Stable Ischemic Heart Disease

Stable ischemic heart disease (SIHD, chronic coronary disease) results from fixed atherosclerotic plaque causing ≥70% luminal stenosis of epicardial coronary arteries (≥50% for left main), producing a supply-demand mismatch during exertion. The stable plaque has a thick fibrous cap, large lipid-poor neite, and does not rupture (unlike the thin-capped, lipid-rich vulnerable plaque of acute coronary syndromes). During exertion, myocardial oxygen demand increases (increased heart rate, contractility, wall stress), but the fixed stenosis limits augmentation of coronary blood flow. Subendocardial ischemia occurs first (subendocardium is most vulnerable to ischemia — farthest from epicardial vessels and highest wall stress during systole). Ischemic cascade: decreased coronary flow → diastolic dysfunction (earliest sign) → wall motion abnormality → ST-segment depression on ECG → anginal chest pain (latest — 'angina is the tip of the iceberg'). Treatment targets the supply-demand equation: reduce demand (beta-blockers reduce HR and contractility; CCBs reduce afterload; nitrates reduce preload/afterload) and improve supply (nitrates cause coronary vasodilation; revascularization for refractory symptoms). Optimal medical therapy (OMT) includes antiplatelet therapy, statin, ACE inhibitor/ARB, beta-blocker, and risk factor modification. The ISCHEMIA trial (2019) demonstrated...