Holay M P, Paunikar N P, Joshi P P, Sahasrabhojney V S, Tankhiwale S R
Department of Medicine Indira Gandhi Medical College, Nagpur.
J Assoc Physicians India. 2004 Feb;52:114-7.
Active smoking predisposes to atherosclerotic vascular disease but recent evidence that inhalation of environmental tobacco smoke (passive smoking) may also have deleterious cardiovascular effects, has enormous public health implications. Endothelial dysfunction is an important early feature of atherogenic process, which may occur due to passive smoking.
To assess the effect of passive smoking on endothelial function (measured by flow-mediated dilatation, a marker of endothelium-dependent arterial dilatation) and compare it with non-smokers.
Case control study.
Out-Patient Department of Medicine, Government Medical College, Nagpur.
Seventy-five young, healthy, male adults between 15-30 years age were studied. There were three groups: (a) Non smokers (n = 25) (b) Passive smokers (n= 25) and (c) Active smokers (n = 25). Subjects with diabetes mellitus, hypertension and ischemic heart disease were excluded. Lipid profile was measured in all. Endothelial function was tested non-invasively by using high frequency linear vascular probe on brachial artery. Resting brachial artery lumen, flow at rest and after hyperemia, flow-mediated dilatation and nitroglycerine-induced dilatation were measured.
The mean brachial artery lumen dilatation and flow at rest were similar in all the three groups. Flow-mediated dilatation (FMD%, a marker of endothelium-dependent dilatation and endothelial function) was significantly higher in non-smokers than passive smokers (8.9 +/- 4.8 Vs 5 +/- 2.3, p < 0.01) and also as compared with active smokers (8.9 +/- 4.8 Vs 6.6 +/- 2.2, p < 0.05). Nitroglycerine-induced dilatation, (a marker of endothelium-independent dilatation ) was similar in all the three groups. Serum lipids (mean cholesterol, LDL, and mean LDL/HDL ratio) were statistically significantly higher in passive and active smokers as compared with non-smokers (p < 0.05).
Like active smoking, passive smoking was also associated with impaired endothelial function, (a key early event in atherogenesis) and altered lipid profile, in healthy young adults.
主动吸烟易引发动脉粥样硬化性血管疾病,但近期有证据表明,吸入环境烟草烟雾(被动吸烟)也可能对心血管产生有害影响,这具有重大的公共卫生意义。内皮功能障碍是动脉粥样硬化形成过程中的一个重要早期特征,被动吸烟可能导致这种情况发生。
评估被动吸烟对内皮功能(通过血流介导的血管扩张来衡量,这是内皮依赖性动脉扩张的一个指标)的影响,并与不吸烟者进行比较。
病例对照研究。
那格浦尔政府医学院内科门诊。
对75名年龄在15至30岁之间的年轻、健康男性成年人进行了研究。分为三组:(a)不吸烟者(n = 25)(b)被动吸烟者(n = 25)和(c)主动吸烟者(n = 25)。排除患有糖尿病、高血压和缺血性心脏病的受试者。对所有人进行了血脂检测。使用高频线性血管探头对肱动脉进行非侵入性检测内皮功能。测量静息肱动脉管腔、静息及充血后的血流、血流介导的血管扩张和硝酸甘油诱导的血管扩张。
三组的平均肱动脉管腔扩张和静息血流相似。不吸烟者的血流介导的血管扩张(FMD%,内皮依赖性扩张和内皮功能的一个指标)显著高于被动吸烟者(8.9±4.8对5±2.3,p < 0.01),与主动吸烟者相比也更高(8.9±4.8对6.6±2.2,p < 0.05)。硝酸甘油诱导的血管扩张(内皮非依赖性扩张的一个指标)在三组中相似。被动吸烟者和主动吸烟者的血清脂质(平均胆固醇、低密度脂蛋白以及平均低密度脂蛋白/高密度脂蛋白比值)与不吸烟者相比在统计学上显著更高(p < 0.05)。
与主动吸烟一样,被动吸烟在健康年轻成年人中也与内皮功能受损(动脉粥样硬化形成的关键早期事件)和血脂改变有关。