Pathophysiology of coronary thrombosis: role of plaque rupture and plaque erosion.
Coronary artery disease is the leading cause of death in much of the western world. Atherosclerotic plaques in the coronary arteries contribute to luminal obstruction leading to myocardial ischemia; however, abrupt coronary artery occlusion most frequently results from superimposition of a thrombus on a disrupted plaque, leading to the most serious clinical manifestations of coronary artery disease, ie, unstable angina, acute myocardial infarction, and sudden death. Plaque that have undergone disruption and, by inference, plaques at risk for disruption (vulnerable plaques), tend to demonstrate outward vessel remodeling, contain a large lipid core, thinned out fibrous cap, reduced collagen content, and increased inflammatory cell infiltration. Plaque stabilization through change in plaque composition may be responsible for reduced frequency of acute vaso-occlusive events observed with lipid and other risk-factor modifying interventions.
Shah
Prediman K
PK
Division of Cardiology and Atherosclerosis Research Center, Burns and Allen Research Institute, and Department of Medicine, Cedars Sinai Medical Center and UCLA School of Medicine, Los Angeles, California 90048, USA.
D003251:Constriction, Pathologic / Q000473:pathology; D003324:Coronary Artery Disease / Q000188:drug therapy / Q000473:pathology*; D003328:Coronary Thrombosis / Q000150:complications / Q000473:pathology* / Q000503:physiopathology; D005109:Extracellular Matrix / Q000473:pathology; D006801:Humans; D007249:Inflammation / Q000473:pathology; D012422:Rupture, Spontaneous / Q000150:complications / Q000473:pathology