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 男 女 瑞典 17% 18% 俄罗斯 60% 16% 冰岛 25% 20% 加拿大 22% 17% 法国 30% 21% 德国 37% 28% 葡萄牙 33% 10% 白俄罗斯 53% 7% 美国 24% 19% 意大利 33% 17% 中国 67% 2% 西班牙 39% 25% 伊朗 22% 2% 墨西哥 13% 5% 埃及 45% 12% Key Point Gender-specific smoking prevalence varies across the world. Background Worldwide, there are marked differences in smoking prevalence rates between men and women from country to country. For example, in South Africa, the Philippines, China, Iran, and Portugal, smoking prevalence is much lower in women than in men. In contrast, in the United States, Canada, Australia, and Iceland, the prevalence of smoking in men is only slightly higher than that in women.1 Overall, the prevalence of smoking in men is declining. However, although smoking prevalence in women is declining in some countries, such as the United States, the United Kingdom, Australia, and Canada, in several southern, central, and eastern European countries, the rate of smoking in women is not in decline or is still increasing.1 Reference 1. Mackay J, Eriksen M, Shafey O. The Tobacco Atlas. Second ed. American Cancer Society Myriad Editions Limited. Atlanta, Georgia, 2006. Also available online at: http://www.myriadeditions.com/statmap/. 肯尼亚 21% 1% 印度 47% 17% 菲律宾 41% 8% 男 女 巴西 22% 14% 南非 23% 8% 澳大利亚 19% 16% 智利 48% 37% Mackay J, et al. The Tobacco Atlas. Second Ed. American Cancer Society Myriad Editions Limited, Atlanta, Georgia, 2006. Also available online at: http://www.myriadeditions.com/statmap/.

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 中国NEHNS IV

冠心病—是吸烟致死疾病的前三位之一 由吸烟引起死亡的前三位疾病： 国外资料为：COPD＞冠心病＞肺癌 国内资料为：COPD＞肺癌＞冠心病 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. 1. Surgeoen General’s Report. Health Consequences of Smoking; 2004. 2. J Natl Cancer Inst. 1993;85(24):1994. 2 3. Crane. Cancer Epidemiol Biomarkers Prev. 1996;5(8):639. 4. Miligi. Am J Ind Med. 1999;36(1):60. 5. Roman. Cerebrovasc Dis, 2005;20(Suppl 2):91. 6. Willigendael. J Vasc Surg. 2004;40:1158. 7. Yang. BMJ. 1999;319:143

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 右冠状动脉粥样硬化 Smoking has been implicated as a cause of both peripheral and coronary endothelial dysfunction and has been shown to be a predictor of long-term cardiovascular events, but its mechanism is not fully understood. Potential mechanisms by which smoking may play a role in cardiovascular events prior to the development of significant coronary artery disease (CAD) include induction of endothelial dysfunction, oxidative stress, increased blood thrombogenicity, and an enhanced inflammatory response. 右冠状动脉粥样硬化 Lavi et al. Circulation. 2007;115:2621-2627; http://www.texasheartinstitute.org /HIC/Topics/Diag/diangio.cfm. Accessed June 14, 2007. Reference Lavi S, Prasad A, Yang EH, et al. Smoking is associated with epicardial coronary endothelial dysfunction and elevated white blood cell count in patients with chest pain and early coronary artery disease. Circulation. 2007; 115:2621-2627.

Factor Xa (FXa) pmol/L/min 吸烟使血栓生成增加 400 组织因子（TF）在动脉粥样硬化斑块有高表达，这可能在血栓形成中发挥重要作用 TF 水平以 Xa因子 (FXa)进行评价 吸烟者与非吸烟者比，循环中TF活性远高于后者 P=.003 283 300 217 200 Factor Xa (FXa) pmol/L/min Key Point Current smokers have elevated levels of tissue factor (TF), which may be one of the mechanisms by which smoking is associated with increased atherothrombotic complications. TF is highly expressed in atherosclerotic plaques and its presence has been related to plaque thrombogenicity. TF may be present in the blood as well, and plays a role in the propagation of thrombosis. Acute coronary syndromes are associated with atherosclerotic lesion disruption and thrombus formation. Smoking has been implicated in both atherosclerotic progression and atherothrombotic complications. The objective of this study was to evaluate whether the increased rate of atherothrombotic complications observed in current smokers, is mediated through increased circulating levels of TF. Levels of TF were assessed by adding factor X, factor VIIa, and calcium to plasma, and then quantifying the concentration of factor Xa (FXa). Circulating TF was reported as changes in factor FXa per unit time (pmol/L/min). Subjects who smoke 10 cigarettes per day with a smoking history of 10 years were evaluated before and 2 hours after smoking 2 cigarettes. Baseline levels of circulating TF were significantly increased 2 hours after smoking 2 cigarettes (21772 pmol/L [before] and 283106 pmol/L/min FXa [after]; P=.003). The authors concluded that smoking has significant modulatory effects on plasma levels of circulating TF. 100 吸烟者吸烟前 （2支烟） 吸烟者吸烟后 (2支烟) Sambola et al. Circulation. 2003;107:973-977. Reference Sambola A, Osende J, Hathcock J, et al. Role of risk factors in the modulation of tissue factor activity and blood thrombogenicity. Circulation. 2003;107:973-977.

吸烟加重动脉粥样硬化 已有病变加重的发生率 新病变发生率 57 P=.002 P=.007 37 36 20 非吸烟者 吸烟者 非吸烟者 患者百分率％ 患者百分率％ 37 36 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. 20 非吸烟者 吸烟者 非吸烟者 吸烟者 Waters et al. Circulation. 1996;94:614-621. 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.

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。 10 9 8 7 6 5 4 3 2 1 OR (95% CI)a 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 current smoking was significantly greater in younger (OR, 3.53; 95% CI, 3.23-3.86) than in older participants (OR, 2.55; 95% CI, 2.35-2.76); P<.0001 for interaction. The effect of current smoking was markedly greater in younger subjects, particularly among the heaviest smokers (20 cigarettes per day) in whom ORs were 5.6 (95% CI, 5.1-6.2) for younger smokers and 3.6 (95% CI, 3.25-3.98) for older smokers (P<.0001 for interaction). 年龄<40 年龄40-49 年龄50-59 年龄60-69 年龄>70 非吸烟者 戒烟者 吸烟20支/天 吸烟1-19支/天 aThe ratio of the odds of development of disease in exposed persons to the odds of development of disease in nonexposed persons. Teo. Lancet. 2006;368:647-658. Reference Teo KK, Ounpuu S, Hawken S, et al; on behalf of the INTERHEART Study Investigators. Tobacco use and risk of myocardial infarction in 52 countries in the INTERHEART study: a case-control study. Lancet. 2006;368:647-658.

