Abstract
An acute coronary syndrome (ACS) is the clinical manifestation of a thrombotic event occurring within a coronary artery narrowed by atherosclerosis. This atherothrombotic event is thought to occur following destabilizing changes within the atherosclerotic plaque, rendering it a surface on which thrombus can develop. The development and progression of this thrombus are determined by deleterious perturbations in the hemostatic equilibrium within the local environment of the plaque that favor thrombosis. Major risk factors for the development of atherosclerotic disease have been clearly established and are targets of aggressive modification in an effort to impede the development or slow the progression of disease. While conferring an increased risk for plaque development, these and other risk factors also establish a prothrombotic milieu within the microenvironment of the atherosclerotic plaque that favors thrombosis. This review seeks to address these traditional and emerging risk factors from the context of their pathologic effects on local hemostatic balance. Aggressive risk factor modification not only reduces atherosclerotic disease development and progression, but also ameliorates the prothrombotic state, and ultimately serves to reduce atherothrombotic events.
