Folts J D, Gering S A, Laibly S W, Bertha B G, Bonebrake F C, Keller J W
Department of Medicine, University of Wisconsin, Madison.
Adv Exp Med Biol. 1990;273:339-58. doi: 10.1007/978-1-4684-5829-9_33.
The causal link between smoking, atherosclerosis and an increased risk for acute platelet mediated coronary events such as acute platelet thrombus formation, myocardial infarction, and sudden coronary death is not clear. Our studies suggest that there may be a transient increase in in vivo platelet activity with each exposure to cigarette smoke or elevated plasma nicotine. It is thought that platelets may contribute to the acceleration of the atherosclerotic process by several mechanisms (5). Thus it may be that each time a person increases their platelet activity, by smoking or some other means, and given other predisposing conditions such as elevated lipids and/or acute intimal damage, such as rupture of an atherosclerotic plaque, the atherosclerotic process may be enhanced. In addition it appears that cigarette smoke makes a developing thrombus more adherent and less likely to embolize distally, although the effect is transient. Finally, cigarette smoke may provide the final stimulus for an occlusive coronary thrombus in a stenosed coronary artery already predisposed to thrombosis by other risk factors. This may account for the fact that the risk of coronary occlusion and myocardial infarction decreases markedly in the first year after quitting (65). It may be that smoking has a greater likelihood of precipitating a fatal thrombus than it does of accelerating the altherosclerotic process. This would be reflected in the inability of aspirin to prevent the smoking induced enhancement of CFR's in our model (23) or the enhancement of platelet function in men with coronary artery disease (66).
吸烟、动脉粥样硬化与急性血小板介导的冠状动脉事件（如急性血小板血栓形成、心肌梗死和心源性猝死）风险增加之间的因果关系尚不清楚。我们的研究表明，每次接触香烟烟雾或血浆尼古丁升高时，体内血小板活性可能会出现短暂升高。人们认为，血小板可能通过多种机制促进动脉粥样硬化进程（5）。因此，可能每次一个人通过吸烟或其他方式提高其血小板活性，并且存在其他易感条件，如血脂升高和/或急性内膜损伤（如动脉粥样硬化斑块破裂）时，动脉粥样硬化进程可能会加速。此外，尽管这种影响是短暂的，但香烟烟雾似乎会使正在形成的血栓更具黏附性，且更不容易向远端栓塞。最后，香烟烟雾可能会为已经因其他危险因素而易发血栓形成的狭窄冠状动脉中的闭塞性冠状动脉血栓提供最终刺激。这可能解释了戒烟后第一年冠状动脉闭塞和心肌梗死风险显著降低这一事实（65）。可能吸烟引发致命血栓的可能性比加速动脉粥样硬化进程的可能性更大。这将体现在阿司匹林无法在我们的模型中预防吸烟引起的冠状动脉血流储备（CFR）增强（23），或无法预防冠心病男性的血小板功能增强（66）。
