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- W2104112841 abstract "textabstractDespite the fact that mortality from cardiovascular diseases has declined considerablyover the last decades, it still represents the leading cause of mortality andmorbidity in industrialized countries. Most clinical manifestations of cardiovasculardisease share the underlying pathophysiological process of atherosclerosis.Atherosclerosis is a diseased state of the intima and media of medium to large sizedarteries characterized by focal plaques preferentially located in areas of low shear.It is assumed that plaques origin from fatty streaks that are initiated by oxidation oflow density lipoprotein. Formation of fatty streaks may also follow initial injuryfrom a wide range of agents including toxins, viral infections and intraluminaldevices such as catheters. The subsequent inflammatory reactions induce smoothmuscle proliferation by growth factor production from a wide range of cellsincluding platelets, endothelial cells, macrophages, and other smooth muscle cells.The development of fatty streaks may already commence early in childhood andprogress over a period of decades to become atherosclerotic plaques which containlipid-filled foam cells, extracellular lipid and a layer of smooth muscle cells justbeneath the endothelium.' Plaque growth is mediated by the proliferation of smoothmuscle cells and extracellular connective tissue elements such as collagen, elastin,and proteoglycans. Growth factors derived from the interaction between plateletsand the underlying artery wall further stimulates this process. This process willlead to the formation of a fibrolipid plaque that constitutes a core of extracellularlipid separated from the media by smooth muscle cells and covered and separatedfrom the lumen by a thick cap of collagen-rich fibrous tissue containing smoothmuscle cells. Surrounding the lipid core are lipid-filled foam cells. Elevatedcoronary plaques may cause clinical symptoms when the plaque size is sufficient toobstruct the normal bloodflow, usually when it occupies more than 40 percent of the original cross-sectional area of the lumen. As the result of a dynamic interplaybetween plaque vulnerability, possibly mediated through a process of inflammation,and external stresses the atherosclerotic plaque surface may eventually rupture." @default.
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- W2104112841 date "1994-11-23" @default.
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- W2104112841 title "Long-term oral anticoagulant treatment after myocardial infarction : results of the 'Anticoagulants in the Secondary Prevention of Events in Coronary Thrombosis' (ASPECT) trial" @default.
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