Nielsen Vance G, Hafner David T, Steinbrenner Evangelina B
Department of Anesthesiology, The University of Arizona College of Medicine, Tucson, AZ 85724-5114, USA.
Blood Coagul Fibrinolysis. 2013 Jun;24(4):381-5. doi: 10.1097/MBC.0b013e32835d53ec.
In the setting of acute myocardial infarction, decreases in early/late mortality, reocclusion after thrombolysis, and restenosis rate after percutaneous intervention are lower in smokers - this phenomenon has been designated as the 'smoker's paradox'. These benefits of smoking, however, are abrogated by stent placement. We hypothesized that fibrinolytic vulnerability would change in response to smoking, and that inhaled carbon monoxide may play a role. Smoking patients (n = 20, two cigarettes consumed within 90 min, average carboxyhemoglobin concentration of 5%) had plasma collected and normal individual (n = 20) plasma was also obtained. Thrombelastographic analyses conducted with addition of tissue-type plasminogen activator revealed that with the exception of the rate of thrombus generation, there was little difference in fibrinolytic kinetics between normal and smoking individuals. Addition of exogenous carbon monoxide resulted in diminished fibrinolytic response to the same extent in both groups. Subanalyses demonstrated that the smoking cohort had both hyperfibrinolytic and hypofibrinolytic patients as defined by confidence interval (5-95%) values generated from normal individuals. Addition of carbon monoxide reduced hyperfibrinolytic parameter values by 80% in smokers, whereas only a 17% decrease in hypofibrinolytic values changed. Our investigation suggests that 'smoker's paradox' involves a marked change in the character of the plasmin-antiplasmin-carbon monoxide interaction. Further investigation will be required to further define the molecular mechanism responsible for the 'smoker's paradox'.
在急性心肌梗死的情况下，吸烟者的早期/晚期死亡率、溶栓后再闭塞率以及经皮介入治疗后的再狭窄率降低——这一现象被称为“吸烟者悖论”。然而，吸烟的这些益处会因置入支架而消除。我们推测，纤溶易感性会因吸烟而改变，并且吸入的一氧化碳可能起作用。收集了吸烟患者（n = 20，90分钟内吸两支烟，平均碳氧血红蛋白浓度为5%）的血浆，同时也获取了正常个体（n = 20）的血浆。添加组织型纤溶酶原激活剂后进行的血栓弹力图分析显示，除血栓生成速率外，正常个体与吸烟个体之间的纤溶动力学几乎没有差异。添加外源性一氧化碳后，两组的纤溶反应均在相同程度上减弱。亚组分析表明，根据正常个体生成的置信区间（5 - 95%）值定义，吸烟队列中既有高纤溶患者也有低纤溶患者。在吸烟者中，添加一氧化碳使高纤溶参数值降低了80%，而低纤溶值仅降低了17%。我们的研究表明，“吸烟者悖论”涉及纤溶酶 - 抗纤溶酶 - 一氧化碳相互作用特征的显著变化。需要进一步研究以进一步明确导致“吸烟者悖论”的分子机制。
