冠状动脉粥样硬化中的炎症和血栓形成机制
Inflammatory and thrombotic mechanisms in coronary atherosclerosis.
作者信息
Tousoulis D, Davies G, Stefanadis C, Toutouzas P, Ambrose J A
机构信息
Cardiology Unit, Athens University Medical School, Athens, Greece.
出版信息
Heart. 2003 Sep;89(9):993-7. doi: 10.1136/heart.89.9.993.
Abstract
Many molecular and cellular mechanisms link inflammation and haemostatic mechanisms. Inflammation, and perhaps chronic infection, may play important roles in the initiation and progression of atherosclerosis. Atherosclerotic lesions are heavily infiltrated by cellular components associated with inflammation (macrophages and T lymphocytes), and acute plaque rupture is also associated with inflammatory components. Several markers of systemic inflammation may predict future cardiovascular events in apparently healthy subjects as well as in patients with chronic and acute syndromes. There may thus be therapeutic potential in modifying the atherosclerotic, vasomotor, and thrombotic components of ischaemic heart disease.
摘要
许多分子和细胞机制将炎症与止血机制联系起来。炎症，或许还有慢性感染，可能在动脉粥样硬化的发生和发展中起重要作用。动脉粥样硬化病变被与炎症相关的细胞成分（巨噬细胞和T淋巴细胞）大量浸润，急性斑块破裂也与炎症成分有关。全身炎症的几种标志物可能预测看似健康的受试者以及患有慢性和急性综合征的患者未来的心血管事件。因此，改变缺血性心脏病的动脉粥样硬化、血管舒缩和血栓形成成分可能具有治疗潜力。
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