title: Molecular mechanisms of plaque instability.
abstract: OBJECTIVE
  Coronary artery thrombosis superimposed on a disrupted atherosclerotic plaque initiates abrupt arterial occlusion and is the proximate event responsible for 60-80% cases of acute coronary syndromes. This article provides a concise update on the evolving concepts in the pathophysiology of plaque rupture and thrombosis.
  
  
  RESULTS
  Over the past several years, the critical role of plaque composition rather than plaque size or stenosis severity, in plaque rupture and thrombosis have been recognized. The necrotic lipid core and plaque inflammation appear to be key factors. Extracellular matrix loss in the fibrous cap, a prelude to rupture, is attributed to matrix degrading enzymes as well as to death of matrix synthesizing smooth muscle cells; inflammation appears to play a critical role in both these processes. Inflammatory cell derived tissue factor is a key contributor to plaque thrombogenicity. Inflammation has also been implicated in plaque neovascularity, intraplaque hemorrhage and plaque expansion. Recent observations have also highlighted the important modulatory role of immune system in atherosclerosis and plaque composition.
  
  
  CONCLUSIONS
  Improved understanding of mechanisms causing plaque instability should provide novel insights into prevention of athero-thrombotic cardiovascular events.
authors: 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. shahp@cshs.org
authors: Prediman K
authors: PK
authors: Shah
mesh_terms: D000818:Animals; D003324:Coronary Artery Disease / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D003328:Coronary Thrombosis / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D005109:Extracellular Matrix / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D008954:Models, Biological