Unstable angina before and after infarction: thoughts on pathogenesis and therapeutic strategies.

The pathophysiology of unstable angina both before and after infarction is incompletely understood, because the patient population with the diagnosis of unstable angina is not uniform and the definition of this condition is not precise. The question must be asked, "Why does a patient suddenly become unstable?" Several conditions can be responsible alone or in combination with each other. These conditions include extracardiac (aggravating) factors, rapid progression of coronary atherosclerosis, rapid decrease in coronary lumen size as a result of hemorrhage into an atherosclerotic plaque, transient platelet aggregation in severely diseased vessels, transient coronary artery thrombosis, and abnormal coronary artery vasoconstriction (spasm) in normal or diseased vessels. Fig. 1 summarizes a hypothetical scheme relating the above conditions to the degree of coronary artery stenosis. In patients with unstable angina before infarction, most investigators believe that severe coronary atherosclerosis and its consequences are the major pathogenic mechanisms when ischemic heart disease is present. If spasm is the mechanism, then the use of vasodilators is warranted. However, if thrombosis is clearly defined, then thrombolytic therapy in the early stages seems reasonable. If severe coronary artery disease is found (with or without thrombosis), therapy with anticoagulants such as intravenous heparin during the acute phase of the illness can be argued strongly. A similar argument could be made for the use of antiplatelet agents during the convalescent phase. If extracardiac (aggravating) factors are present, they must be corrected appropriately.(ABSTRACT TRUNCATED AT 250 WORDS)