1. 吸烟与心血管疾病

2. 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

3. 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Ca 国内资料为：COPD＞肺Ca＞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):
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:
4. Ezzati M, Lopez AD. Regional, disease specific patterns of smoking-attributable mortality in Tobacco Control. 2004;13:
1. Surgeoen General’s Report. Health Consequences of Smoking; J Natl Cancer Inst. 1993;85(24):1994.
3. Crane. Cancer Epidemiol Biomarkers Prev. 1996;5(8): Miligi. Am J Ind Med. 1999;36(1):60.
5. Roman. Cerebrovasc Dis, 2005;20(Suppl 2): Willigendael. J Vasc Surg. 2004;40: Yang. BMJ. 1999;319:143

4. 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: ; 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:

5. 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:
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:

6. 吸烟使一氧化氮生物合成减少 5000 不吸烟者 吸烟者 4000 3000 2000 1000 NO浓度 (nmol/L)
不吸烟者
吸烟者
4000
3000
2000
1000
NO浓度 (nmol/L)
P<.0001
1266
3613
Key Point
Smoking is associated with reduced nitric oxide (NO) biosynthesis.
NO is the primary vasodilatory substance produced by endothelial cells. Smokers have been noted to have impaired endothelium-dependent vasodilation (EDV). Barua et al hypothesized that reduction in NO biosynthesis contributes to the impaired EDV noted in current smokers.
Twenty-three male patients (15 current smokers, 8 nonsmokers) had fasting bloodwork drawn, while abstaining from smoking for a 6 to 8 hour period. Human umbilical vein endothelial cells (HUVECs) were incubated with serum from participants, and after 12 hours basal NO production in the supernatant was determined. NO production in the cell culture supernatant was evaluated by chemiluminscence.
HUVECs incubated with current smoker’s serum showed significantly lower basal NO production compared with HUVECs incubated with nonsmoker’s serum (P<.0001).
The authors concluded that smoking is associated with reduced basal NO production.
Barua et al. Circulation. 2001;104:
Reference
Barua R, Ambrose JA, Eales-Reynolds LJ, DeVoe MC, Zervas JG, Saha DC. Dysfunctional endothelial nitric oxide biosynthesis in healthy smokers with impaired endothelium-dependent vasodilatation. Circulation. 2001;104:

7. 吸烟使血管内皮舒张功能受损 与不吸烟者相比，吸烟者根据流量调节的内皮血管舒张功能明显减弱 P<.01 P<.001 20 30
动脉造影正常的不吸烟者
与不吸烟者相比，吸烟者根据流量调节的内皮血管舒张功能明显减弱
动脉造影不正常的不吸烟者
P<.01
动脉造影正常的吸烟者
动脉造影不正常的吸烟者
P<.001 20 30 40 60 50 10
–10
P<.01
P<.01
流量调节的内皮血管舒张功能％
P<.01
Key Point
Flow-dependent dilation was significantly blunted in current smokers compared with nonsmokers.
Zeiher et al evaluated whether long-term smoking is associated with impaired endothelial vasodilator function, irrespective of preexisting atherosclerotic disease.
Blood vessels were distinguished as either normal or irregular, according to their angiographic appearance.
Ninety-six long-term current smokers (at least 2 pack/years of cigarette smoking immediately before the study) underwent diagnostic cardiac catheterization. Patients were excluded from the study if they had evidence of >30% stenosis in the left anterior descending (LAD) coronary artery or a history of variant angina, valvular heart disease, clinical evidence of heart failure, or diabetes. Intracoronary ultrasound examination was performed in 24 patients.
LAD diameter was evaluated angiographically before and after a 7-mg papaverine infusion. Papaverine maximally increases coronary blood flow without affecting global hemo-dynamics. Changes in LAD diameter were utilized to assess flow-dependent dilation.
Flow-dependent dilation was significantly blunted in current smokers compared with nonsmokers (P<.0001). When vessel segments were divided into normal and irregular segments based upon their angiographic appearance, both smoking groups demonstrated significantly blunted response in flow-dependent vasodilation compared with the nonsmoking groups (P<.01).
The authors concluded that long-term cigarette smoking is associated with a reduction in endothelium-dependent vasodilation, regardless of the presence or absence of coronary atherosclerotic lesions.
不吸烟者
吸烟者
Zeiher et al. Circulation. 1995;92:
Reference
Zeiher AM, Schächinger V, Minners J. Long-term cigarette smoking impairs endothelium-dependent coronary arterial vasodilator function. Circulation. 1995;92:

