Initially, narrowing (plaques) of the coronary arteries occurs may be severe enough to cause stable angina with exertion or stress. This narrowing, however, may not cause any symptoms at all. For reasons not well understood, the plaques reach a point at which they rupture. Under these circumstances, a plug formed by platelets and blood clots may form causing an already narrowed blood vessel to become "high-grade." This inherently unstable situation may progress to complete occlusion and infarction (cell death) or the lesion may heal. When this plug completely occludes a coronary artery, a heart attack occurs.

Once this type of lesion exists, onset of chest pain is "unstable." Unlike stable angina, in which chest pain can be induced by exercise or stress, chest pain secondary to unstable angina may occur at rest and without any precipitating factors at all. Pain may increase in the severity, frequency, or duration at low levels of activity or for no identifiable reason. Diabetes mellitus, hypertension, myxedema, peripheral vascular disease, heart valve disease, cardiomyopathy, and atherosclerosis may also produce this type of angina.

Risk factors for unstable angina are similar to those for stable angina, and include:

• male gender
• cigarette smoking
• high cholesterol levels (in particular, high LDL cholesterol and low HDL cholesterol)
• high blood pressure
• diabetes
• family history of coronary heart disease before age 55
• sedentary lifestyle
• being more than 30% over ideal body weight

Occasionally, sudden overwhelming stress can precipitate an episode of angina.

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