Coronary Artery Spasm

Disease affecting mostly middle- and old-aged men and postmenopausal women

Gender difference: Higher incidence in women

Periop CAS: Prevalent in elderly male pts with coronary risk factors

Teenagers and young adults with illicit substance abuse, primarily cocaine

Occurs in 1–5% of percutaneous coronary interventions

Ethnic differences: Higher frequency in eastern populations

Type A behavior pattern, severe anxiety, and panic disorder

Age, smoking, and high sensitivity C-reactive protein (marker of inflammation)

Change of sympathetic activity: may trigger CAS

CAS can lead to myocardial ischemia.

• Chest pain and ischemic ST segment changes on ECG

May be result of or associated with myocardial infarction

• Coronary thrombosis: May trigger CAS, leading to acute MI, unstable angina, or ischemic sudden death

Cardiogenic shock: Decreased LV and RV compliance and decreased pump function

In pts with CAS, tachyarrhythmias associated with anterior ST segment elevations, ventricular arrhythmias, and even ventricular fibrillation

Bradyarrhythmias: More frequent with inferior CAS, potentially resulting in complete atrioventricular block, associated with hypotension and syncope

Abnormal constriction of epicardial coronary arteries

Classical CAS (Prinzmetal for variant or spastic angina):

• Diagnosed if pt has severe chest pain, usually at rest, with concurrent ST segment elevation on ECG

• Characterized by spasm of normal coronary arteries on arteriography

Other forms of CAS:

• Silent angina (without chest pain), diagnosed with Holter monitoring

• CAS with concurrent atherosclerotic disease at the site or distant from the organic stenosis

• Effort angina, unstable angina, or microvascular angina (female prevalence)

• ECG changes, which may include either ST segment elevation, ST depression, or T wave abnormalities

• Coronary arteriography: Can demonstrate normal or diseased coronary arteries

The exact mechanism of CAS is unknown. Several contributing factors are thought to play a role:

• Change in sympathetic activity

• Vagal withdrawal

• Coronary thrombosis

• Smooth muscle dysfunction

• Compromised endothelium-mediated vasodilation

• Increased Ca ²⁺ sensitivity

• Reduced endothelial NO activity

• eNOS gene polymorphism

• Signs of chronic low-grade inflammation

• Oxidative stress