摘要目的 探讨吸烟对轻中度颈动脉狭窄患者口服阿司匹林预防脑卒中效果的影响.方法 收集2011年8月至2015年3月本院就诊的轻中度颈动脉狭窄患者300例,均口服阿司匹林预防脑卒中.按吸烟情况将患者分为未吸烟组(n=94)与吸烟组(n=206),并按吸烟指数将吸烟组患者分为轻度吸烟组(n=88)、中度吸烟组(n=70)与重度吸烟组(n=48).治疗前、治疗6个月和12个月所有患者进行美国国立卫生研究院卒中量表(NIHSS)评分和改良Rankin评分(mRS).采用颈部超声检测各组患者颈动脉内膜中层厚度(CIMT)变化,记录治疗6个月颈动脉内膜增厚例数、斑块形成例数及斑块面积.随访12个月,记录脑卒中发病情况和不良出血事件发生情况.结果 颈部超声检查显示,治疗6个月未吸烟组患者颈动脉内膜增厚比例及斑块形成率均低于吸烟各组(均P<0.05);随着吸烟指数上升,颈动脉内膜增厚比例及斑块形成率均增加.治疗6个月未吸烟组患者CIMT低于吸烟各组,且斑块面积小于吸烟各组(均P<0.05);重度、中度吸烟组CIMT高于轻度吸烟组,且重度吸烟组高于中度吸烟组(均P<0.05).治疗前各组患者NIHSS、mRS评分组间比较,差异无统计学意义(均P>0.05);治疗6个月、12个月,各组患者NIHSS、mRS评分较治疗前均显著降低(均P<0.05).治疗6个月、12个月,未吸烟组患者NIHSS、mRS评分较吸烟各组均显著降低(均P<0.05);随着吸烟指数增加,患者NIHSS、mRS评分降低速度减缓.未吸烟组和轻度、中度、重度吸烟组患者的脑卒中发病率分别为14.9%(14/94)、28.4%(25/88)、38.6%(27/70)、45.8%(22/48).吸烟各组脑卒中发病率均高于未吸烟组(均P<0.05);且重度吸烟组高于中度、轻度吸烟组,中度吸烟组高于轻度吸烟组(均P<0.05).重度、中度吸烟组脑出血发病率高于未吸烟组(均P<0.05).结论 吸烟可影响轻中度颈动脉狭窄患者应用阿司匹林预防脑卒中的效果,增加脑卒中发病风险和不良事件发生率.

abstractsObjective To investigate the impact of smoking on the efficacy of oral aspirin for stroke prevention in patients with mild to moderate carotid artery stenosis. Methods Included in this study were 300 patients with mild to moderate carotid artery stenosis treated in our hospital between August 2011 and March 2015. All the patients were given oral aspirin for stroke prevention. According to smoking habits,these patients were divided into non-smokers(n=94)and smokers(n=206). The smokers were further divided into mild smokers(n=88),moderate smokers(n=70)and heavy smokers(n=48)according to smoking index. Before and at 6,12 months of treatment,all the patients were evaluated with the National Institutes of Health Stroke Scale(NIHSS)score and modified Rankin score(mRS). The changes in carotid intima-media thickness(CIMT)were examined by carotic ultrasound screening. The number of patients with carotid intima thickening,or with plaque formation(as well as the plaque area)was recorded at 6 months of treatment. During a follow-up for 12 months,the incidence of stroke and the adverse hemorrhage events was recored. Results The carotic ultrasonography showed that non-smokers had less carotid intima thickening and plaque formation than the smokers at 6 months of treatment(all P<0.05). With the increase in smoking index,there was an increase in rates of carotid artery intima thickening and plaque formation. At 6 months of treatment,non-smokers had lower CIMT and smaller plaque areas than smokers(all P<0.05);While the CIMT was greater in moderate to heavy smokers than in mild smokers,and in heavy smokers than in moderate smokers(all P<0.05). There were no significant differences in NIHSS score and mRS among all patients before treatment(all P>0.05). At 6 and 12 months of treatment,the NIHSS score and mRS were significantly reduced in all groups(all P<0.05);and non-smokers had lower NIHSS score and mRS than smokers(all P<0.05). With the increase in smoking index,the reduction in NIHSS score and mRS appeared slower. The incidence rates of stroke in non-smokers,mild,moderate and heavy smokers were 14.9%(14/94), 28.4%(25/88),38.6%(27/70),and 45.8%(22/48),respectively. The incidence rate of stroke was higher in smokers than in non-smokers(all P<0.05),in heavy smokers than in moderate to mild smokers,and in moderate smokers than in mild smokers(all P<0.05). The incidence rate of cerebral hemorrhage in heavy and moderate smokers was higher than that in non-smokers(both P<0.05). Conclusion Smoking may interfere with the efficacy of aspirin for stroke prevention in patients with mild to moderate carotid artery stenosis ,and may increase the risk of stroke and the incidence of adverse events.