8. 吸烟致心外膜血管内皮功能障碍 与不吸烟者相比，吸烟者更容易发生心外膜内皮功能障碍 60 45 30 15 不吸烟者 戒烟者 吸烟者
不吸烟者
戒烟者
吸烟者
P=.03
46%
内皮功能障碍％
35%
34%
Key Point
Current smokers, without evidence of significant coronary artery disease (CAD), are more likely to have epicardial endothelial dysfunction than nonsmokers.
In an attempt to establish whether or not smoking is associated with coronary endothelial dysfunction and inflammation, Lavi et al evaluated 881 patients referred for evaluation of chest pain, who did not have evidence of significant CAD on diagnostic coronary angiography. Patients consisted of 115 current smokers (smoking within the last month) and 766 ex-smokers and nonsmokers. Nonsmokers included both previous and never smokers.
All patients underwent diagnostic coronary angiography. Microvascular coronary flow reserve was assessed after infusion with incremental doses of adenosine. Coronary vasoreactivity was assessed after infusion of incremental doses of acetylcholine. Endothelium-independent epicardial coronary artery function was assessed by the change in coronary artery diameter in response to an intracoronary bolus of nitroglycerine. All patients had baseline bloodwork prior to angiography to evaluate white blood cell (WBC) count and other systemic markers of inflammation.
Significantly more current smokers were found to have epicardial endothelial dysfunction, 46%, than ex-smokers, and nonsmokers, 34% and 35%, respectively.
Lavi et al. Circulation. 2007;115:
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:

9. 吸烟使白细胞计数升高 白细胞计数升高与更高心血管事件风险相关 与不吸烟者相比，吸烟者的白细胞计数明显升高 P<.0001 不吸烟者 86 4 2
戒烟者
细胞计数
吸烟者
P=.03
Key Point
Current smokers without evidence of significant coronary artery disease have significantly increased WBC counts compared with nonsmokers.
Elevated WBC counts have been associated with a greater long-term cardiovascular risk. In an attempt to establish whether or not smoking is associated with coronary endothelial dysfunction and inflammation, Lavi et al evaluated 881 patients referred for evaluation of chest pain, who did not have evidence of significant coronary artery disease on diagnostic coronary angiography. Patients consisted of 115 current smokers (smoking within the last month) and 766 ex-smokers and nonsmokers. Nonsmokers included both previous and never smokers.
All patients underwent diagnostic coronary angiography. Microvascular coronary flow reserve was assessed after infusion with incremental doses of adenosine. Coronary vasoreactivity was assessed after infusion of incremental doses of acetylcholine. Endothelium-independent epicardial coronary artery function was assessed by the change in coronary artery diameter in response to an intracoronary bolus of nitroglycerine. All patients had baseline bloodwork prior to angiography to evaluate WBC count and other systemic markers of inflammation.
Both total WBC count and leukocyte subtypes were higher in current smokers than in nonsmokers.
109/L
P<.0001
P<.0001
白细胞
中性粒细胞
淋巴细胞
单核细胞
Lavi et al. Circulation. 2007;115: ; Stewart et al. Circulation. 2005;111:
References
Stewart R, White H, Kirby A; et al; The Long-term Intervention With Pravastatin in Ischemic Disease (LIPID) Study Investigators. White blood cell count predicts reduction in coronary heart disease mortality with pravastatin. Circulation. 2005;111:
Lavi S, Prasad A, Yang E, 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:

