Vasospastic Angina (Prinzmetal)

Vasospastic angina, also known as Prinzmetal’s angina, is a form of angina caused by a transient coronary vasospasm, leading to a temporary reduction in blood flow to the myocardium.
Unlike stable angina, which is triggered by exertion and caused by fixed atherosclerotic stenoses, vasospastic angina can occur at rest and is not clearly correlated with physical activity.

The main pathophysiological mechanisms involved are:

• Coronary vasospasm: Abnormal contraction of the coronary arteries, independent of atherosclerotic plaques.
• Endothelial dysfunction: Reduced nitric oxide production and altered vascular tone regulation.
• 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 vascular tone instability.

Risk Factors

Vasospastic angina is more common in younger individuals and smokers, whereas other traditional cardiovascular risk factors (hypertension, diabetes, dyslipidemia) play a less significant role compared to classic ischemic heart disease.

Clinical Presentation and Diagnosis

Patients with Prinzmetal’s angina experience chest pain episodes with the following characteristics:

• Severe, constrictive chest pain, often occurring at rest or during nighttime.
• Typically short duration (5-15 minutes), resolving spontaneously or with nitrate administration.
• No clear relationship with physical exertion.
• Possible association with ventricular arrhythmias or syncope.

The most useful diagnostic tools include:

• ECG during an episode: Transient ST-segment elevation that resolves once symptoms disappear.
• Provocative tests with ergonovine or acetylcholine: Induce coronary vasospasm under controlled conditions.
• 24-48 hour Holter monitoring: Identification of silent ischemic episodes.
• Coronary angiography: Useful for ruling out significant stenosis and confirming coronary vasospastic reactivity.

Treatment of Vasospastic Angina

Treatment aims to reduce the frequency of episodes and prevent arrhythmic complications.

Lifestyle modifications: Smoking cessation, avoiding extreme cold exposure, and reducing the intake of vasoconstrictive substances (caffeine, cocaine) are fundamental for managing the condition.

Pharmacological therapy:

• Calcium channel blockers: First-line agents for preventing vasospasm (amlodipine, verapamil, diltiazem).
• Long-acting nitrates: Reduce the 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 stenosis and documented ischemia.

Prognosis and Complications

Vasospastic angina generally has a favorable prognosis when adequately treated, but in some cases, it may lead to malignant ventricular arrhythmias, acute myocardial infarction, and sudden cardiac death.
Timely treatment and management of triggering factors are crucial to reducing the risk of major cardiac events.

References
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