Lewis B
University of London, UK.
Isr J Med Sci. 1996 Jun;32(6):360-3.
The characteristics of a subset of atherosclerotic plaques that is responsible for myocardial infarction (infarctogenic plaques) are increasingly well defined. They include moderate size, a thin fibrous cap, and a large lipid pool. Fissuring of the cap leads to thrombotic occlusion and often to an acute coronary event. Physical stresses on, and proteolytic weakening of, the cap--both related to effects of hyperlipidemia on the plaque--increase the risk of fissuring. Treatment of hyperlipidemia leads to regression of experimental atherosclerosis, promotes regression and reduces progression of human coronary artery disease. The arterial changes in humans are predictive of reduced incidence of coronary events. This sequence of events may reflect gradual depletion of plaque lipids, and also a more rapid depletion of chronic inflammatory cells in the plaque cap that are the source of collagenase and other proteases. The primary objective of lipid-lowering therapy appears to be the induction of these changes in infarctogenic plaques, and vigorous treatment should be targeted on patients likely to harbor such plaques.
导致心肌梗死的动脉粥样硬化斑块亚组（致梗死斑块）的特征越来越明确。它们包括中等大小、薄纤维帽和大脂质池。帽的破裂会导致血栓形成性阻塞，并常常引发急性冠状动脉事件。帽上的物理应力和蛋白水解弱化——两者均与高脂血症对斑块的影响有关——会增加破裂风险。高脂血症的治疗会导致实验性动脉粥样硬化的消退，促进人类冠状动脉疾病的消退并减少其进展。人类的动脉变化可预测冠状动脉事件发生率的降低。这一系列事件可能反映了斑块脂质的逐渐消耗，以及斑块帽中慢性炎症细胞的更快消耗，这些细胞是胶原酶和其他蛋白酶的来源。降脂治疗的主要目标似乎是在致梗死斑块中诱导这些变化，并且应针对可能存在此类斑块的患者进行积极治疗。