10. 吸烟使血小板聚集功能增强 被动吸烟的人血小板聚集功能与吸烟者接近 不吸烟者 吸烟者 5.6 2.5 3.2 3.6 4.0 4.4 4.8
5.2
36.8
34.8
32.8
30.8
28.8
26.8
24.8
22.8
11-脱氢血栓烷素B2
丙二醛 ns ns ns ns ns ns ns ns ns ns ns
Min/10° Plateletsa ns
pg/mLa ns
Key Point
Nonsmokers repeatedly exposed to cigarette smoke have platelet function similar to that of current smokers (ie, increased thrombogenicity).
Schmid et al evaluated the effect of single and repeated exposure to environmental tobacco smoke on platelet thromboxane formation. Twenty-four subjects (12 nonsmokers, 12 current smokers) were exposed to the smoke of 30 cigarettes for 60 minutes. Blood was drawn immediately before, immediately after, and 6 hours after environmental tobacco smoke exposure, and assessed for levels of malondialdehyde, serum and plasma thromboxane B2, 11-dehydro-thrombaxane B2 as well as conversion of arachidonic acid to thromboxane B2 and hydroxy-5, 8,10-heptadecatrienoic acid . Smokers abstained from smoking for 10 hours prior to the experiment; however, they were allowed to reinitiate smoking 7 hours after the experiment was initiated. The experiment was repeated for 6 sequential days and on day 12.
The above graph demonstrates that nonsmokers repeatedly exposed to cigarette smoke have platelet function similar to that of current smokers (ie, increased thrombogenicity).
This study also demonstrated that the effects of even brief exposure to environmental tobacco smoke (minutes to hours) are often nearly as great (averaging 80% to 90%) as the effects of chronic active smoking. 天 天 1 2 3 4 5 12 1 2 3 4 5 12
ns=not significant.
a Unless marked as “ns,” differences for each value between groups were statistically significant at a level of P<.05.
Schmid et al. Thromb Res. 1996;81:
Reference
Schmid P, Karaniks G, Kritz H, et al. Passive smoking and platelet thromboxane. Thromb Res. 1996;81(4):

11. 吸烟增加氧化修饰 640 1000 560 酯化异构前列腺素F2 900 自由异构前列腺素F2 480 800 400 700 320
600
Key Point
Current smokers have higher levels of oxidative modification in vivo than do nonsmokers.
F2-isoprostane level is an accurate method of detecting lipid peroxidation, and thereby oxidant injury, in vivo. In this study Morrow et al determined whether smoking induces oxidative modification by evaluating whether production of F2-isoprostanes are increased in smokers.
Twenty subjects (10 smokers, 10 nonsmokers) had fasting bloodwork drawn on 2 separate occasions. Participants were not allowed to smoke prior to venipuncture. The average of the 2 measurements of F2-isoprostanes are demonstrated above.
Levels of free F2-isoprostanes in plasma from current smokers were significantly higher than those measured in age- and sex-matched nonsmokers (242147 and 10319 pmol/L, respectively) (P=.02). The levels of F2-isoprostanes esterified to lipids in plasma from smokers were also significantly higher than those measured in nonsmokers (574217 and 34565 pmol/L, respectively; P=.03).
The authors concluded that elevated levels of F2-isoprostanes in current smokers indicate that smoking induces oxidative modification of biologic components in humans.
240
500
160
400
pmol/L
pmol/L 80
300
不吸烟者
吸烟者
不吸烟者
吸烟者
异构前列腺素F2 水平是体内脂质过氧化反应的指标
The dots representing subjects who smoked are each connected to a dot representing a nonsmoker matched to the subject for age and sex.
Adapted from Morrow et al. N Engl J Med. 1995;332(18):
Reference
Morrow JD, Frei B, Longmire AW, et al. Increase in circulating products of lipid peroxidation (F2-isoprostanes) in smokers: smoking as a cause of oxidative damage. N Engl J Med. 1995;332(18):

12. 吸烟与心血管疾病的流行病学

13. 吸烟流行10年后出现吸烟相关疾病的流行

14. 吸烟与冠心病 (CAD)

15. 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:
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:

