Lipid lowering therapy in atherosclerosis.

Masanori Aikawa, Peter Libby
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引用次数: 30

Abstract

Dyslipidemia plays critical roles in the pathogenesis of coronary atherosclerosis, a chronic inflammatory disease. Vascular inflammation also triggers the onset of acute complications of atherosclerosis, such as myocardial infarction. Advances in cardiovascular medicine demonstrate that lipid-lowering therapy by 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) likely prevents acute coronary complications by limiting vascular inflammation. In particular, recent clinical evidence indicates aggressive lipid-lowering treatment for patients at risk. Preclinical studies also support the concept of anti-inflammatory properties of lipid lowering by either diet or statins. Therefore, dyslipidemia is the primary target of therapy for the prevention of coronary atherosclerosis and its acute thrombotic complications. Nevertheless, even aggressive statin therapy does not forestall many adverse events. Thus, current cardiovascular medicine also seeks mechanisms to mitigate vascular inflammation and atherosclerosis other than addressing low-density lipoprotein, and new therapeutic strategies beyond lipid lowering.

动脉粥样硬化中的降脂治疗。
血脂异常在冠状动脉粥样硬化这一慢性炎症性疾病的发病机制中起着至关重要的作用。血管炎症也会引发动脉粥样硬化的急性并发症,如心肌梗死。心血管医学的进展表明,3-羟基-3-甲基戊二酰辅酶A还原酶抑制剂(他汀类药物)的降脂治疗可能通过限制血管炎症来预防急性冠状动脉并发症。特别是,最近的临床证据表明,积极的降脂治疗患者的风险。临床前研究也支持通过饮食或他汀类药物降脂的抗炎特性。因此,血脂异常是预防冠状动脉粥样硬化及其急性血栓并发症的主要治疗目标。然而,即使是积极的他汀类药物治疗也不能预防许多不良事件。因此,目前的心血管医学还在寻找除低密度脂蛋白外减轻血管炎症和动脉粥样硬化的机制,以及除降脂外的新的治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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