A pathophysiologic basis for the clinical classification and management of unstable angina.

Recent clinical observations have extended our classification of unstable angina to include new groups of patients now recognized at high risk of subsequent infarction. Patients with non-Q wave myocardial infarction and those with early postinfarction ischemia share a prognosis similar to that of patients with crescendo angina or with acute coronary insufficiency. Unstable angina after coronary angioplasty and after coronary artery surgery also form particular subsets of patients. Pathologic, coronary angiographic, and coronary angioscopic studies have extended the role of the obstructive atherosclerotic plaque to include a dynamic component to explain the unstable state. Recognized dynamic components are rapid progression of the disease, active vasomotion, plaque fissuring, and thrombus formation. Activation of platelets and blood coagulation factors may play a major role in triggering the syndrome. Our therapeutic approach has also become more specific for the correction of the cause of the disease. Our understanding of unstable angina now appears to be at a turning point, and a pathophysiologic basis for its clinical classification and for its management may soon be available.