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吸烟对血小板聚集的影响。

Effect of cigarette smoking on platelet aggregation.

机构信息

Istanbul University, Istanbul Faculty of Medicine, Department of Cardiology, Istanbul, Turkey.

出版信息

Clin Appl Thromb Hemost. 2011 Nov-Dec;17(6):E175-80. doi: 10.1177/1076029610394440. Epub 2011 Mar 14.

DOI:10.1177/1076029610394440
PMID:21406413
Abstract

BACKGROUND

Cigarette smoking may increase platelet aggregation and cause atherothrombotic cardiovascular events. We aimed to investigate the impact of cigarette smoking on platelet function in patients with ischemic coronary heart disease (CHD).

METHODS

Twenty patients with ischemic stable CHD under aspirin therapy (300 mg/d), who continue to smoking despite all warnings, and 20 nonsmokers with CHD are enrolled in the study. Platelet function is studied at the morning, before and 15 minutes after the first cigarette, by the Platelet Function Analyzer (PFA)-100, with collagen and epinephrine and collagen and adenosine diphosphate cartridges. Post aspirin platelet hyperactivity is defined as having a closure time (CT) shorter than 186 seconds despite regular aspirin intake. Serial CT measurements are analyzed by paired samples t test.

RESULTS

Persistent platelet activity was present in 4 smoker (20%) and 3 nonsmoker (15%) patients at the beginning. Platelet activity measured by the PFA-100 is been increased significantly after cigarette smoking (P = .004). Shorter CTs were determined after smoking in all patients with and without baseline persistent platelet activity, and 4 more participants became aspirin nonresponder (P = .004). No significant differences in demographic, hematological, and biochemical parameters were determined between aspirin responders and nonresponders.

CONCLUSIONS

We determined that cigarette smoking may increase platelet aggregation in patients with ischemic CHD in an aspirin nonresponsive manner. Our results emphasize the importance of quitting cigarette smoking in patients with CHD.

摘要

背景

吸烟可能会增加血小板聚集,并导致动脉粥样硬化血栓形成的心血管事件。我们旨在研究吸烟对缺血性冠心病(CHD)患者血小板功能的影响。

方法

研究纳入 20 例正在服用阿司匹林(300mg/d)治疗的缺血性稳定型 CHD 患者,尽管已多次警告,但这些患者仍继续吸烟,同时纳入 20 例不吸烟的 CHD 患者。使用血小板功能分析仪(PFA-100),通过胶原和肾上腺素以及胶原和二磷酸腺苷检测试剂盒,在早晨、吸烟前和吸烟后 15 分钟测量血小板功能。将阿司匹林后血小板高反应性定义为尽管常规服用阿司匹林,但闭合时间(CT)仍短于 186 秒。通过配对样本 t 检验分析连续 CT 测量值。

结果

开始时,有 4 名吸烟者(20%)和 3 名不吸烟者(15%)存在持续的血小板活性。吸烟后,PFA-100 测量的血小板活性显著增加(P=0.004)。在有和没有基线持续血小板活性的所有患者中,吸烟后 CT 更短,另外 4 名患者成为阿司匹林无反应者(P=0.004)。阿司匹林反应者和无反应者之间的人口统计学、血液学和生化参数无显著差异。

结论

我们确定吸烟可能以阿司匹林无反应的方式增加缺血性 CHD 患者的血小板聚集。我们的研究结果强调了戒烟对 CHD 患者的重要性。

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