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血栓形成的多种机制使动脉粥样硬化斑块复杂化。

Multiple mechanisms of thrombosis complicating atherosclerotic plaques.

作者信息

Libby P

机构信息

Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.

出版信息

Clin Cardiol. 2000 Nov;23 Suppl 6(Suppl 6):VI-3-7. doi: 10.1002/clc.4960231103.

DOI:10.1002/clc.4960231103
PMID:11129684
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6655212/
Abstract

Atherosclerosis is a highly prevalent disorder and remains a leading cause of morbidity and mortality in the United States. Recent advances in vascular biology have led to a better understanding of the mechanisms underlying atherogenesis. The central role played by plaque disruption, and by adhesion, activation, and aggregation of platelets that trigger activation of the coagulation cascade in the pathogenesis of acute thrombotic events is also better understood. Combination antithrombotic therapy targeting various platelet activation mechanisms and the coagulation cascade may help optimize the management of atherosclerosis.

摘要

动脉粥样硬化是一种高度常见的疾病,在美国仍然是发病和死亡的主要原因。血管生物学的最新进展使人们对动脉粥样硬化发生的潜在机制有了更好的理解。斑块破裂以及血小板的黏附、激活和聚集在急性血栓形成事件的发病机制中触发凝血级联反应所起的核心作用也得到了更好的理解。针对各种血小板激活机制和凝血级联反应的联合抗栓治疗可能有助于优化动脉粥样硬化的管理。

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Molecular biology of atherosclerosis.动脉粥样硬化的分子生物学
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