16. 吸烟增加心绞痛风险 2.6 2.0 1.6 1.0 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％
2.0
Key Point
The risk of angina may be directly related to the amount smoked.
Willett et al prospectively evaluated the incidence of coronary artery disease 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. Criteria for confirmed angina was presence of one of the following: documented evidence of coronary artery bypass surgery, coronary angiography demonstrating more than 70% obstruction of any coronary artery, or ST-segment depression of more than 1 mm on exercise stress testing together with a positive response to a mailed version of the Rose questionnaire.
Compared with nonsmokers, the age-adjusted RR of angina, increased with increasing daily cigarette use, 1.6, 2.0, and 2.6, for 1-14/day, 15-24/day, and 25/day, respectively.
1.6
1.0
非吸烟者
1-14/日
15-24/日
25/日
吸烟者每日吸烟量
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. Willett et al. N Engl J Med. 1987;317(1):
References
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):
Willigendael EM, Teijink JAW, Bartelink ML, Peter RJG, Büller HR, Prins MH. Smoking and the patency of lower extremity bypass grafts: a meta-analysis. J Vasc Surg. 2005;42(1):67-74.

17. 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
风险比
可信区间
95％
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 ; 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, ) than in older participants (OR, 2.55; 95% CI, ); 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, ) for younger smokers and 3.6 (95% CI, ) for older smokers (P<.0001 for interaction).
年龄<40 y
年龄40-49 y
年龄50-59 y
年龄60-69 y
年龄>70 y
非吸烟者
戒烟者
1-19支/日
支/日20
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:
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:

18. 每日吸烟量与心肌梗死发生有量效关系
OR (99% CI)
Y usuf S et al . Lancet. 2004;364:937-52

19. 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):
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):

20. 吸烟增加心源性猝死的风险 4.0 3.0 2.3 2.0 1.0 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, ).
1.0
1.0
0.0
不吸烟者
吸烟者
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:
Reference
Wannamethee G, Shaper AG, Macfarlane PW, Walker M. Risk factors for sudden cardiac death in middle-aged British men. Circulation. 1995;91:

21. 吸烟使冠脉介入治疗后发生Q波心梗的风险增高
4.0
相对风险
可信区间
95％
3.0
2.08
2.0
1.28
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 [ ]), than nonsmokers.
1.0
1.0
0.0
不吸烟者
戒烟者
吸烟者
Q波心梗 (MI)
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:
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:

22. 被动吸烟与冠心病

23. 被动吸烟增加冠心病发生风险 被动吸烟发生心脏疾病的风险比不吸烟者增加30％ 随访时间（年） 5 10 15 20 0.05 0.105 10 15 20
0.05
0.10
0.15
0.20
轻度主动吸烟a
重度被动吸烟b
轻度被动吸烟c
严重冠心病发生比例
Key Point
Exposure to environmental tobacco smoke increases the risk of heart disease among nonsmokers by 30%.
Whincup et al prospectively evaluated the relationship between environmental tobacco smoke exposure (quantified by serum cotinine levels) and risk of coronary artery disease (CAD) and stroke in 4729 subjects enrolled in the British Regional Heart Study. Participants were male nonsmokers aged 40 to 59 years, initially evaluated from 1978 to Baseline examination included assessment of blood pressure and nonfasting cholesterol and cotinine levels in addition to a nurse-administered questionnaire, from which data on smoking and medical history were obtained. Men were classified as “current nonsmokers” at baseline if they reported that they did not smoke and had a cotinine concentration <14.1 ng/mL. Nonsmokers were further subclassified into light and heavy passive smokers. Light passive smokers were nonsmokers who had the lowest levels of cotinine concentration (0-0.7). Heavy passive smokers were nonsmokers who had the highest cotinine concentration (0.8 to 14.0). Light active smokers were men who reported smoking 1 to 9 cigarettes a day, irrespective of cotinine concentration.
All men were followed up for all-cause mortality and cardiovascular mortality. The graph depicts the Kaplan-Meier plot showing the cumulative proportions of men with major CAD over time among the light active, heavy passive and light passive smokers. Age, systolic blood pressure, diastolic blood pressure, total cholesterol, high-density lipoprotein (HDL) cholesterol, forced expiratory volume in 1 second (FEV1), height, preexisting CAD, body mass index, triglycerides, WBC, diabetes, physical activity (none, occasional, light, moderate, or more), alcohol intake (none/occasional, light/moderate, heavy), and social class (I, II, III non-manual, III manual, IV, V, and Armed Forces) were fitted as dichotomous variables.
Heavy passive and light passive smokers had the highest incidence of major CAD. Although the groups diverged markedly in the early follow-up period, they remained almost parallel during later years.
The authors concluded that environmental tobacco smoke exposure is associated with an increased risk of CAD of approximately 25% to 30%.
Adjusted for age, systolic blood pressure, diastolic blood pressure, total cholesterol, HDL cholesterol, FEV, height, preexisting CAD, body mass index, triglycerides, white cell count, diabetes, physical activity, alcohol intake, and social class.
aLight active refers to men smoking 1-9 cigarettes a day. bHeavy passive refers to upper three quarters of cotinine concentration combined (0.8 to 14.0 ng/mL). cLight passive refers to lowest quarter of cotinine concentration among nonsmokers ( ng/mL).
Whincup et al. BMJ. 2004;329:
Reference
Whincup PH, Gilg JA, Emberson JR, et al. Passive smoking and risk of coronary heart disease and stroke: prospective study with cotinine measurement. BMJ. 2004;329:

