Sumida H, Watanabe H, Kugiyama K, Ohgushi M, Matsumura T, Yasue H
Division of Cardiology, Kumamoto Rosai Hospital, Japan.
J Am Coll Cardiol. 1998 Mar 15;31(4):811-5. doi: 10.1016/s0735-1097(98)00010-2.
This study sought to examine whether passive smoking is associated with endothelial dysfunction in the coronary arteries.
Long-term exposure to cigarette smoking has been reported to suppress endothelium-dependent arterial dilation in humans. Endothelial dysfunction is an early feature of atherogenesis, and the impairment of acetylcholine (ACh)-induced coronary artery dilation indicates coronary endothelial dysfunction.
We studied 38 women (40 to 60 years old) who had no known risk factors for coronary artery disease other than tobacco smoking: 11 nonsmokers who had never smoked and had never been regularly exposed to environmental tobacco smoke; 19 passive smokers with self-reported histories of exposure to environmental tobacco smoke of > or = 1 h/day for > or = 10 years; and 8 active smokers. We examined the response of the epicardial coronary artery diameters (proximal and distal segments of the left anterior descending [LAD] and left circumflex [LCx] coronary arteries) to the intracoronary injection of ACh into the left coronary artery by means of quantitative coronary angiography.
ACh significantly dilated the distal segment in nonsmokers (percent change from baseline diameter: LAD 13.7+/-3.4%, p < 0.05; LCx 18.8+/-2.9%, p < 0.01) but not the proximal segment (LAD 7.4+/-3.5%; LCx 3.1+/-5.0%). ACh significantly constricted all segments of the left coronary artery in passive smokers (LAD: proximal -20.3+/-3.7%, p < 0.05; distal -22.3+/-4.1%, p < 0.01; LCx: proximal -20.8+/-3.1%, p < 0.05; distal -17.3+/-2.9%, p < 0.01) and active smokers (LAD: proximal -14.8+/-3.4%, p < 0.05; distal -27.2+/-6.0%, p < 0.01; LCx: proximal -14.5+/-6.6%, p < 0.05; distal -22.4+/-4.0%, p < 0.01). Thus, ACh constricted most coronary arteries in both passive and active smokers and dilated the coronary arteries in nonsmokers.
Impairment of ACh-induced coronary artery dilation, indicating coronary endothelial dysfunction, may occur diffusely in passive smokers as well as in active smokers.
本研究旨在探讨被动吸烟是否与冠状动脉内皮功能障碍有关。
据报道，长期接触香烟烟雾会抑制人体内皮依赖性动脉扩张。内皮功能障碍是动脉粥样硬化形成的早期特征，乙酰胆碱（ACh）诱导的冠状动脉扩张受损表明冠状动脉内皮功能障碍。
我们研究了38名年龄在40至60岁之间、除吸烟外无已知冠状动脉疾病危险因素的女性：11名从不吸烟且从未经常接触环境烟草烟雾的非吸烟者；19名自述每天接触环境烟草烟雾≥1小时、持续≥10年的被动吸烟者；以及8名主动吸烟者。我们通过定量冠状动脉造影检查了心外膜冠状动脉直径（左前降支[LAD]和左旋支[LCx]冠状动脉的近端和远端节段）对向左冠状动脉内注射ACh的反应。
ACh使非吸烟者的远端节段显著扩张（相对于基线直径的百分比变化：LAD为13.7±3.4%，p<0.05；LCx为18.8±2.9%，p<0.01），但近端节段未扩张（LAD为7.4±3.5%；LCx为3.1±5.0%）。ACh使被动吸烟者（LAD：近端-20.3±3.7%，p<0.05；远端-22.3±4.1%，p<0.01；LCx：近端-20.8±3.1%，p<0.05；远端-17.3±2.9%，p<0.01）和主动吸烟者（LAD：近端-14.8±3.4%，p<0.05；远端-27.2±6.0%，p<0.01；LCx：近端-14.5±6.6%，p<0.05；远端-22.4±4.0%，p<0.01）的左冠状动脉所有节段显著收缩。因此，ACh使被动吸烟者和主动吸烟者的大多数冠状动脉收缩，而使非吸烟者的冠状动脉扩张。
ACh诱导的冠状动脉扩张受损，表明冠状动脉内皮功能障碍，可能在被动吸烟者和主动吸烟者中广泛发生。
