Pathoanatomic studies indicate that the atheromatous component enlarges with plaque growth, 8 35 36 but the variability is great, and data on a possible relation between size and composition of plaques are incomplete. 19 Therefore, the soft lipid-rich core within a plaque is also called a “necrotic core” and “atheronecrosis.” 28 29 30 Recent observations, however, suggest that the core does not originate primarily from dead foam cells in the superficial intima (fatty streaks) but rather arises from lipids accumulating gradually in the extracellular matrix of the deep intima as a result of complex binding between insudating LDL and glycosaminoglycans, collagen, and/or fibrinogen. 17 18 19 The relative contribution of direct lipid trapping versus foam cell necrosis in the formation of the atheromatous core and its growth is unknown, although foam cell necrosis is widely believed to be more important. Insudated blood-derived lipid, preferentially LDL, may be trapped and accumulate directly within the extracellular space, or it may be endocytosed by macrophages, probably via their scavenger receptors after oxidative modification, and accumulate indirectly after necrosis of the lipid-filled macrophages (foam cells). 27 28 The pathogenesis of this, the clinically more important plaque component, however, remains controversial. The atheromatous core within a plaque is devoid of supporting collagen, avascular, hypocellular (except at the periphery of the core), rich in extracellular lipids, and soft like gruel. 7 8Ītherosis: Lipid Trapping and/or Cell Death? 6 This review will explore potential mechanisms responsible for the sudden conversion of a stable atherosclerotic plaque to an unstable and life-threatening atherothrombotic lesion-an event known as plaque fissuring, rupture, or disruption. The composition and vulnerability of plaque rather than its volume or the consequent severity of stenosis produced have emerged as being the most important determinants for the development of the thrombus-mediated acute coronary syndromes lipid-rich and soft plaques are more dangerous than collagen-rich and hard plaques because they are more unstable and rupture-prone and highly thrombogenic after disruption. 1 2 3 4 5 Therefore, for event-free survival, the vital question is not why atherosclerosis develops but rather why, after years of indolent growth, it suddenly becomes complicated by life-threatening thrombosis. Customer Service and Ordering InformationĬoronary atherosclerosis is by far the most frequent cause of ischemic heart disease, and plaque disruption with superimposed thrombosis is the main cause of the acute coronary syndromes of unstable angina, myocardial infarction, and sudden death.Stroke: Vascular and Interventional Neurology. Journal of the American Heart Association (JAHA).Circ: Cardiovascular Quality & Outcomes.Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB).
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