Angina pectoris is due to myocardial ischemia and occurs when myocardial oxygen demand exceeds the capacity of the coronary vessels to supply oxygen to the myocardium. The major determinants of oxygen consumption are heart rate, contractility and systolic wall tension. The major determinants of wall tension are blood pressure and ventricular cavity size. Pharmacologic therapy is often directed at reducing heart rate and wall tension.

In some patients with myocardial ischemia, the typical symptoms of angina pectoris are absent. They may have "anginal equivalent" symptoms, usually associated with exertion and relieved by rest and nitroglycerin. The most common examples are exertional dyspnea and exertional fatigue. Other patients have "silent" myocardial ischemia, that is, ischemia unaccompanied by symptoms.

There are important differences between stable angina, unstable angina and a special variant of angina called prinzmetal's angina.

Stable angina is characterized by chest discomfort precipitated by a predictable level of exertion or stress. Its frequency, severity and response to therapy are also predictable. The pathogenesis of stable angina is usually an atheromatous plaque that limits an increase in blood flow in the face of increasing demand.

Angina is considered unstable when it occurs at rest, is of recent onset, or when there is a change in a previously stable pattern with prolonged duration or increased severity. Angina in the early post-myocardial infarction setting is also considered unstable.

The underlying pathology associated with unstable angina is usually a ruptured atheromatous plaque with a superimposed, platelet-rich non-occlusive thrombus. Unstable angina carries a high risk for myocardial infarction and sudden death.