[Atherosclerosis].

Abstract

Atherosclerosis is vascular disease characterized by thickening, hardening, and remodelling of the arterial wall. Occlusive vascular disease most often results from thrombosis superimposed on atherosclerotic plaque. Lipoproteins enter the vessel wall, promoting the recruitment of monocytes, which imbibe lipids and become foam cells. Smooth muscle cells invade these early plaques, producing connective tissue fibrils that form a fibrous cap over the lipid center; rupture of this cap is an important cause of thrombosis. The specific topography of early atherosclerotic lesions is primarily attributed to wall shear stress, one of hemodynamic forces. Inflammatory mediators regulate processes that determine the composition of the plaque's fibrous cap, a structure that separates blood from the thrombogenic lipid core. Factors involved in coagulation, such as thrombin, can regulate non-thrombotic functions of vascular wall cells such as smooth muscle proliferation or cytokine release. Tissue factor is a major regulator of coagulation and hemostasis. When the plaques are ruptured or eroded, exposure of cellular and extracellular tissue factor to circulating blood play a pivotal role in mediating fibrin-rich thrombus formation leading to acute coronary syndromes. Several serial angiographic studies have demonstrated that over 70% of acute coronary syndromes evolve from mildly to moderately obstructive atherosclerotic plaques.