每日吸烟量与心肌梗死发生有量效关系 OR (99% CI) OR Linear (OR) 1 3 5 7 9 never 1~5 6~10 11~15 16~20 21~25 26~30 31~40 >40 OR Linear (OR) Yusuf S et al . Lancet. 2004;364:937-52

吸烟增加冠心病死亡风险 致死冠心病的相对风险 非吸烟者 1-14/日 15-24/日 25/日 吸烟者每日吸烟量 相对风险 可信区间 95％ Key Point The risk of fatal CAD may be directly related to the amount smoked. Willett et al prospectively evaluated the incidence of CAD in a cohort of 119,404 female nurses enrolled in the Nurses’ Health Study. Participants completed questionnaires at baseline (1976) and were followed up over a 6-year period. Smoking status was identified. Deaths among nonrespondents were identified through searches of state records and the National Death Index or were reported by family members. More than 98% of the deaths were identified. Fatal CAD was defined as fatal myocardial infarction (MI) confirmed by hospital records or at autopsy, or as CAD recorded on the death certificate, if this was the only cause given and there was previous evidence of CAD. Compared with nonsmokers, the age-adjusted relative risk (RR) of fatal CAD, increased with increasing daily cigarette use: 1.7, 3.7, and 5.4, for 1-14/day, 15-24/day, and 25/day, respectively. 非吸烟者 1-14/日 15-24/日 25/日 吸烟者每日吸烟量 a The probability of an event (developing a disease) occurring in exposed people compared with the probability of the event in nonexposed people. Adjusted for age. Willett et al. N Engl J Med. 1987;317(21):1303-1309. Reference Willett WC, Green A, Stampfer MJ, et al. Relative and absolute excess risks of coronary heart disease among women who smoke cigarettes. N Engl J Med. 1987;317(21):1303-1309.

吸烟增加心源性猝死的风险 4.0 3.0 2.3 2.0 1.0 0.0 不吸烟者 吸烟者 相对风险 可信区间 95％ Key Point Current smoking is associated with an increased risk of sudden cardiac death. Wannamethee et al prospectively evaluated 7735 British men, aged 40 to 59 years from the British Regional Heart Study (BRHS). All participants completed questionnaires regarding their smoking habits, alcohol intake, and medical history. Subjects had complete physical exams that included fasting bloodwork, pulmonary function tests (PFTs), and ECG. Participants were followed up for 8 years. Fatal events were defined as death from ischemic heart disease. Sudden cardiac death was defined as an event in which death occurred within 1 hour after the onset of symptoms. Only those men for whom clear information was available about their death within 1 hour were included in the category of sudden death. A Cox proportional hazards model was used to evaluate contribution of risk factors to the risk of sudden cardiac death and to derive the age-adjusted RRs. When adjusted for age, current smokers had an increased risk of sudden cardiac death (RR, 2.3, 95% CI, 1.2-4.0). aThe probability of an event (developing a disease) occurring in exposed people compared with the probability of the event in nonexposed people. Adjusted for age. Wannamethee et al. Circulation. 1995;91:1749-1756. Reference Wannamethee G, Shaper AG, Macfarlane PW, Walker M. Risk factors for sudden cardiac death in middle-aged British men. Circulation. 1995;91:1749-1756.

吸烟使冠脉介入治疗后发生Q波心梗的风险增高 Q波心梗 (MI) 1.0 1.28 2.08 相对风险 可信区间 95％ 0.0 2.0 3.0 4.0 不吸烟者 戒烟者 吸烟者 Key Point Current smokers have a higher risk of Q-wave MI after successful percutaneous transluminal coronary angioplasty (PTCA) than nonsmokers and ex-smokers. Patients (N=6600) who underwent PTCA at the Mayo Clinic from 1979 through 1995 were followed for up to 16 years by Hasdai et al. Patients were questioned about their smoking status at baseline and follow-up. Study population was divided into 4 groups on the basis of smoking status at baseline: nonsmokers, defined as patients who had never smoked cigarettes regularly; ex-smokers, who had quit smoking a minimum of 6 months before the procedure; quitters, those who had permanently quit smoking immediately after the procedure; and current smokers, who smoked before and after the procedure. The study end points were death from any cause, Q-wave acute MI or severe angina, and the need for coronary artery bypass grafting (CABG) or repeated PTCA. When adjusted for baseline variables significantly associated with each end point, current smokers had a greater risk of Q-wave MI (RR, 2.08 [1.16-3.72]), than nonsmokers. aThe probability of an event (developing a disease) occurring in exposed people compared with the probability of the event in nonexposed people. Adjusted for the baseline variables significantly associated with each end point. Hasdai et al. N Engl J Med. 1997;336:755-761. Reference Hasdai D, Garratt KN, Grill DE. Effect of smoking status on the long-term outcome after successful percutaneous coronary revascularization. N Engl J Med. 1997;336:755-761.

吸烟增加致命性和非致命性脑卒中风险 青年、中年女性，发生脑卒中的风险可能与吸烟量相关 1-14 15-24 不吸烟者 ≥25 吸烟者每日吸烟量（支） 相对风险 可信区间 95％ 青年、中年女性，发生脑卒中的风险可能与吸烟量相关 Key Point In young and middle-aged women, the risk of stroke may be related to the amount smoked. Colditz et al evaluated 118,539 women from the Nurses’ Health Study in the United States. The Nurses’ Health Study consisted of a cohort of 121,700 female nurses, aged 30 to 55 who completed baseline and follow-up self-administered questionnaires evaluating social and past medical history. Subjects were followed up for a period of 8 years (1976-1984). Primary end points were incidence of nonfatal and fatal stroke. Stroke was defined as a clinical syndrome consisting of a constellation of neurologic findings of sudden or rapid onset, persisting for more than 24 hours, with vascular origins limited to thrombosis of a cerebral artery resulting in infarction or vessel rupture resulting in hemorrhage. There were 274 incidents of stroke in the 8-year follow-up period. Current smokers had a significantly higher rate of stroke, both nonfatal and fatal. Risk of stroke increased with the number of cigarettes smoked daily. The adjusted RR of fatal and nonfatal stroke increased from 2.5 (1.6-3.8) to 2.9 (2.0-4.2) to 3.8 (2.6-5.5) in 25 cigarettes, respectively. Relative risk was adjusted for age in 5-year intervals, history of diabetes, history of hypertension, history of high cholesterol, and relative weight. aThe probability of an event (developing a disease) occurring in exposed people compared with the probability of the event in nonexposed people. Adjusted for age, follow-up period, history of diabetes, hypertension, high cholesterol levels, and relative weight (in 5 categories). Colditz et al. N Engl J Med. 1988;318(15):937-941. Reference Colditz GA, Bonita R, Stampfer MJ, et al.. Cigarette smoking and risk of stoke in middle-aged women. N Engl J Med. 1988;318(15):937-941.

