Cardiology

Coronary Artery Spasm song

Listen to the preview here. The full song is free on YouTube.

Coronary Artery Spasm

Full song on YouTube ↗

Key points in this song10

Coronary artery spasm (Prinzmetal/variant angina) causes chest pain at rest, typically in the early morning hours, due to transient vasospasm of a coronary artery, often overlying an atherosclerotic plaque.
ECG during an episode shows transient ST-segment elevation (not depression), which resolves spontaneously or with nitrates — this distinguishes it from classic stable angina.
The spasm is caused by increased vascular smooth muscle reactivity and endothelial dysfunction, with alpha-adrenergic stimulation and reduced nitric oxide bioavailability as key mechanisms.
Classic triggers include cocaine use, cigarette smoking, cold exposure, hyperventilation, and ergotamine — all cause vasoconstriction or alpha-adrenergic activation.
Cocaine is the classic trigger: it blocks norepinephrine reuptake and causes direct coronary vasospasm, leading to MI even in young patients with normal coronaries.
Diagnosis is confirmed by provocative testing with ergonovine (ergometrine) or acetylcholine during coronary angiography, which induces spasm in susceptible vessels.
Coronary angiography classically shows normal or near-normal coronary arteries between episodes, differentiating it from obstructive CAD.
First-line treatment is calcium channel blockers (e.g., amlodipine, diltiazem) and long-acting nitrates, which prevent spasm by promoting coronary vasodilation.
Beta-blockers are contraindicated in isolated coronary artery spasm — unopposed alpha-adrenergic activity worsens vasospasm and can precipitate MI.
Prinzmetal angina is associated with other vasospastic disorders such as Raynaud phenomenon and migraine headaches, suggesting a systemic vascular hyperreactivity syndrome.