Primary Causes & Pathophysiology
Stable angina results from an imbalance between myocardial oxygen supply and demand. Atherosclerotic plaques cause fixed luminal narrowing of the epicardial coronary arteries, typically exceeding 70% stenosis. At rest, coronary blood flow is sufficient to meet basal metabolic needs. However, during physical exertion or emotional stress, increased heart rate, contractility, and wall tension elevate myocardial oxygen demand. The stenotic artery cannot adequately augment flow due to exhausted coronary vasodilatory reserve, leading to transient subendocardial ischaemia. This ischaemia triggers the release of metabolites such as adenosine and bradykinin that stimulate cardiac sympathetic afferent nerves, transmitting pain signals to the thalamus and cortex.
Progressive accumulation of lipid-rich plaques in epicardial arteries causes fixed stenosis, limiting coronary flow reserve during exertion.
Impaired vasodilation and structural remodelling of the coronary microcirculation despite angiographically normal epicardial arteries, causing ischaemia (microvascular angina).
A band of heart muscle overlies a segment of a coronary artery, compressing it during systole and potentially causing exertional ischaemia due to delayed diastolic relaxation.