吸烟增加出血性卒中风险 不吸烟者 (n=20,339) 每日吸烟量少于15支 (n=1914) 每日吸烟量多于15支 (n=3265) 相对风险 可信区间 95％ 2.06 1.74 4.04 Key Point Female smokers have an increased risk of total hemorrhagic stroke as well as intracerebral hemorrhage and subarachnoid hemorrhage. In an attempt to evaluate the impact of smoking on the risk of hemorrhagic stroke, Kurth et al evaluated data obtained from the Women’s Health Study. The Women’s Health Study is a randomized, double-blind, placebo-controlled trial (1993-2003) in which 39,876 healthy women were followed up to determine the benefits of low-dose aspirin and vitamin E for the prevention of cardiovascular disease (CVD). Kurth et al determined subjects’ smoking habits from responses to baseline self-administered questionnaires. Stroke was defined as a focal neurologic deficit of sudden onset and vascular mechanism that lasted more than 24 hours. Hemorrhagic stroke was further classified into intracerebral hemorrhage, subarachnoid hemorrhage, or intraventricular hemorrhage. During a mean of 9 years of follow-up, a total of 70 hemorrhagic strokes occurred. Analysis was adjusted for age, exercise (<4 times per week vs 4 times per week), alcohol consumption (<1 drink per week, 1-6 drinks per week, and 1 drink per day), body mass index (continuous), history of hypertension (self-reported systolic pressure 140 mm Hg, or diastolic blood pressure 90 mm Hg, or current treatment of hypertension, regardless of blood pressure), and history of diabetes. Risk of total hemorrhagic stroke, intracerebral hemorrhage, and subarachnoid hemorrhage increased with quantity of cigarettes smoked. 3.43 2.39 2.89 总出血性脑卒中 脑内出血 蛛网膜下腔出血 aThe probability of an event (developing a disease) occurring in exposed people compared with the probability of the event in nonexposed people. Adjusted for age, exercise, alcohol consumption, body mass index, history of hypertension, and history of diabetes. Kurth et al. Stroke. 2003;34:2792-2795. Reference Kurth T, Kase CS, Berger K, Gaziano JM, Cook NR, Buring JE. Smoking and risk of hemorrhagic stroke in women. Stroke. 2003;34:2792-2795.

吸烟增加脑卒中死亡风险 1-15 15-24 ≥25 吸烟者每日吸烟量（支） 死亡率 /10000人*年 Key Point Cigarette smoking increases the risk of mortality from stroke. Hart et al evaluated data derived from the Renfrew/Paisley study, a prospective cohort study initiated in the 1970s in West Scotland. Residents (7052 male and 8354 female) of Renfrew and Paisley, Scotland, aged 45 to 64 years were evaluated prospectively over a period of 20 years. Subjects underwent a thorough baseline physical exam, which included fasting bloodwork, ECG and pulmonary function tests, and responded to a self-administered questionnaire in which smoking habits and other cardiovascular risk factors were assessed. The age-adjusted 20-year stroke mortality rate was similar for men and women. There was a dose-related increase in stroke-related mortality in men. Cigarette smoking increased the risk of mortality from stroke in women as well; however, the dose-related increase was not as pronounced as in men. 1-15 15-24 ≥25 吸烟者每日吸烟量（支） aTwenty-year age-adjusted mortality per 10,000 person-years for men. P<.014 for trend. Hart et al. Stroke. 1999;30:1999-2007. Reference Hart CL, Hole DJ, Smith GD. Risk factors and 20-year stroke mortality in men and women in the Renfrew/Paisley Study in Scotland. Stroke. 1999;30:1999-2007.

吸烟增加外周血管疾病危险 吸烟与下列血管疾病的风险增加有关: 吸烟使发生PVD的时间早10年 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 Freund KM, The Framingham Study: 34 years of follow-up. Ann Epidemiol 1993; 3:417-424

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 Witteman JC,. Circulation 1993; 88:2156-2162 Wilmink TB, J Vasc Surg 1999; 30:1099-1105

戒烟使冠心病风险减少 戒烟 CAD危险与正常不吸烟者相似 肺癌发生率是继续吸烟者的30-50% 卒中危险恢复到正常不吸烟者水平 1/CDC/SGR/ p. 2 & 3 of printout 2/ACS/p 4/¶1-6. 3/USDHHS 1990/p vi/¶1,2 CAD危险与正常不吸烟者相似 肺癌发生率是继续吸烟者的30-50% 卒中危险恢复到正常不吸烟者水平 CAD危险减少50% 肺功能改善减少咳嗽鼻窦充血呼吸急促等 戒烟 1年 5 年 10 年 15 年 3个月 Key Point The health benefits of quitting smoking start immediately and are sustained such that 15 years after quitting smoking, the coronary heart disease risk of a former smoker is equal to that of a nonsmoker. Background When gauging the health benefits from smoking cessation one is encouraged to assess both the short-term and long-term improvements. Within 2 weeks to 3 months lung function may begin to improve and there may be notable decreases in coughing, sinus congestion, fatigue and shortness of breath. Around the year mark, coronary heart disease risk, the leading cause of death in the United States, improves with smoking cessation to a point where excess risk is reduced by 50% and continues to decline thereafter. Within the 5-15 year range, the risk of stroke for smoking cessators returns to the level of a person who has never smoked. Other potential long-term benefits include: the risk of lung cancer, the most common cause of cancer death in the United States, declines steadily after smoking cessation; and by 10 years after cessation, the risk of lung cancer is 30-50% that of continuing smokers. And beyond this, smoking cessation may also reduce the risk of cancers of the larynx, oral cavity, esophagus, pancreas, urinary bladder and of developing ulcers of the stomach or duodenum. Other long-term benefits include the rate of decline in lung function among former smokers returns to that of never smokers, reducing the risk of COPD. And, the risk of coronary heart disease, after 15 years of abstinence, becomes similar to that of a person who has never smoked. Clearly, a patient has health benefits to gain if they successfully cessate. References 1. CDC. Surgeon General’s 2004 Report. The Health Consequences of Smoking on the Human Body. Online slides. http://www.cdc.gov/tobacco/sgr/sgr_2004/sgranimation/flash/index.html Accessed on April 15, 2006. 2. American Cancer Society. Guide to Quitting Smoking. Available at: http://www.cancer.org. Accessed June 2006. 3. US Department of Health & Human Services. The Health Benefits of Smoking Cessation: A Report of the Surgeon General. Centers for Disease Control and Prevention (CDC), Office on Smoking and Health. 1990. Available at: http://profiles.nlm.nih.gov/NN/B/B/C/T/. Accessed July 2006. 1/CDC/SGR/p. 2 & 3 of printout ¶2; 2/ACS/ p 3/¶9,10 2/ACS/p 4/ ¶1-6. 3/USDHHS 1990/p vi/¶1,2 1. CDC. Surgeon General Report 2004 2. American Cancer Society. Guide to Quitting Smoking2006

