Angina pectoris is, until proven otherwise, the result of myocardial ischemia, secondary to coronary artery disease. Angina pectoris can be divided into typical and atypical angina pectoris. In typical angina pectoris, the discomfort or pain is located substernally and often radiates. It is precipitated by exertion or emotion and promptly relieved by rest.

Atypical chest pain is located in the left chest, sometimes confined to a small area, does not radiate, and is described as sharp, stabbing, or tearing. In atypical angina pectoris the pain can occur repetitively for short periods of time (seconds) or last for hours. It is unrelated to exercise and not relieved by rest or nitroglycerin.

Stable and Unstable Angina Pectoris. The distinction between stable and unstable angina pectoris is of great clinical importance. In chronic stable angina pectoris the discomfort is predictably provoked by exertion and relieved by rest. A chronic stable coronary stenosis is, in most cases, the pathophysiological explanation of chronic stable angina pectoris.

Unstable angina pectoris occurs with minimal exertion or at rest. The pain is new in onset or increasing in intensity. Character and location are typical, however the intensity is often more severe and the duration longer than in chronic stable angina pectoris.

Pathophysiologically, unstable angina pectoris is associated with ruptured plaques and thrombi, which obstruct the coronary lumina. Occasionally, coronary vasoconstriction or spasms contribute to the typical dynamic clinical manifestation of unstable angina pectoris.

It is important to note that myocardial ischemia may present itself in forms other than angina pectoris. Particularly in elderly patients, myocardial ischemia may cause nausea and stomach ache without chest pain.

In those patients the first manifestation of coronary artery disease may be an acute myocardial infarction, heart failure, or cardiac arrest.