Pathophysiology of CAD

Ischemic Heart Disease

Coronary Artery Anatomy and Ischemia Ischemic Syndromes & Myocardial Infarction Diagnostic and Prognostic Testing Treatment & Prevention of Ischemia and Infarction

Coronary Angiography

NORMAL CORONARY ANATOMY

DOMINANCE (Right or Left): Refers to the coronary artery( Posterior Descending Artery) that supplies the inferior wall and AV node artery 80-90% of individuals are right dominant (the LCA nonetheless supplies more myocardium) The LV, being more massive and doing more work, gets the bulk of the coronary blood flow.

Collateral Coronary Circulation

Collaterals appear in the presence of severe coronary stenosis Collaterals connect generally wellperfused segments to segments distal to a stenosis/occlusion Collaterals may exist in form fruste. enlarging when needed Collaterals probably help maintain viability

MYOCARDIAL OXYGEN SUPPLY

O2 CARRYING CAPACITY OF BLOOD (Hgb) CORONARY BLOOD FLOW: 1.Directly proportional to perfusion pressure (Diastolic BP) 2.Inversely proportional to coronary vascular resistance a. External compression (myocardium) b. Intrinsic vascular resistance (Arteriolar vessels)endothelial factors, neural innervation 3. Coronary artery patency

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

MYOCARDIAL O2 DEMAND
HEART RATE CONTRACTILITY WALL STRESS Law of LaPlace: stress=Pxr/2h P-interventricular pressure, rventricular radius, h-ventricular wall thickness

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 ISCHEMIA AND INFARCTION

Conditions Provoking or Exacerbating Ischemia

Increased Oxygen Demand Non-Cardiac
Hyperthermia Hyperthyroidism Sympathomimetic toxicity (cocaine use) Hypertension Anxiety Arteriovenous fistula

Decreased Oxygen Supply Non-Cardiac

Anemia Hypoxemia pneumonia, asthma, COPD, pulmonary hypertension, interstitial pulmonary fibrosis, obstructive sleep apnea Sickle-cell disease Sympathomimetic toxicityc (cocaine use) Hyperviscosity polycythemia, leukemia, thrombocytosis, hypergammaglobulinemia

Cardiac
Hypertrophic cardiomyopathy Aortic stenosis Dilated cardiomyopathy Tachycardia ventricular supraventricular

Cardiac
Aortic stenosis Hypertrophic cardiomyopathy

EFFECTS OF MYOCARDIAL 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 pressure 3. Pain (Not always present)

Atherosclerosis Timeline
Foam Cells Complicated Lesion/ Fatty Intermediate Fibrous Rupture Streak Lesion Atheroma Plaque

Endothelial Dysfunction From First Decade From Third Decade From Fourth Decade

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

LAD Stenosis

RCA Stenosis

CBF and ATHEROSCLEROSIS

LESIONS OF CAD ARE IN EPICARDIAL VESSELS ALTERATION IN CORONARY BLOOD FLOW MAY IN PART BE DUE TO ALTERED VASCULAR TONE LUMEN REDUCTION OF .60-70% REDUCES MAXIMAL BLOOD FLOW LUMEN REDUCTION OF >90% MAY REDUCE RESTING BLOOD FLOW

Angina

Substernal chest pain Precipitated by exercise and relieved with rest Responds to sublingual nitroglycerine.

Typical angina

All three symptoms

Atypical angina

2/3 symptoms

Atypical chest pain

1/3 symptoms

Differential Diagnosis of Chest Pain

Cardiac

Myocardial ischemia Pericarditis Aortic dissection

GI reflux Peptic ulcer disease Esophageal spasm Biliary colic Acute cholecystitis

Gastrointestinal

Musculoskeletal Costrochondral syndrome Cervical radiculitis Pulmonary Pulmonary embolism Pneumonia Pneumothorax

Stable Angina

Typically exertion related (increased demand) Variable threshold in some: alterations in vascular tone Fixed atherosclerotic plaque is flowlimiting Risk factors

Diagnostic Studies

Stress testing Standard exercise Nuclear imaging (exercise or persantine) Echo imaging (exercise or dobutamine) Coronary angiography Cardiac CT angiography

Treatments to Prevent Ischemia

Medical nitrates, B-blockers, calcium channel blockers, ranolazine Percutaneous coronary intervention (PCI) Coronary Artery Bypass Graft Surgery (CABG)

UNSTABLE ANGINA

Prolonged episodes of pain, rest pain, with increasing frequency Thrombus formation, partially occlusive, at site of ruptured plaque Ischemic changes on ECG Prognosis: increase in likelihood of near-term acute MI Negative biomarkers (by definition)

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

Symptoms of MI (prolonged chest pain, shortness of breath, nausea, others) ECG: ischemic changes without ST segment elevation or Q-waves Enzymes (troponin, CPK-MB) indicative of myocardial cell death Usually subtotal occlusion by thrombus on ruptured plaque

ST-Elevation MYOCARDIAL INFARCTION (Q-wave)

Clinical presentation (Pain, etc.) ECG: ST segment elevation, evolution of Q waves Enzymes elevated Totally occlusive thrombus at site of ruptured plaque

Medical Treatment of Acute 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

Acute Treatment of ST-Elevation MI

Fibrinolytic therapy- tPA, rPA, TNK-tPA, streptokinase Primary Percutaneous coronary intervention (PCI) Coronary Artery Bypass Graft Surgery (CABG)

ELECTRICAL COMPLICATIONS OF ACUTE MI

Ventricular Arrhythmias (vtach & vfib) Supraventricular Arrhythmias (afib) Conduction Blocks ( temporary & permanent pacemaker)

MECHANICAL COMPLICATIONS OF ACUTE MI

Congestive heart failure: Loss of pumping function Mitral valve insufficiency (papillary muscle dysfunction) Myocardial rupture (septum, free wall, papillary muscle, right ventricle) Cardiogenic Shock Ventricular aneurysm Dressler Syndrome Thromboembolism

PROGNOSIS OF ACUTE MI

Extent of coronary vascular disease (number of diseased vessels, location of stenoses or occlusions) State of LV function Ejection fraction Ongoing ischemia

Risk Stratification With 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 survival rate

Coronary arteries normal coronary arteries one-vessel disease two-vessel disease three-vessel disease 91% 74% 59% 40%

Ejection fraction 50% to 100% 35% to 49% <35% 73% 54% 21%

Circulation 1994;90:2645-57

Thank you for your attention.

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