戒烟使急性心梗风险降低 戒烟数年后，发生急性心梗的风险明显降低 P<.0001 吸烟者 >1-3 >5-10 >10-15 20 戒烟者 (戒烟年数) >3-5 >15-20 4 2 1 比值比 可信区间 95％ 戒烟数年后，发生急性心梗的风险明显降低 Key Point Risk of acute MI associated with smoking is significantly reduced within a few years of quitting. Teo et al evaluated 12,461 cases of first acute MI and 14,637 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. Risk of acute MI associated with smoking was markedly reduced within a few years of quitting. Risk of acute MI decreased progressively with time since becoming abstinent; however, some increased risk persisted, even in those who had quit more than 20 years prior. aThe ratio of the odds of development of disease in exposed persons to the odds of development of disease in nonexposed persons. Adjusted for sex, region, diet, alcohol, physical activity, consumption of fruits, vegetables, and alcohol. Adapted from Teo. Lancet. 2006;368:647-658. Reference Teo KK, Ounpuu S, Hawken S, et al, on behalf of the INTERHEART Study Investigators. Tobacco use and risk of myocardial infarction in 52 countries in the INTERHEART study: a case-control study. Lancet. 2006;368: 647-658.

戒烟使冠状动脉介入治疗后死亡率下降 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 100 80 60 生存率 (%) 40 Key Point Persistent smokers had a significantly greater risk of overall mortality after percutaneous coronary revascularization. Patients (N=6600) who underwent percutaneous coronary revascularization at the Mayo Clinic from 1979 through 1995 were followed for up to 16 years by Hasdai et al. Patients were questioned about their smoking status at baseline and follow-up. Study population was divided into 4 groups on the basis of smoking status at baseline: nonsmokers, defined as patients who had never smoked cigarettes regularly; ex-smokers, who had quit smoking a minimum of 6 months before the procedure; quitters, those who had permanently quit smoking immediately after the procedure; and persistent smokers, who smoked before and after the procedure. The study end points were death from any cause, Q-wave acute myocardial infarction or severe angina, and the need for coronary artery bypass grafting or repeated percutaneous coronary revascularization. After adjusting for significant differences in baseline variables, risk of death from all causes among persistent smokers was compared with risk among quitters. Persistent smokers had significantly greater risk of overall mortality (RR, 1.44; 95% CI, 1.02-2.11). The estimated survival curves diverged soon after the initial revascularization procedure. The difference between the curves continued to increase throughout the follow-up period. 40 戒烟者 持续吸烟者 20 2 3 4 5 6 7 8 9 10 11 12 时间（年） Hasdai. N Engl J Med. 1997;336(11):755-761. Reference Hasdai D, Garratt KN, Grill DE, Lerman A, Holmes DR Jr. Effect of smoking status on the long-term outcome after successful percutaneous coronary revascularization. N Engl J Med. 1997;336(11):755-761.

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％。 100 80 60 P<.0001 (戒烟者 vs 吸烟者) 生存概率 (%) Key Point Patients who continue to smoke after Coronary Artery Bypass Graft (CABG) surgery have a greater risk of death than those who stop smoking. van Domburg et al sought to evaluate the influence of smoking cessation on mortality in patients undergoing CABG surgery. The authors identified 1041 patients undergoing their first CABG procedure between February 1971 and June 1980. Baseline smoking history was obtained at the time of surgery. Patients were followed up for a median of 20 years (range: 13-26 years). Postoperative smoking status was obtained in 985 patients. Mortality was divided into perioperative mortality (death occurring within 28 days after surgery) and late mortality. Late mortality was subdivided into death at re-CABG or PTCA, acute cardiac death, death caused by MI, death due to chronic heart failure, death due to noncardiac cause, and unknown causes of death. The study population was divided into smokers and nonsmokers. Nonsmokers included ex- and never smokers. Smokers before surgery were further subdivided as quitters (those who stopped smoking in the first year after their CABG) and persistent smokers (those who had smoked before CABG and continued to smoke for at least one year after CABG). Persistent smokers had a significantly greater risk of death from all causes, (RR, 1.68; 95% CI, 1.33-2.13) and of cardiac death, (RR, 1.75; 95% CI, 1.30-2.37) compared with patients who abstained from smoking after bypass surgery. The above graph depicts the survival curves for ex-smokers, current smokers, and nonsmokers. Benefits of smoking abstinence were demonstrated as early as 4 years after the initial CABG, at which point the curves diverged. The estimated benefit in survival associated with smoking abstinence increased from 3% at 5 years (98% vs 95%), to 10% at 10 years (88% vs 78%), and 15% at 15 years (70% vs 55%). 戒烟者 40 不吸烟者 持续吸烟者 20 5 10 15 20 年 Adapted from van Domburg et al. J Am Coll Cardiol. 2000;36(3):878-883. Reference van Domburg RT, Meeter K, van Berkel DFM, Veldkanys RF, van Herwerden LA, Bogers AJJC. Smoking cessation reduces mortality after coronary artery bypass surgery: a 20-year follow-up study. J Am Coll Cardiol. 2000;36(3):878-883.

戒烟使心脏骤停风险减低 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 P=.038 30 27 25 19 20 15 3年内发生率 (%) Key Point Smoking cessation is associated with a significant reduction in risk of recurrent cardiac arrest. Hallstrom et al performed a life-table analysis of 310 survivors of out-of-hospital cardiac arrest who were current smokers at the time of the cardiac arrest to determine if immediate smoking cessation after hospitalization was associated with a decrease in risk of recurrent cardiac arrest. The life-table analysis included information about smoking cessation following hospital discharge, which was obtained through surveys of the families of the survivors and a review of medical records. Patients with coronary artery disease were stratified according to mortality risk into 5 prognostic strata on the basis of recognized clinical variables. Ninety-one patients quit smoking immediately following the sudden cardiac arrest, while 219 continued to smoke. At 3 years, the risk of recurrent cardiac arrest was significantly lower for ex-smokers than current smokers across all strata except the highest risk stratum (19% ex-smokers vs 27% smokers; P=.038). Total mortality due to recurrence of cardiac arrest was lower for ex-smokers (P=.062); however, there was no difference between mortality due to other causes (P=.91).   10 5 吸烟者 戒烟者 a 心脏骤停反复发作 aAbstention period of 3 years. Hallstrom et al. N Engl J Med. 1986;314:271-275. Reference Hallstrom AP, Cobb LA, Ray R. Smoking as a risk factor for recurrence of sudden cardiac arrest. N Engl J Med. 1986;314:271-275.

