title: [Mechanisms of coronary plaque formation and disruption].
abstract: We review here the evolutional understanding of the pathophysiology of chronic and acute phase of coronary artery disease (CAD). Although we previously considered CAD as a cholesterol storage disease, we currently understand that atherosclerosis is an inflammatory disorder and inflammation plays a major role in all stages of atherogenesis. We formerly focused our attention on luminal narrowing due to the atheroma. However, we now recognize the need to attend to non-obstructive lesions and their biological attributes as well. Moreover, plaque disruption is thought to occur due to, not only local changes in the plaque itself, but also systemic changes in the patient. Thus, treatment of CAD should involve the approach of mechanical revascularization and systemic preventive intervention.
authors.affiliation: Department of Cardiovascular Medicine, Wakayama Medical University.
authors.forename: Yoshiki
authors.initials: Y
authors.lastname: Matsuo
authors.forename: Takashi
authors.initials: T
authors.lastname: Akasaka
mesh_terms: D001777:Blood Coagulation; D002465:Cell Movement; D003324:Coronary Artery Disease / Q000209:etiology* / Q000473:pathology* / Q000517:prevention & control / Q000628:therapy; D003328:Coronary Thrombosis / Q000209:etiology; D003331:Coronary Vessels / Q000473:pathology*; D005109:Extracellular Matrix / Q000378:metabolism; D005110:Extracellular Space / Q000378:metabolism; D005355:Fibrosis; D006801:Humans; D007249:Inflammation / Q000150:complications; D007962:Leukocytes / Q000276:immunology; D050356:Lipid Metabolism; D020782:Matrix Metalloproteinases / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000166:cytology; D009389:Neovascularization, Pathologic
chemical_list: D020782:Matrix Metalloproteinases