy, sensitivity
• Supplemental oxygen:
– Indications: First 6 hrs, especially patients
with oxygen desaturation (< 90% by pulse ox)
QUESTIONS
QUESTIONS