医学
氯吡格雷
白细胞减少症
中性粒细胞绝对计数
阿司匹林
心肌梗塞
风险因素
发病机制
中性粒细胞胞外陷阱
入射(几何)
内科学
孟德尔随机化
免疫学
疾病
心脏病学
炎症
化疗
中性粒细胞减少症
化学
遗传变异
基因型
物理
光学
基因
生物化学
作者
Stefano De Servi,Antonio Landi,Elena Gualini,Rossana Totaro,Stefano Savonitto,Sergio Leonardi
标识
DOI:10.2459/jcm.0000000000001668
摘要
Neutrophils activation plays a pivotal role in the pathogenesis of atherosclerotic plaque formation, progression and rupture. An association between the leukocyte count and the risk of developing myocardial infarction has been well known for many years; however, only recently did Mendelian randomization studies show that a high neutrophil count is a causal risk factor for atherosclerotic cardiovascular disease. On the other hand, experimental studies show that depletion of circulating neutrophils impairs plaque development. Clopidogrel, an antiplatelet agent, is widely used in combination with aspirin to reduce the incidence of ischemic events in patients treated with coronary stenting. Chronic treatment with this drug reduces inflammatory markers and neutrophil numbers, rarely causing severe leukopenia. The purpose of this review is to present recent evidence showing the link between neutrophil number and the development of cardiovascular diseases and to discuss how the clopidogrel-induced reduction in the neutrophil count may be a beneficial off-target effect of this drug.
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