Thrombotic and Fibrinolytic Factors in Acute Coronary Syndrome
AbstractIt is now generally accepted that intracoronary thrombosis after plaque disruption is a major cause of the acute coronary syndromes (ACS) of unstable angina, myocardial infarction, and sudden cardiac death. Thrombus arises from procoagulant changes in complex plaques, which trigger both platelet activation and coagulation pathways.1 The magnitude of the local thrombogenic response also contributes to occlusive complications after percutaneous coronary intervention (PCI), either via thrombus formation or by other mechanisms.2,3 High levels of the biochemical markers of the activation of the hemostatic mechanism have been found in patients with ongoing intracoronary thrombosis and may therefore be helpful in identifying patients who are at the greatest risk of an unfavorable outcome.
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