戒烟使卒中风险降低 与持续吸烟的患者比较，戒烟者非致死性脑卒中的发生风险降低 P <.0001(趋势) 不吸烟者 戒烟者 相对风险 可信区间 95％ P <.0001(趋势) Key Point Compared with current smokers, male ex-smokers have a reduced risk of nonfatal stroke. Robbins et al prospectively evaluated 22,071 male physicians in the Physicians’ Health Study, a randomized, double-blind, placebo-controlled study evaluating the effect of low-dose aspirin on cardiovascular disease, as well as the effect of beta-carotene on cancer and cardiovascular disease. Subjects were men aged 40 to 84 years, without history of myocardial infarction (MI), stroke, or transient ischemic attacks. Data regarding smoking habits was derived from a self-completed questionnaire. Smokers were defined as nonsmokers, ex-smokers, current smokers smoking less than 20 cigarettes per day, or current smokers smoking more than 20 cigarettes per day. Every 6 months during the first year, then annually thereafter, subjects completed a questionnaire regarding compliance with the prescribed regimen and incidence of cardiac events (stroke, MI, etc). Follow-up continued either until participants experienced nonfatal or fatal stroke, or any other fatal event. Participants were followed up for an average of 9.7 years. After adjusting for age and treatment assignment, ex-smokers had lower relative risk of total nonfatal stroke (1.2; 95% CI, 0.95-1.63) than physicians currently smoking less than 20 and more than 20 cigarettes daily, (2.0, 95% CI, 1.04-3.33) and (2.5, 95% CI, 1.84-3.98), respectively. 不吸烟者 戒烟者 吸烟者 (<20支/日) 吸烟者 (≥20 支/日） aThe probability of an event (developing a disease) occurring in exposed people compared with the probability of the event in nonexposed people. Adjusted for age and treatment assignment. Robbins et al. Ann Intern Med. 1994;120(6):458-462. Reference Robbins AS, Manson JE, Lee I-M, Satterfield S, Hennekens CH. Cigarette smoking and stroke in a cohort of US male physicians. Ann Intern Med. 1994;120(6):458-462.

戒烟使外周血管疾病症状改善 对于间歇性跛行（IC）患者，戒烟可减缓外周血管病的进一步加重。 30 吸烟 戒烟 20 P=.049 累积静息痛 (%) Key Point Smokers with intermittent claudication (IC), who discontinue smoking demonstrate reductions in progression of peripheral vascular disease (PVD). Three hundred forty-three Swedish patients with IC were evaluated at baseline, at follow-up 12 months later, and 7 years after the follow-up exam. Subjects were designated ex-smokers if they had stopped smoking within 6 months before or 12 months after the initial examination. Patients who continued to smoke or stopped more than 12 months after the initial examination were designated as current smokers. At baseline, evidence of PVD was determined based upon the results of a combination of segmental blood pressure measurements as well as Doppler assessment of the velocity and direction of the blood flow in the popliteal and common femoral arteries. Walking tolerance was also estimated by a symptom-limited treadmill test. Rest pain was defined as pain in the leg or foot when the patient was recumbent that was relieved when the leg was lowered. Patients who had stopped smoking within 6 months before or within 12 months after the initial examination were designated nonsmokers. Patients who continued to smoke or stopped smoking more During the 7-year follow-up period, rest pain developed in 26 patients, all of whom were current smokers. None of the ex-smokers developed rest pain. After 7 years, the cumulative proportion of patients with rest pain was 16% among the current smokers (P=.049). 10 2 7 1 6 5 4 3 年 Jonason et al. Acta Med Scand. 1987;221:253-260. Reference Jonason T, Bergstrom R. Cessation of smoking in patients with intermittent claudication: effects on the risk of peripheral vascular complications, myocardial infarction and mortality. Acta med Scand. 1987;221:253-260.

戒烟是冠心病强效干预措施 Critchley JA, Capewell S. JAMA; 2003; 290: 86-97

戒烟是降低心血管风险最经济的干预方式 平均每挽救一个生命年（人年）的成本: 戒烟 $ 2,000 – 6,000 戒烟 $ 2,000 – 6,000 降血压药物 $ 9,000 – 26,000 降血脂药物 $ 50,000 – 196,000 Benowitz, Prog Cardiovasc Dis, 2003;46:91

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 尼古丁在中枢神经主要与位于腹侧核 (VTA)的包含尼古丁乙酰胆碱受体受体的42亚单位结合 b b2 4b2 尼古丁受体 Key Point Nicotine stimulates dopamine release in areas of the brain that are believed to be involved in the reward and satisfaction effect associated with smoking. After inhalation, nicotine preferentially binds to nAChR located in the mesolimbic-dopamine system of the brain within seconds. Nicotine specifically activates 4β2 nicotinic receptors in the ventral tegmental area (VTA), causing an immediate dopamine release at the nAcc. The dopamine release is believed to be a key component of the reward circuitry associated with cigarette smoking. 尼古丁在中枢神经主要与位于腹侧核 (VTA)的包含尼古丁乙酰胆碱受体受体的42亚单位结合 尼古丁在VTA与42受体结合, 在伏核(nAcc) 产生多巴胺，后者与奖赏有关 nAcc= Nucleus Accumbens. Adapted from Picciotto et al. Nicotine Tob Res. 1999;1:S121-S125. Reference Picciotto MR, Zoli M, Changeux J-P. Use of knock-out mice to determine the molecular basis for the actions of nicotine. Nicotine Tob Res. 1999;1:S121-S125.

尼古丁促多巴胺释放 尼古丁刺激脑腹侧被盖区42尼古丁乙酰胆碱受体, 引起伏核多巴胺释放. 这导致了吸烟后短暂的奖赏/满足感。 D 奖赏效应 轴突 Key Point Nicotine stimulates dopamine release in areas of the brain that are believed to be involved in the reward and satisfaction effect associated with smoking. Nicotine activates 42 nicotinic receptors that are localized to the neuronal bodies and terminal axons of the cells in the VTA. This activation causes dopamine release at the nAcc, which is believed to result in the short-term reward/satisfaction effect associated with cigarette smoking. 脑腹侧被盖区 伏核 D – 包含nAChR 的β2 亚单位 - 尼古丁 - 多巴胺 Adapted from Picciotto et al. Nicotine Tob Res. 1999;1:S121-S125. Reference Picciotto MR, Zoli M, Changeux J-P. Use of knock-out mice to determine the molecular basis for the actions of nicotine. Nicotine Tob Res. 1999;1:S121-S125.

长期的尼古丁暴露会上调尼古丁受体 长期暴露于尼古丁，尼古丁会刺激42 尼古丁受体活化和失敏感，随后则上调受体，导致42 尼古丁受体数量增加。 D D 奖赏效应 Key Point Chronic exposure to nicotine initiates the activation, then desensitization, of 42 nicotine receptors. This process is followed by long-term up-regulation of the nicotine receptors, increasing the number of high-affinity nAChRs and likely contributing to nicotine addiction. Typically, down-regulation occurs as a result of overstimulation due to drug exposure. However, in the case of nicotine, increased exposure leads to up-regulation of its own receptors. As is shown in this figure, the β2 subunit containing nAChR proliferates upon increased exposure to nicotine. Nicotine acts both at the neuron cell bodies in the VTA to increase the neuron’s firing rate and at the terminals in the nACC to increase dopamine release. 轴突 脑腹侧被盖区 伏核 D – 包含 nAChR 的β2 亚单位 - 尼古丁 - 多巴胺 Adapted from Picciotto et al. Nicotine Tob Res. 1999;1:S121-S125; Corringer et al. J Phys Paris. 2006;99:62-171. Reference Picciotto MR, Zoli M, Changeux J-P. Use of knock-out mice to determine the molecular basis for the actions of nicotine. Nicotine Tob Res. 1999;1:S121-S125.

