Cardiology · Ischemic Heart Disease
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Caused by coronary artery vasospasm; pain occurs at rest, classically between midnight and early morning, not with exertion.
ECG during an attack shows transient ST-segment elevation that resolves as the pain subsides.
Troponins are typically normal because there is no infarction, unless spasm is prolonged.
Strongly associated with tobacco smoking and cocaine use; coronaries are often angiographically normal.
Calcium-channel blockers (and nitrates) are first-line therapy and are highly effective at preventing spasm.
Beta-blockers are contraindicated: unopposed alpha-adrenergic tone can worsen coronary spasm; also avoid triptans/ergots.
Definitive diagnosis is by provocative testing with ergonovine or acetylcholine during coronary angiography.
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A 42-year-old woman presents to the emergency department with recurrent episodes of substernal chest pressure that wake her from sleep around 3 AM and resolve within 10 minutes. She has a 20-pack-year smoking history and exercises without chest pain between episodes. During an episode in the ED, ECG shows transient ST-segment elevation in the inferior leads that normalizes as the pain resolves; serial troponins are normal. Coronary angiography reveals no fixed obstructive lesions.
Which of the following is the most appropriate first-line pharmacologic therapy?
Diltiazem (a calcium-channel blocker)
Rest/nocturnal angina with transient ST elevation, normal troponins, and normal coronary arteries is classic for Prinzmetal (vasospastic) angina. Calcium-channel blockers (and nitrates) are first-line. Beta-blockers are contraindicated because unopposed alpha-adrenergic tone can worsen coronary spasm.
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Etiology / Epidemiology
Spasm of epicardial coronary arteries; arteries are normal in ~1/3 and atherosclerotic in ~2/3 of cases.
Clinical Manifestations
Chest pain at rest, often nocturnal/early morning; triggered by tobacco or cocaine.
Diagnosis
Transient ST-segment elevation during attack that resolves with symptoms; confirm with provocative testing.
Treatment
Calcium-channel blockers and nitrates; beta-blockers are contraindicated (can worsen spasm).
Prognosis
Generally good with CCB therapy and risk-factor control; risk of arrhythmia/MI during severe spasm.
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Epidemiology & Etiology
Variant (Prinzmetal) angina is caused by spasm of the epicardial coronary arteries, occurring in patients with angiographically normal coronaries (about one-third) or with underlying atherosclerotic disease (about two-thirds). It typically affects younger patients than classic atherosclerotic angina and is strongly associated with tobacco smoking and cocaine use. Hyperventilation, cold, and emotional stress can also provoke attacks.
Pertinent Anatomy
Spasm occurs in the large epicardial coronary arteries (especially the RCA), at or near sites that may or may not have a fixed plaque. Smooth muscle hyperreactivity of the medial layer transiently and severely narrows the lumen, producing transmural ischemia of the territory supplied.
Pathophysiology
Focal or diffuse hyperreactivity of coronary smooth muscle, with endothelial dysfunction and altered nitric oxide signaling, causes intense transient vasoconstriction. The resulting near-total occlusion produces transmural ischemia, hence ST-segment elevation, without thrombotic plaque rupture. Spasm resolves spontaneously or with vasodilators, restoring flow before infarction in most cases, but prolonged spasm can cause MI or ventricular arrhythmias.
Clinical Manifestations
Pain typically occurs at rest, classically between midnight and early morning, rather than with exertion, and may be precipitated by tobacco or cocaine. Episodes are recurrent and self-limited, lasting minutes, and respond to nitroglycerin. Exercise tolerance is often preserved between attacks. Severe spasm can cause syncope from transient bradyarrhythmia or ventricular tachyarrhythmia.
Diagnosis
The ECG typically shows transient ST-segment elevation during an acute attack that normalizes as symptoms resolve, distinguishing it from fixed obstructive disease. Capturing the ECG during pain (or ambulatory monitoring) is key. Coronary angiography with provocative testing (ergonovine or acetylcholine) reproduces focal spasm and confirms the diagnosis; troponins are usually normal unless prolonged spasm causes infarction.
Treatment
Calcium-channel blockers (e.g., diltiazem, amlodipine, verapamil) are first-line and highly effective at preventing spasm, combined with nitrates for acute and prophylactic relief. Aggressive smoking cessation and avoidance of cocaine and other vasoconstrictors are essential. Beta-blockers are contraindicated, unopposed alpha-mediated vasoconstriction can worsen spasm. Aspirin should be used cautiously, as high doses may aggravate spasm.
Prognosis
Prognosis is generally favorable, especially in patients without significant fixed atherosclerosis, and most do well on calcium-channel blockers with risk-factor modification. However, severe or prolonged spasm can cause myocardial infarction, life-threatening ventricular arrhythmias, or sudden death, so symptom suppression and trigger avoidance are important.
Differential Diagnosis
Stable angina: pain provoked by exertion and relieved by rest, with reproducible ischemic threshold.
STEMI: ST elevation that persists, with troponin rise and a culprit thrombotic lesion on angiography.
Cocaine-induced chest pain: temporally linked to use; like Prinzmetal, avoid beta-blockers.
GERD/esophageal spasm: burning or food-related pain, no ECG changes, responds to PPIs.
Stress (Takotsubo) cardiomyopathy: catecholamine surge with apical ballooning on echo, normal coronaries.