Antianginal Drugs

Introduction & pathophysiology

• Antianginal drugs — agents that prevent, abort or terminate attacks of angina pectoris — a heavy, pressing substernal discomfort from accumulation of metabolites when myocardial O₂ demand exceeds O₂ supply. Pain classically radiates to the left arm/jaw/epigastrium; women, the elderly and diabetics often present atypically.
• O₂ demand — set by heart rate, contractility and ventricular wall tension (preload + afterload). Wall tension follows the law of Laplace — tension ∝ (pressure × radius)/(2 × wall thickness), so a dilated ventricle costs more O₂.
• O₂ supply — depends on coronary blood flow (flow ∝ radius⁴). The heart already extracts ~75% of O₂ at rest, so demand can only be met by raising flow. Coronary flow occurs almost entirely in diastole — tachycardia (short diastole) worsens ischaemia, bradycardia improves perfusion.
• Substrate — atherosclerosis with endothelial dysfunction (↓ NO), inflammation and plaque rupture → thrombosis. A rising LV end-diastolic pressure (~5 → ~25 mmHg) compresses the diastolically-perfused subendocardium ("subendocardial crunch").

• Classical / stable (effort) angina — predictably provoked by exertion/emotion, relieved by rest; substrate is a fixed atherosclerotic stenosis.
• Variant / Prinzmetal (vasospastic) — at rest, due to localised coronary vasospasm; therapy aims to relieve spasm (CCBs/nitrates, not β-blockers).
• Unstable angina / ACS — plaque rupture + platelet deposition; a spectrum graded by troponin — UA (no necrosis) → NSTEMI (partial necrosis, ST not elevated) → STEMI (complete occlusion, ST elevated). Microvascular angina has normal epicardial vessels with reduced flow reserve.