variant angina

Prinzmetal (variant) angina results from focal or diffuse spasm of epicardial coronary arteries, leading to transient myocardial ischemia. Unlike typical angina, it is not reliably provoked by exertion and commonly occurs at rest, frequently between midnight and early morning. Risk factors include smoking, cocaine use, and other triggers like hyperventilation, alcohol withdrawal, and cold exposure; it is more common in younger women and those with fewer traditional atherosclerotic risk factors, though underlying atherosclerosis can coexist. Pathophysiology involves endothelial dysfunction and hyperreactivity of vascular smooth muscle, with increased vasoconstrictor tone (e.g., due to reduced nitric oxide bioavailability, increased Rho-kinase activity) leading to spasm. ECG during an episode shows transient ST-segment elevation (rather than depression) due to transmural ischemia, which normalizes once spasm resolves; this can sometimes be mistaken for acute MI. Diagnosis is confirmed by coronary angiography demonstrating spasm, often provoked with ergonovine or acetylcholine challenge testing. Treatment includes calcium channel blockers (first-line, e.g., diltiazem, amlodipine) and nitrates to relax vascular smooth muscle and prevent spasm; beta-blockers are generally avoided as they may exacerbate spasm by allowing unopposed alpha-adrenergic vasoconstriction. Smoking cessation is critical. Complications can include myocardial infarction, arrhythmias (including ventricular tachycardia/fibrillation), and sudden cardiac death due to severe or prolonged spasm.