Prinzmetal's, or variant, angina is characterized by chest pain at rest associated with transient ST-segment elevation on the electrocardiogram. It is related to epicardial coronary artery spasm, often at the site of a stenotic lesion. The attacks are usually cyclical, often occurring in the early morning hours and are more prolonged than classic angina. The ST-segment Angina Pectoris normalizes with the recession of chest pain. Exercise tolerance may be well preserved. Prinzmetal's angina occurs more commonly in females with other forms of vasoreactivity, such as migraine or Raynaud's phenomenon.

Angina pectoris is most commonly due to atherosclerotic disease of the epicardial coronary arteries. Disease of the coronary microvasculature may also contribute. More rarely, it may reflect non-atherosclerotic coronary artery disease such as spasm, emboli, or congenital anomalies or spontaneous coronary artery dissection. It may also be due to non-coronary disease, such as left ventricular outflow tract obstruction from valvular aortic stenosis or hypertrophic cardiomyopathy. On rare occasions, angina may be due to pulmonary hypertension.

Angina may be precipitated or aggravated by non-cardiac factors. These factors either increase myocardial oxygen demand, decrease supply or both. They include anemia, tachydysrhythmias, hyperthyroidism, hypotension and severe hypertension.