Heitzer T, Meinertz T
Universitäres Herzzentrum Hamburg, Universitätsklinikum Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany.
Z Kardiol. 2005;94 Suppl 3:III/30-42. doi: 10.1007/s00392-005-1306-y.
Smoking is the leading preventable cause of illness and premature death in Germany, claiming over 110,000 lives a year because it directly increases the risk of dying from heart disease, stroke, emphysema and a variety of cancers. The overwhelming majority of smokers begin tobacco use before they reach adulthood. Among those young people who smoke, the average age is now 13-14. In Germany, about 39% of male and 31% of female adults (age 18-60 years) continue to smoke, despite information about the unequivocally negative health consequences of smoking. The exact mechanisms of smoking-related vascular disease are not yet known. Smoking causes acute hemodynamic alterations such as increase in heart rate, systematic 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 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 mainly by increased inactivation of nitric oxide by oxygen-derived free radicals. Smoking also increases oxidative modification of LDL and is associated with lower HDL plasma levels. Smoking induces a systemic inflammatory response with increased leukocyte count and elevation of the C-reactive protein level. Importantly, the prothrombotic effects of smoking have been repeatedly demonstrated to cause alterations in platelet function, imbalance of antithrombotic vs prothrombotic factors, and decrease of fibrinolytic activity. Given the enormous health hazard of tobacco use, complete abstinence from smoking should be achieved. Smoking cessation counselling 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 smoker 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. A framework for tobacco control measures is necessary to reduce tobacco consumption and exposure to tobacco smoke. Recommendations on specific tobacco control interventions are: 1. increase in tobacco taxes; 2. comprehensive tobacco advertising bans; 3. legislation prohibiting smoking in work and public places; 4. prohibiting the sales of tobacco products to persons under 18; 5. comprehensive disclosure of the physical, chemical and design characteristics of all tobacco products; 6. training of health professionals to promote smoking prevention and cessation interventions; and 7. development of a national network of smoking cessation treatment services.
在德国,吸烟是可预防的主要致病和过早死亡原因,每年导致超过11万人死亡,因为它直接增加了死于心脏病、中风、肺气肿和多种癌症的风险。绝大多数吸烟者在成年前就开始使用烟草。在吸烟的年轻人中,平均年龄现在是13 - 14岁。在德国,尽管有关于吸烟对健康明确的负面后果的信息,但仍有大约39%的成年男性(18 - 60岁)和31%的成年女性继续吸烟。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,如心率增加、全身和冠状动脉阻力增加、心肌收缩力增加以及心肌需氧量增加。这些短期影响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类内皮细胞有直接毒性作用并导致结构改变。最近的研究表明内皮在通过合成和释放一氧化氮等多种物质来调节血管张力、血小板 - 内皮相互作用、白细胞黏附和平滑肌细胞增殖方面具有重要的功能作用。有强有力的证据表明吸烟主要通过氧衍生自由基增加一氧化氮的失活而导致内皮功能障碍。吸烟还会增加低密度脂蛋白的氧化修饰,并与血浆高密度脂蛋白水平降低有关。吸烟会引发全身炎症反应,白细胞计数增加,C反应蛋白水平升高。重要的是,吸烟的促血栓形成作用已被反复证明会导致血小板功能改变、抗血栓与促血栓因子失衡以及纤溶活性降低。鉴于吸烟对健康的巨大危害,应实现完全戒烟。应向健康人群提供戒烟咨询,对于已患病的患者更应大力提供。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,每次门诊就诊时都应至少为每位吸烟者提供简短治疗。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。有必要建立一个烟草控制措施框架以减少烟草消费和接触烟草烟雾。关于具体烟草控制干预措施的建议如下:1. 提高烟草税;2. 全面禁止烟草广告;3. 立法禁止在工作场所和公共场所吸烟;4. 禁止向18岁以下人员销售烟草制品;5. 全面披露所有烟草制品的物理、化学和设计特征;6. 培训卫生专业人员以促进吸烟预防和戒烟干预;7. 建立全国戒烟治疗服务网络。