The cause of a heart attack in the majority of cases is a blockage of a coronary artery by a blood clot. This clot usually occurs on the surface of a partially obstructing plaque of atheroma (see the figures in the chapter Atherosclerosis/Atherothrombosis). The surface of a plaque ruptures and the plaque contains substances that increase the clotting of blood. A clot therefore forms on the surface of the rupture and also inside the plaque. The ruptured plaque, by direct release of tissue factor and exposure of the subintima, is highly thrombogenic. Exposed collagen further provokes platelet aggregation. Some plaques, particularly those that have a high lipid content and a thin fibrous cap, are prone to rupture (see the chapter Atherosclerosis/Atherothrombosis). Considerable research has been done during the past decade on the complexity and the instability of vulnerable plaques.
Coronary angiography performed during the early hours of infarction confirms the presence of total occlusion of the infarct-related artery in over 90% of patients. It is not surprising that aspirin, through inhibition of platelet aggregation, reduces the incidence of coronary thrombosis and prevents the progression of unstable angina to thrombosis and myocardial infarction. Aspirin is particu¬larly useful when given at the onset of chest pain produced by an infarction. However, it does not block all pathways that relate to platelet aggregation (see the chapter Antiplatelet Agents).

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