尼古丁成瘾环 多巴胺 尼古丁 多巴胺带来平静愉快感 尼古丁与受体结合导致多巴胺释放增加 1/Jarvis/ p 278, para 1 多巴胺带来平静愉快感 2/Picciotto, p. S121, para 1 1/Jarvis/ p 278, para 1 尼古丁与受体结合导致多巴胺释放增加 多巴胺 尼古丁 1/Jarvis/ p 278, para 1 1/Jarvis/ p 278, para 2 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 Key Point Nicotine addiction is a cycle which begins with nicotine binding to receptors in the brain causing the release of dopamine which in turn results in feelings of pleasure and calmness. Background The distribution of nicotine is very rapid. It can reach the brain within 10 to 20 seconds after inhaling cigarette smoke.1 The binding of nicotine to its relevant receptors results in the release of multiple neurotransmitters, most critically dopamine. The release of dopamine in the nucleus accumbens neurons is thought to play a critical role in the addictive nature of nicotine. This release of dopamine requires binding of nicotine to 42 receptors.1,2 Absorption of cigarette smoke from the lungs is rapid and complete, producing with each inhalation a high concentration of arterial nicotine that reaches the brain within 10 to 16 seconds. Nicotine has a terminal half-life in blood of 2 hours. Smokers therefore experience a pattern of repetitive and transient high blood nicotine concentrations from each cigarette. Nicotine’s activation of acetylcholinergic receptors induces the release of dopamine in the nucleus accumbens. This is similar to the effect produced by other drugs of misuse, such as amphetamines and cocaine. The symptoms of nicotine withdrawal are a major barrier to smoking cessation. Smokers start to experience impairment of mood and performance within hours of their last cigarette. These effects are completely alleviated by smoking a cigarette. Withdrawal symptoms include irritability, restlessness, feeling miserable, impaired concentration, and increased appetite, as well as craving for cigarettes. Cravings, sometimes intense, can persist for many months. References Jarvis MJ. Why people smoke. BMJ. 2004;328:277-279. Picciotto MR, Zoli M, Changeux J. Use of knock-out mice to determine the molecular basis for the actions of nicotine. Nicotine Tob Res. 1999; Suppl 2:S121-S125. 吸烟者为了恢复平静愉快感渴求尼古丁 每支烟之间，多巴胺减少引起易怒和紧张等戒断症状 1/Jarvis/ p 277, para 5 1/Jarvis/ p 278, para 1, 2, 3 Jarvis MJ. BMJ. 2004; 328:277-279. 2. Picciotto MR, et al. Nicotine and Tob Res. 1999: Suppl 2:S121-S125. 2/Picciotto, p. S121, para 1 1/Jarvis/ p 277, para 5

‘‘人们为什么吸烟. 为了放松; 有味道; 消遣时间; 手上有些事情干. 但，最重要的，人们不停地吸烟是因为他们戒烟以后会非常难受” ‘‘人们为什么吸烟 . . . 为了放松; 有味道; 消遣时间; 手上有些事情干. . . . 但，最重要的，人们不停地吸烟是因为他们戒烟以后会非常难受” Philip Morris, 1984 Philip Morris. Internal presentation. 1984, 20th March; Kenny et al. Pharmacol Biochem Behav. 2001;70:531-549.

戒断症状 戒断症状：躯体及情感的共同作用 易怒,受挫感或生气 (<4周) 失眠/睡眠紊乱 (<4周) 焦虑 1/DSM IV-TR p 1 of printout, table 292.0 2/West/ p 37/Table;p. 39, ¶2 戒断症状 易怒,受挫感或生气 (<4周) 失眠/睡眠紊乱 (<4周) 焦虑 (可能随着戒烟加重或减轻) 食欲增加或体重增加 (>10周) Key Point Nicotine withdrawal syndrome is characterized by a combination of physical and psychological conditions, which make smoking difficult to treat. Background Recognizing that nicotine withdrawal results in clinically significant impairment in a person’s ability to function, the American Psychiatric Association’s Diagnostic and Statistical Manual (DSM) classifies these symptoms as a distinct condition: nicotine withdrawal syndrome. The symptoms of nicotine withdrawal syndrome can develop rapidly after a smoker tries to quit, and characteristics include the psychological symptoms of dysphoric or depressed mood; anxiety; irritability, frustration, or anger; and restlessness or impatience and the physical symptoms of insomnia, increased appetite/weight gain, and difficulty concentrating. Although present in those who use other nicotine-containing products, the manifestations of nicotine withdrawal syndrome are more intense in individuals who smoke compared with those who use other forms of tobacco. The rapidity of onset and intensity of withdrawal syndrome in smokers may suggest a greater dependence on tobacco.1 The typical duration of most of these symptoms is <4 weeks. Increased appetite is an exception, often lasting for >10 weeks. Although anxiety is listed as a classic symptom of nicotine withdrawal in the DSM, additional information is available about the relationship between anxiety and smoking. Some evidence suggests that while smokers increase their smoking when stressed, smoking does not help relieve the stress. As smokers stop smoking, levels of stress and anxiety actually decrease.2 References 1. Diagnostic and Statistical Manual of Mental Disorders, IV-TR. Washington, DC: APA; 2006: Available at http://psychiatryonline.com. Accessed November 7, 2006. 2. West R, Shiffman S. Fast Facts: Smoking Cessation. 1st ed. Oxford, United Kingdom. Health Press Limited. 2004. 坐立不安或性急 (<4周) 烦躁或抑郁情绪 (<4周) 难集中注意力 (<4周) 1/DSM IV-TR p 1 of printout, table 292.0, 2/West/ p 37/Table3p. 39, ¶2 Diagnostic and Statistical Manual of Mental Disorders, IV-TR. Washington, DC: APA; 2006: Available at http://psychiatryonline.com. Accessed November 7, 2006. West RW, et al. Fast Facts: Smoking Cessation. 1st ed. Oxford, United Kingdom. Health Press Limited. 2004.

