心血管医生戒烟知识及策略烟草依赖是一种慢性成瘾性疾病 WHO 国际疾病分类(ICD-10, F17.2) 中国的男性吸烟率居高不下吸烟是中国人心血管疾病的重要危险因素高血压 	 160M 血脂异常 160M 糖尿病 	 20M IFG 	 	 	 20M 肥胖 	 	 60M 超重200M 吸烟 		 350M 被动吸烟540M 冠心病—是吸烟致死疾病的前三位之一吸烟促发心血管疾病的发病机理内皮功能紊乱血栓生成增加炎症反应加强氧化修饰吸烟使血栓生成增加吸烟加重动脉粥样硬化吸烟增加急性非致死性心梗的风险与非吸烟者相比，吸烟者发生急性非致死性心梗的风险增加3 倍。每日吸烟量与心肌梗死发生有量效关系吸烟增加冠心病死亡风险吸烟增加心源性猝死的风险吸烟使冠脉介入治疗后发生Q 波心梗的风险增高吸烟增加致命性和非致命性脑卒中风险吸烟增加脑卒中死亡风险吸烟增加外周血管疾病危险吸烟使发生PVD 的时间早10 年吸烟使发生PVD 的风险增加10-16 倍，高于冠心病的发生风险吸烟与下列血管疾病的风险增加有关: 无症状的PVD 间歇性跛行PVD 的进展因PVD 并发症引起的截肢股帼动脉旁路失败血管手术后的死亡吸烟与主动脉瘤发生有量效关系吸烟促进主动脉扩张吸烟增加主动脉瘤死亡风险戒烟使急性心梗风险降低与吸烟者相比，冠状动脉介入治疗后戒烟者整体死亡风险明显下降戒烟使冠状动脉旁路移植术后死亡率减低对戒烟的生存收益进行评估，戒烟5 年，生存率提高3 ％，戒烟5 年可提高10 ％，戒烟15 年则可提高15 ％。戒烟者与持续吸烟者相比，反复发生心脏骤停风险明显降低戒烟使卒中风险降低戒烟使外周血管疾病症状改善戒烟是冠心病强效干预措施戒烟	 $ 2,000 –6,000 降血压药物 $ 9,000 –26,000 降血脂药物 $ 50,000 –196,000 烟草依赖的病理生理机制尼古丁依赖是烟草依赖的基础尼古丁在中枢神经中的作用机制尼古丁成瘾环吸烟者一般来讲会增加吸烟量，以获得更大的愉快感并避免戒断症状和对烟草的渴求戒断症状：躯体及情感的共同作用尼古丁成瘾: 慢性复发性成瘾性医学问题戒烟——医生责无旁贷约70% ～90% 的吸烟者每年与医生接触50% ～70% 的吸烟者对戒烟感兴趣约70% 的戒烟成功者因医生的劝告实现医生的行为被视为楷模和榜样医生是协助人们戒烟的最佳人选医生一份耕耘一份收获与对照组相比3 分钟以下咨询帮助，成效增加30 ％：3~10 分的咨询，增加60 ％：10 分以上的帮助咨询，增加130 ％，4 次以上的咨询，成功率也会加倍。医生的力量在中国：190 万临床医生每人每年帮助10 个病人戒烟如果有一个能戒烟成功每年190 万吸烟人戒烟近100 万人今后免于死于吸烟相关疾病哪一项临床手段，公共卫生措施能取得如此效果？医生在戒烟中的作用榜样的作用——自己不吸烟帮助吸烟病人戒烟积极参与政策的制定如何将控烟融入临床工作？应用科学方法，有效控烟5A―烟草依赖干预的医学支持（经典版）第一步ASK —询问：了解患者是否吸烟清晰的、强烈的、个性化的方式建议每一位吸烟者戒烟联系病情、量身定做、切中要害列举数据、实例询问每一个吸烟者语气严肃不希望戒烟者：强化戒烟意愿发放宣传资料（时间有限）吸烟危害的数字安排下次随诊电话热线5R （时间充足）相关（Relevance ）危害（Risk ）回报（Rewards ）障碍（Roadblocks ）重复（Repetition ）随访时间: 　　６个月近期频繁: 　　第１周　　第２周　　第一个月总随访次数不少于６次随访内容：表扬戒烟成功者鼓励偶尔吸烟者帮助失败者：分析原因复吸者：解释复吸是常见现象，多数需多次戒烟才成功治疗生理依赖（躯体依赖）：戒烟药物治疗心理依赖：心理支持其它: 行为疗法等烟草依赖最佳方案：药物和行为治疗结合尼古丁替代治疗(NRT)1 长效1-3 贴片短效1-3 咀嚼制剂吸入剂鼻喷雾舌下含片抗抑郁药物4 盐酸安非他酮4 去甲替林尼古丁乙酰胆碱受体部分激动剂酒石酸伐尼克兰戒烟药物9-12 周持续戒烟率比较戒烟药物短期观察最后4 周戒烟率比较与NRT 治疗相比，伐尼克兰减轻吸烟者的烟草渴求、戒断症状、吸烟满意度作用更优P<0.001 戒烟门诊专业人员帮助戒烟辅助材料电话咨询将戒烟融入慢病管理模式戒烟生活方式改变冠心病二级预防降压达标降脂达标降糖达标戒烟指导模式门诊或住院患者常规询问吸烟史及吸烟相关疾病史认真记录于门诊手册或住院病历中门诊戒烟指导3 分钟，并在门诊手册中记录指导时间病房戒烟指导5 分钟，并在出院医嘱中明确要求患者“戒烟”不要在患者面前吸烟，鼓励吸烟医生戒烟大赛推广时间表Key Point Smoking is causally linked to a host of cardiovascular, respiratory, reproductive, and other conditions, as well as many types of cancer. The top 3 smoking-attributable causes of death in the United States are lung cancer, ischemic heart disease, and chronic obstructive pulmonary disease (COPD). Background In 2004, the US Surgeon General published a report on the health effects of active smoking, focusing specifically on the evidence for a causal relationship between smoking and disease and death. According to the research summarized in the report, many serious conditions are caused by smoking, including cardiovascular, respiratory, reproductive, and other conditions, as well as cancer affecting diverse areas and organs of the body. In addition to the widely-known consequences of lung cancer and respiratory disease, smoking has been causally linked to such diverse morbidities as low-bone density, nuclear cataract, bladder cancer, and reduced fertility.1 Other studies have linked smoking to vascular dementia2 and peripheral arterial disease.3 These conditions can affect young and middle-aged smokers and, in general, as a smoker’s age increases, the frequency of smoking-caused diseases rises.1 References 1. US Department of Health and Human Services. The Health Consequences of Smoking. A Report of the Surgeon General. Atlanta, Ga: Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health; 2004. 