Vasospastic angina, also known as Prinzmetal angina, is a form of angina caused by a transient coronary vasospasm, which leads to a temporary reduction of blood flow to the myocardium.
Unlike stable angina, which is effort-induced and caused by fixed atherosclerotic stenoses, vasospastic angina can occur at rest and shows no clear correlation with physical activity.
The main pathophysiological mechanisms involved are:
Coronary vasospasm: Abnormal contraction of the coronary arteries, regardless of the presence of atherosclerotic plaques.
Endothelial dysfunction: Reduced nitric oxide production and altered regulation of vascular tone.
Vasomotor hyperreactivity: Increased sensitivity to vasoconstrictive stimuli such as cold, stress, or substances like cocaine and cigarette smoke.
Vascular inflammation: Chronic inflammatory state contributing to instability of vascular tone.
Risk Factors
Vasospastic angina is more frequent in young individuals and smokers, while other traditional cardiovascular risk factors (arterial hypertension, diabetes, dyslipidemia) play a less relevant role compared to classic ischemic heart disease.
Clinical Presentation and Diagnosis
Patients with Prinzmetal angina report episodes of chest pain with the following features:
Severe, constrictive chest pain, often at rest or during nighttime hours.
Typically brief duration (5–15 minutes), with spontaneous resolution or after taking nitrates.
No relation to physical exertion.
Possible association with ventricular arrhythmias or syncope.
The most useful diagnostic tools include:
ECG during episode: Presence of transient ST-segment elevation, resolving with disappearance of symptoms.
Provocative testing with ergonovine or acetylcholine: Induction of coronary vasospasm in a controlled setting.
24–48 hour Holter monitoring: Identification of silent ischemic episodes.
Coronary angiography: Useful to exclude significant stenoses and confirm vasospastic reactivity of the coronary arteries.
Treatment of Vasospastic Angina
Treatment aims to reduce the frequency of episodes and prevent arrhythmic complications.
Lifestyle modifications:
Smoking cessation, avoiding intense cold, and reducing exposure to vasoconstrictive substances (caffeine, cocaine) are fundamental for managing the disease.
Pharmacological therapy:
Calcium channel blockers: First-line drugs for the prevention of vasospasm (amlodipine, verapamil, diltiazem).
Long-acting nitrates: Reduction of frequency and severity of episodes.
Statins and ACE inhibitors: Useful in patients with documented endothelial dysfunction.
Beta-blockers: Generally contraindicated, as they may promote vasospasm.
Revascularization:
Indicated only in patients with concomitant coronary stenoses and documented ischemia.
Prognosis and Complications
Vasospastic angina generally has a favorable prognosis if treated adequately, but in some cases it may be complicated by malignant ventricular arrhythmias, acute myocardial infarction, and sudden cardiac death.
Timely treatment and management of trigger factors are essential to reduce the risk of major cardiac events.
References
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Patel R, et al. Microvascular dysfunction and endothelial role in coronary spasm. Circulation. 2018;137(10):1015-1025.
JCS Joint Working Group. Guidelines for diagnosis and treatment of vasospastic angina. Circulation Journal. 2020;84(4):621-635.
Gori T, et al. Endothelial dysfunction and coronary vasospasm. J Am Coll Cardiol. 2018;71(4):423-432.
Shah SJ, et al. Coronary artery spasm: Mechanisms and management. New England Journal of Medicine. 2019;380(7):709-717.
Takagi Y, et al. Long-term prognosis of patients with vasospastic angina. Circulation. 2021;143(2):129-137.
Hung MJ, et al. Coronary vasospasm in young patients with chest pain. BMJ. 2019;366:l3859.
Fox K, et al. Management of vasospastic angina. European Heart Journal. 2020;41(22):2064-2071.