尼古丁成瘾: 慢性复发性成瘾性医学问题 戒 烟 复 吸 干 预 做为一个成瘾性医学问题，尼古丁成瘾需要长期临床干预，戒烟是一个反复的长期过程 1/Fiore/ pg 9, para 6 1/Fiore/ pg 9, para 3 临床常见， 属于成瘾特性，不能完全靠个人毅力解决, 长期吸烟者凭个人努力戒断者仅 3%–5% 复 吸 2/Jarvis, p. 278, para 1 治疗的手段常需联合药物、行为及社会环境支持等方法: 药物干预应使用指南推荐药物，并按照指南完成疗程才能取得较好的疗效 其他干预心理、社会、生理及环境等多种因素的介入使得戒烟是一个系统工程 Key Point Cigarette smoking is a chronic relapsing medical condition. Tobacco dependence is a chronic condition with addiction comparable to that caused by other drugs of abuse.1 Long-term clinical intervention for nicotine addiction is needed, just as it is for other addictive disorders. Clinicians may fail to appreciate the chronic nature of nicotine addiction and, therefore, fail to treat smoking consistently and over the long term. It should be considered a chronic condition, such as diabetes, hypertension, or hyperlipidemia, and treated as such.2 Smoking is a relapsing condition, and it is easy to understand why the vast majority of smokers who attempt to quit fail over multiple attempts.2 References Jarvis MJ. Why people smoke. BMJ. 2004;328:277-279. Fiore MC, Bailey WC, Cohen SJ, et al. Clinical Practice Guideline: Treating Tobacco Use and Dependence. US Department of Health and Human Services. Public Health Service; June 2000. Available at: www.surgeongeneral.gov/tobacco/default.htm. 干 预 1/Jarvis, p. 278, para 1 2/Fiore/ pg 9, para 6 2/Fiore/ pg 9, para 3 Fiore MC, Bailey WC, Cohen SJ, et al. Clinical Practice Guideline: Treating Tobacco Use and Dependence. US Department of Health and Human Services. Public Health Service; June 2000. Available at: www.surgeongeneral.gov/tobacco/default.htm. Jarvis MJ. Why people smoke. BMJ. 2004;328:277-279.

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

2002年中国流行病学调查： 国人对吸烟与心血管病间的关系尤其缺乏认识 吸烟易患气管炎 吸烟易患肺癌 孕妇吸烟对胎儿有严重危害 吸烟有严重危害 被动吸烟有严重危害 2002年 1996年 吸烟易患冠心病 10 20 30 40 50 60 70 80 90 比例（％） 杨功焕等，中华流行病学杂志2005年2月第26卷第2期

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 哪一项临床手段，公共卫生措施能取得如此效果？ 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 US guideline (AHRQ, 2000) UK guideline (1998) New Zealand guideline (2007)

5A―烟草依赖干预的医学支持（经典版） Ask ：询问烟草应用情况 Advise：建议戒烟 Assess：评估尝试戒烟的意愿 Assist：帮助制定戒烟计划 Arrange：安排随访 重要生命体征 Fiore MC, et al. US Department of Health and Human Services. Public Health Service. June 2000.

第一步 ASK —询问：了解患者是否吸烟 评估尼古丁依赖程度 评估内容 0分 1分 2分 3分 自我评分 早晨醒来后多长时间吸第1支烟 >60分钟 31-60分钟 6-30分钟 5分钟以内 您是否在许多禁烟场所感到很难控制吸烟的需要? 否 是 您最不想放弃的是哪一支烟? 其他时间 早晨第一次 您每天吸多少烟? 10支 11-20支 21-30支 31支 您是否在早晨醒来后的第1小时内吸烟最多? 如果您患病卧床是否还会吸烟? 评分1-3分： 尼古丁轻度依赖。建议使用戒烟辅助药，或靠毅力戒烟。 评分4-6分： 尼古丁中度依赖。建议使用戒烟辅助药。 评分大于7分： 尼古丁重度依赖。建议使用戒烟辅助药。

第二步 ADVISE—建议：强化吸烟者的 戒烟意识 “您必须完全戒烟” ―Say to each smoker 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

第三步 Assess — 评估：明确吸烟者戒烟的意愿 “您希望尝试戒烟吗？” ―Ask each smoker 询问每一个吸烟者 语气严肃

第四步 ASSIST — 帮助：帮助吸烟者戒烟 希望尝试戒烟者 ―明确障碍，具体支持 您希望尝试戒烟吗？ 是 否 策略：明确障碍，具体支持 信息：戒烟是一个艰难的过程，经常需要医生和药物的协助；可能需多次尝试，但最终会成功 行动：发放宣传资料 确定戒烟日期 戒烟的策略：心理治疗＋药物治疗 建议患者咨询戒烟门诊或电话热线 行动：发放宣传资料 安排下一次的随诊

不希望戒烟者：强化戒烟意愿 5R（时间充足） 戒烟对于保护您和您周围人的健康非常重要， 希望您能加入戒烟者的行列！ 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） 戒烟对于保护您和您周围人的健康非常重要， 希望您能加入戒烟者的行列！

第五步 ARRANGE — 随访 安排随访 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： 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

戒烟方法 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

烟草依赖的药物治疗 尼古丁替代治疗 (NRT)1 抗抑郁药物4 尼古丁乙酰胆碱受体部分激动剂 长效1-3 短效1-3 盐酸安非他酮4 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 Key Point Pharmacotherapies for quitting smoking include NRT and the antidepressants bupropion SR and nortriptyline. Background NRTs assist smokers in quitting by replacing nicotine that would otherwise be smoked, thereby reducing the need to smoke to obtain nicotine.1 Nicotine replacement therapy is available in many forms. Nicotine replacement gum, lozenges, sublingual tablets, inhalers and nasal spray deliver nicotine through the oral or nasal mucosa. Nicotine replacement patches, which deliver nicotine through the skin, provide a passive, longer acting system of delivery.2,3 A Cochrane systematic review of the NRT literature found that all types of NRT significantly increase the odds of quitting with little difference between methods.1 Antidepressant therapies, specifically bupropion SR and nortriptyline, are also used to help smokers quit. The antidepressant bupropion SR is the more widely used and studied agent.2,4 Nortriptyline has not been as widely studied and has not been approved for smoking cessation.4 References 1. Silagy C, Lancaster T, Stead L, Mant D, Fowler G. Nicotine replacement therapy for smoking cessation. Cochrane Database Syst Rev. 2004;(3):CD000146. 2. Stead L, Lancaster T. Nicotine replacement therapy for smoking cessation: Cochrane systematic review. Int J Epidemiol. 2005;34:1001-1003. 3. Henningfield JE, Fant RV, Buchhalter AR, Stitzer ML. Pharmacotherapy for nicotine dependence. CA Cancer J Clin. 2005;55:281-299. 4. Hughes JR, Stead LF, Lancaster T. Antidepressants for smoking cessation. Cochrane Database Syst Rev. 2004;(4):CD000031. 1. Silagy C, et al. Cochrane Database Syst Rev. 2004;(3):CD000146. 2. Stead L, et al. Int J Epidemiol. 2005;34:1001-1003. 3. Henningfield JE, et al. CA Cancer J Clin. 2005;55:281-299. 4. Hughes JR et al. Cochrane Database Syst Rev. 2004;(4):CD000031.