2. Roman GC. Vascular dementia prevention: a risk factor analysis. Cerebrovasc Dis. 2005;20(Suppl 2):91-100. 3. Willigendael EM, Teijink JA, Bartelink ML, et al. Influence of smoking on incidence and prevalence of peripheral arterial disease. J Vasc Surg. 2004;40:1158-1165. 4. Ezzati M, Lopez AD. Regional, disease specific patterns of smoking-attributable mortality in 2000. Tobacco Control. 2004;13:388-395. Key Point When evaluated by serial quantitative coronary arteriography, it is seen that smoking accelerates progression of existing coronary artery disease (CAD) and new lesion formation. Waters et al evaluated 331 participants (90 current smokers, 241 nonsmokers) with angiographically documented coronary atherosclerosis and fasting cholesterol levels between 220 and 300 mg/dL, enrolled in the randomized, double-blind, placebo-controlled Canadian Coronary Atherosclerosis Intervention Trial (CCAIT). Patients were randomized to receive either placebo or lovastatin 20 mg once daily. In an attempt to achieve a target low-density lipoprotein (LDL) cholesterol level 130 mg/dL, drug doses were increased over the initial 16 weeks of the trial to a maximum dose of 40 mg twice daily. Participants were evaluated over a 2-year period. Repeat angiography was performed at the conclusion of the study period (except in 21 patients in whom it was performed earlier). Baseline and follow-up coronary angiograms were compared, and a change in minimal lumen diameter 0.4 mm was considered a true change (either progression or regression). A new lesion was defined as a stenosis that was not apparent on the initial angiogram or was <25% in diameter stenosis but that narrowed by ≥0.4 mm in minimal lumen diameter at the second angiogram. Significantly more current smokers showed evidence of progression. Progression occurred in 41 of 72 (57%) current smokers and 83 of 227 (37%) nonsmokers, P=.002. Significantly more current smokers developed new atherosclerotic lesions, 36% vs 20%, P=.007. The authors therefore concluded that coronary atherosclerosis progresses more rapidly in current smokers than in nonsmokers. Reference Waters D, Lesperance J, Gladstone P, et al; the CCAIT Study Group. Effects of cigarette smoking on the angiographic evolution of coronary atherosclerosis: a Canadian Coronary Atherosclerosis Intervention Trial (CCAIT) substudy. Circulation. 1996;94:614-621. Key Point Overall, current smoking was associated with a 3-fold increase in the odds of having a nonfatal acute myocardial infarction (MI) compared with nonsmokers. Teo et al evaluated 12,133 cases of first acute MI and 14,435 age-matched and sex-matched controls in the international, multicenter INTERHEART study. Trained staff administered a questionnaire to both cases and controls in which participants were asked detailed questions about their smoking status. Overall, current smoking was associated with a 3-fold increase in the odds of having a non-fatal acute MI, compared with nonsmokers (odds ratio [OR] 2.95; 95% CI 2.77-3.14; P<.0001). Risk increased with the number of cigarettes smoked. The effect of