pathophys of cad 2011

8/12/2019 Pathophys of CAD 2011

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Pathophysiology of CAD


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Ischemic Heart Disease

Coronary Artery Anatomy and

Ischemia

Ischemic Syndromes &Myocardial Infarction

Diagnostic and Prognostic

Testing

Treatment & Prevention of

Ischemia and Infarction


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Coronary Angiography


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NORMAL CORONARY ANATOMY

DOMINANCE (Right or Left): Refers to thecoronary artery( Posterior Descending Artery)that supplies the inferior wall and AV nodeartery

80-90% of individuals are right dominant (theLCA nonetheless supplies moremyocardium)

The LV, being more massive and doing morework, gets the bulk of the coronary bloodflow.


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Collateral Coronary Circulation

Collaterals appear in the presence ofsevere coronary stenosis

Collaterals connect generally well-

perfused segments to segmentsdistal to a stenosis/occlusion

Collaterals may exist in form fruste.

enlarging when needed

Collaterals probably help maintain

viability


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MYOCARDIAL OXYGEN SUPPLY

O2 CARRYING CAPACITY OF BLOOD (Hgb)

CORONARY BLOOD FLOW:

1.Directly proportional to perfusion pressure (DiastolicBP)

2.Inversely proportional to coronary vascularresistance

a. External compression (myocardium)

b. Intrinsic vascular resistance (Arteriolar vessels)-endothelial factors, neural innervation

3. Coronary artery patency


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UNIQUE FEATURES OF

CORONARY BLOOD FLOW:1. AUTOREGULATION: Control of

vascular resistance locally (endothelial

function and metabolites)

2. O2 extraction is MAXIMAL even under

basal conditions


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MYOCARDIAL O2 DEMAND

HEART RATE

CONTRACTILITY

WALL STRESSLaw of LaPlace:

stress=Pxr/2h

P-interventricular pressure, r-ventricular radius, h-ventricularwall thickness


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DISTRIBUTION OF

CORONARY FLOW LV IS MOST MASSIVE CHAMBER

AND DOES MOST OF THE WORK

HENCE, MOST BLOOD GOES TO

THE LV (even RCA blood)

LV IS MOST SUBJECT TO ISCHEMIAAND INFARCTION


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EFFECTS OFMYOCARDIAL ISCHEMIA

1. Impairment of systolic and diastolic

ventricular function (I.e., contraction and

relaxation)

2. Result: Lower cardiac output, and

increase in diastolic LV filling pressure3. Pain (Not always present)


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Atherosclerosis Timeline

FoamCells

FattyStreak

IntermediateLesion Atheroma

FibrousPlaque

ComplicatedLesion/Rupture

Adapted from Pepine CJ. Am J Cardiol .1998;82(suppl 104).

From FirstDecade

From ThirdDecade

From FourthDecade

Endothelial Dysfunction


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LAD Stenosis


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RCA Stenosis


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CBF and ATHEROSCLEROSIS LESIONS OF CAD ARE IN

EPICARDIALVESSELS ALTERATION IN CORONARY

BLOOD FLOW MAY IN PART BE

DUE TO ALTERED VASCULAR TONE

LUMEN REDUCTION OF .60-70%

REDUCES MAXIMALBLOOD FLOW LUMEN REDUCTION OF >90% MAY

REDUCE RESTINGBLOOD FLOW


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Angina

Substernal

chest pain

Precipitated by

exercise andrelieved with

rest

Responds to

sublingualnitroglycerine.

Typical angina

All three

symptoms

Atypical angina 2/3 symptoms

Atypical chest

pain

1/3 symptoms


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Differential Diagnosis ofChest Pain

Cardiac Myocardial ischemia

Pericarditis

Aortic dissection

Gastrointestinal GI reflux Peptic ulcer disease

Esophageal spasm

Biliary colic

Acute cholecystitis

Musculoskeletal

Costrochondralsyndrome

Cervical

radiculitis Pulmonary

Pulmonaryembolism

Pneumonia

Pneumothorax


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Stable Angina

Typically exertion related (increaseddemand)

Variable threshold in some: alterations in

vascular tone

Fixed atherosclerotic plaque is flow-

limiting Risk factors


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Diagnostic Studies

Stress testing

Standard exercise

Nuclear imaging (exercise or persantine)

Echo imaging (exercise or dobutamine)

Coronary angiography

Cardiac CT angiography


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Treatments to Prevent Ischemia

Medicalnitrates, B-blockers, calcium

channel blockers, ranolazine

Percutaneous coronary intervention

(PCI)

Coronary Artery Bypass Graft Surgery(CABG)


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UNSTABLE ANGINA

Prolonged episodes of pain, rest pain,with increasing frequency

Thrombusformation, partially

occlusive, at site of ruptured plaque Ischemic changes on ECG

Prognosis: increase in likelihood ofnear-term acute MI

Negative biomarkers (by definition)


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Non-ST-Elevation MI(non-Q wave MI)

Symptoms of MI (prolonged chest pain,

shortness of breath, nausea, others)

ECG: ischemic changes without STsegment elevation or Q-waves

Enzymes (troponin, CPK-MB)

indicative of myocardial cell death Usually subtotal occlusion by thrombus

on ruptured plaque


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Medical Treatment ofAcute Coronary

Syndromes General measures- O2, morphine

Anti-ischemic therapy- b-blocker,

nitrates, calcium channel blockers

Aniplatelet agents- aspirin, clopidogrel

(or prasugrel),GP IIB/IIIa Inhibitors

Anticoagulants- LMWH, Unfractionated

IV heparin, bivalirudin

Adjuctive therapies- statin, ACE inhibitor


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Acute Treatment of ST-Elevation

MI Fibrinolytic therapy- tPA, rPA, TNK-tPA,

streptokinase

Primary Percutaneous coronary

intervention (PCI)

Coronary Artery Bypass Graft Surgery(CABG)


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MECHANICAL COMPLICATIONS

OF ACUTE MI Congestive heart failure: Loss of pumpingfunction

Mitral valve insufficiency (papillary muscle

dysfunction) Myocardial rupture (septum, free wall, papillary

muscle, right ventricle)

Cardiogenic Shock Ventricular aneurysm

Dressler Syndrome

Thromboembolism


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Risk Stratification


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Risk StratificationWith Coronary Angiography

The extent and severity of coronary disease and LV dysfunction are the

most powerful clinical predictors of long-term outcome

proximal coronary stenoses

severe left main coronary artery stenosis

CASS registry of medically treated patients, the 12-year survivalrate

Coronary arteries Ejection fraction

normal coronary arteries 91% 50% to 100% 73%

one-vessel disease 74% 35% to 49% 54%. two-vessel disease 59%


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Thank you for yourattention.

Questions?

pathophys of cad 2011

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