NRT 以非烟草的形式，提供部分原来从烟草中获得尼古丁，而治疗量的尼古丁远远低于从烟草中的获得量 降低吸烟的冲动、减轻戒断症状 避免吸烟产生的有害物质对身体的毒害 包括尼古丁咀嚼片、尼古丁贴片、尼古丁含片

盐酸安非他酮 直接作用于成瘾通路 增加脑内多巴胺(DA)和去甲肾上腺素(NA)含量 消除吸烟的渴望、减轻戒断症状 DA NA

伐尼克兰 尼古丁 伐尼克兰 与中脑腹侧背盖区尼古丁乙酰胆碱42受体结合可以导致多巴胺释放 伐尼克兰是一种高选择性42 受体部分激动剂，具有激动剂和拮抗剂双重活性。可缓解对尼古丁的渴求与戒断症状,并可阻断尼古丁与受体的结合，减少伏核(nAcc) 释放多巴胺，从而降低吸烟的奖赏效应。 Coe JW et al. Presented at the 11th Annual Meeting and 7th European Conference of the Society for Research on Nicotine and Tobacco. 2005. 2. Picciotto MR et al. Nicotine Tob Res. 1999

戒烟药物应用后9-12周的持续戒烟率 研究 1 研究 2 伐尼克兰 1 mg bid (n=352) 比值比 伐尼克兰比安慰剂 3.91 P<0.0001 伐尼克兰比盐酸安非他酮1.96 P<0.0001 研究 2 比值比 伐尼克兰比安慰剂 3.85 P<0.0001 伐尼克兰比盐酸安非他酮1.89 P<0.0001 60 60 1/Champix Summary of Product doc/p. 7/¶7 /Table 50 50 43.9% 44.0% 40 40 持续戒烟率 (%) 29.8% 29.5% 30 持续戒烟率（ %) 30 20 17.6% 20 17.7% 10 10 Key Point In both studies, varenicline resulted in continuous abstinence (CA) rates at weeks 9 through 12 that were significantly higher than for placebo or bupropion Background: For the primary endpoint of carbon monoxide (CO)–confirmed, 4-week CA rates were defined as patient report and exhaled CO <10 ppm. 4-week CA rates with varenicline treatment were significantly higher compared with bupropion treatment or placebo.1 In Study 1, 44.4% of participants in the varenicline group were continuously abstinent from smoking during Weeks 9 to 12 compared with 29.5% of participants in the bupropion group and 17.7% of participants in the placebo group (both P<0.0001). This translated to an abstinence OR of 3.91 for varenicline versus placebo and an OR of 1.96 versus bupropion.1 Similarly, in Study 2, 4-week abstinence rates for varenicline, bupropion, and placebo were 44.0%, 30.0%, and 17.7%, respectively. Varenicline was significantly more effective compared with placebo (OR, 3.85; P<0.0001) and bupropion (OR, 1.89; P<0.0001).1 Subjects were provided with an educational booklet on smoking cessation and received up to 10 minutes of smoking cessation counseling at each clinic visit in accordance with Agency for Healthcare Research and Quality Guidelines. Reference 1. Champix Summary of Product Characteristics. Pfizer Ltd, Sandwich, UK. 2006. 伐尼克兰 1 mg bid (n=344) 盐酸安非他酮 150 mg bid (n=342) 安慰剂 (n=341) 伐尼克兰 1 mg bid (n=352) 盐酸安非他酮 150 mg bid (n=329) 安慰剂 (n=344) 1/Champix Summary of Product doc/p. 7/¶7/Table Jorenby DE et al. JAMA. 2006;296:56-63. Gonzales D et al. JAMA. 2006;296:47-55.

戒烟药物短期观察最后4周戒烟率比较 60 55.9% 50 43.2% 40 持续戒烟率 (%) P<0.01 30 20 10 伐尼克兰（9-12周） (n=376) 尼古丁贴剂（7-10周） (n=370) 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 研究在比利时、荷兰、法国、英国、美国展开。受试者被随机分配到伐尼克兰和尼古丁替代治疗组，分别接受伐尼克兰1mg，2次/日，共12周和尼古丁贴剂21mg/日逐渐减至7mg/日，共10周的治疗。 对伐尼克兰的远期戒烟率和不良反应需进一步积累经验 H-J Aubin,A Bobak,et al.Varenicline versus transdermal nicotine patch for smoking cessation: results from a randomised openlabel trial. Downloaded from thorax.bmj.com on 8 February 2008

走出吸烟认识的误区 吸烟的人戒烟后会不舒服，甚至会得病 烟有过滤嘴、焦油含量低，危害就小 吸烟能减肥，戒烟会增加体重 我吸烟多年也没有健康问题 SARS期间有一种说法，吸烟的人不得SARS …

戒烟干预措施 审查戒烟的理由 让吸烟者记吸烟日记观察自己的吸烟类型 在1周或2周的准备期后，开始戒烟 回顾以往的戒烟经历 对面临的挑战要有思想准备 戒断症状与心理依赖 选择适当的戒烟方法 “逐渐减量法”与“突然停止法”，推荐后者 签一份戒烟协议 给自己一些适当的奖励

控制持续的吸烟欲望 改变行为类型： 改善环境： 建立一些补偿行为： 清晨改变吸烟者的行为顺序，不喝咖啡或酒精饮料、饭后迅速从座位上起来等 扔掉所有烟草制品、打火机、烟灰缸和其他吸烟用品、远离吸烟者、避免停留在很有可能使吸烟者想吸烟的地方，如酒吧 建立一些补偿行为： 吸烟者可以借用一些烟草替代物，例如饮水或茶、咀嚼干海藻或无糖口香糖、进行深呼吸、刷牙、散步等，或找到适合自己的方法，以便能够应付持续的吸烟欲望

处理阶段症状 “我一直有吸烟的欲望”：饮水喝茶，咀嚼干海藻或无糖口香糖 “我感觉易激动，不能平静”：散步或适度锻炼 “我不能够集中精力”：减少工作负担1周 “我感觉身体疲乏，而且总想睡觉”：充分睡眠，适度锻炼、洗热水澡 “我不能睡觉”：避免饮用含咖啡因的饮料，适度锻炼，用温水洗澡 “我开始便秘了”：大量饮水 “我总想吃东西”：多吃蔬菜水果，多喝水，避免吃高热量零食，以防发胖

容易使吸烟者复吸的危险情况 戒烟阶段会不时有吸烟的冲动 可能再次吸烟的危险情况包括： 要求吸烟者观察自己的吸烟习惯，告诉吸烟者事先准备好有针对性的对抗措施，以防再次吸烟 可能再次吸烟的危险情况包括： 当吸烟者在工作和人际关系方面感觉不安时； 心情抑郁时； 外出饮酒时； 戒烟者看到有人正在吸烟时

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