Meinertz T, Heitzer T
Abteilung für Kardiologie Universitätsklinikum Hamburg-Eppendorf Martinistrasse 52 20246 Hamburg, Germany.
Z Kardiol. 2002;91 Suppl 2:3-11.
Although smoking is one of the major risk factors for the development of atherosclerosis, the exact mechanism of smoking-related vascular disease is not known. Smoking causes acute hemodynamic alterations such as increase in heart rate, systemic and coronary vascular resistance, myocardial contractility, and myocardial oxygen demand. These short-term effects could lower the ischemic threshold in smokers with coronary artery disease and contribute to the increased risk for acute cardiovascular events. Endothelial damage is thought to be an initiating event in atherosclerosis and early studies have demonstrated that long-term smoking has direct toxic effects with structural changes of human endothelial cells. Recent research has shown the importance of the functional role of the endothelium in regulating normal vascular tone, platelet-endothelial interactions, leukocyte adhesion and smooth muscle cell proliferation via synthesis and release of a variety of substances such as nitric oxide. There is strong evidence that smoking leads to endothelial dysfunction in both conductance and resistance vessels. This effect seems to be dose-related and reversible. The mechanism of endothelial dysfunction in smokers is not known, but increased degradation of nitric oxide by oxygen-derived free radicals has been suggested. In addition, smoking could cause oxidative inactivation of tetrahydrobiopterin, a critical cofactor of nitric oxide, leading to an uncoupling of the endothelial nitric oxide synthase with increased superoxide production and decreased nitric oxide bioactivity. Other pro-atherosclerotic effects of smoking are discussed. Given the enormous health hazard of tobacco use, complete abstinence from smoking should be achieved. Smoking cessation counseling should be given to healthy subjects and even more vigorously to patients with manifested disease. Every effort should be undertaken to prevent children and adolescents from starting to smoke. Brief tobacco dependence treatment is effective, and every tobacco user should be offered at least brief treatment at every office visit. More intensive treatment is more effective in producing long-term abstinence from tobacco. Nicotine replacement therapy (nicotine patches or gum), clinician-delivered social support, and skills training are the three most effective components of smoking cessation treatment.
尽管吸烟是动脉粥样硬化发展的主要危险因素之一，但吸烟相关血管疾病的确切机制尚不清楚。吸烟会引起急性血流动力学改变，如心率加快、全身及冠状动脉血管阻力增加、心肌收缩力增强和心肌需氧量增加。这些短期效应可能会降低冠心病吸烟者的缺血阈值，并增加急性心血管事件的风险。内皮损伤被认为是动脉粥样硬化的起始事件，早期研究表明，长期吸烟对人内皮细胞的结构变化具有直接毒性作用。最近的研究表明，内皮通过合成和释放一氧化氮等多种物质，在调节正常血管张力、血小板-内皮相互作用、白细胞黏附和平滑肌细胞增殖方面发挥着重要的功能作用。有强有力的证据表明，吸烟会导致传导血管和阻力血管的内皮功能障碍。这种效应似乎与剂量相关且是可逆的。吸烟者内皮功能障碍的机制尚不清楚，但有人提出氧衍生自由基会增加一氧化氮的降解。此外，吸烟可能导致四氢生物蝶呤氧化失活，四氢生物蝶呤是一氧化氮的关键辅助因子，从而导致内皮一氧化氮合酶解偶联，超氧化物生成增加，一氧化氮生物活性降低。本文还讨论了吸烟的其他促动脉粥样硬化作用。鉴于吸烟对健康的巨大危害，应完全戒烟。应对健康受试者提供戒烟咨询，对已患病的患者则应更积极地进行咨询。应尽一切努力防止儿童和青少年开始吸烟。简短的烟草依赖治疗是有效的，每次门诊时都应至少为每位烟草使用者提供简短治疗。更强化的治疗在实现长期戒烟方面更有效。尼古丁替代疗法（尼古丁贴片或口香糖）、临床医生提供的社会支持和技能培训是戒烟治疗最有效的三个组成部分。
