Pathophysiology
Clinical meaning
Stable angina pectoris results from a fixed atherosclerotic narrowing (typically 70% or greater stenosis) of one or more coronary arteries that limits coronary blood flow during periods of increased myocardial oxygen demand. Unlike acute coronary syndrome, the plaque in stable angina has a thick fibrous cap, small lipid core, and is not prone to rupture. During physical exertion, emotional stress, cold exposure, or after heavy meals, the myocardium requires increased oxygen delivery. When the narrowed artery cannot augment flow to meet demand, the subendocardial myocardium (most vulnerable to ischemia due to compression during systole) shifts to anaerobic metabolism. Lactic acid and adenosine accumulate, stimulating cardiac afferent nerve fibers that travel via the sympathetic chain to the upper thoracic dorsal root ganglia, producing the sensation of chest pain or pressure. The pain is characteristically predictable: provoked by consistent levels of exertion, lasting 3-5 minutes, and relieved by rest or nitroglycerin (which dilates coronary arteries and reduces preload). The Canadian Cardiovascular Society (CCS) classification grades angina severity: Class I (ordinary activity does not cause angina), Class II (slight limitation of ordinary activity),...