24. 被动吸烟增加急性心梗发生风险 被动吸烟使发生非致死性心梗的风险量级增加 4 2 1 无 1-7 8-14 15-21 22 0.75
比值比
可信区间
95％ 2
Key Point
Exposure to environmental tobacco smoke increased the risk of nonfatal acute (MI) in a graded manner.
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.
After adjusting for age, sex, region, physical activity, and consumption of fruits, vegetables, and alcohol, nonsmokers who had no previous environmental tobacco smoke exposure showed increasing risk of nonfatal acute MI with increasing levels of exposure to environmental tobacco smoke. Although the etiology is unclear, this increase in risk was slightly attenuated in subjects with 22 hours per week of environmental tobacco smoke exposure. 1 无
1-7
8-14
15-21
22
0.75
被动吸烟暴露持续时间（小时/周）
aThe ratio of the odds of development of disease in exposed persons to the odds of development of disease in nonexposed persons. Adjusted for age, sex, region, physical activity, and consumption of fruits, vegetables, and alcohol. Adapted from Teo et al. Lancet. 2006;368:
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:

25. 吸烟与脑卒中

26. 吸烟增加急性缺血性卒中风险 大量吸烟后急性作用： 脑血管急性血栓形成 脑核磁共振像 急性缺血性脑卒中
Cigarette smoking has been identified as a significant risk factor for ischemic stroke, hemorrhagic stroke, as well as subarachnoid hemorrhage. The annual number of stroke deaths attributed to smoking in the United States has been estimated to be between 17,800 and 21,400, or 12% to 14%. Smoking may also potentiate the effects of other stroke risk factors, such as oral contraceptive use.
Smoking is thought to increase stroke risk both acutely, through its effect on thrombus formation, and chronically, by increasing the risk of atherosclerosis.
脑核磁共振像 急性缺血性脑卒中
Goldstein et al. Stroke. 2006;37: ; Accessed October 19, 2007.
Reference
Goldstein LB, Adams R, Alberts MJ., et al. Primary Prevention of Ischemic Stroke: A Guideline From the American Heart Association/American Stroke Association Council: Cosponsored by the Atherosclerotic Peripheral Vascular Disease Interdisciplinary Working Group; Cardiovascular Nursing Council; Clinical Cardiology Council; Nutrition, Physical Activity, and Metabolism Council; and the Quality of Care and Outcomes Research Interdisciplinary Working Group: The American Academy of Neurology affirms the value of this guideline. Stroke. 2006;37:

27. 吸烟促进颈动脉粥样硬化进展 无论是主动还是被动吸烟都会加快颈动脉粥样硬化 43.0 38.8 31.6 32.8 25.9
颈动脉内膜中层厚度增加
43.0
38.8
31.6
32.8
Key Point
Both active smoking and environmental tobacco smoke exposure are associated with increased progression of carotid atherosclerosis.
Howard et al evaluated 10,914 participants enrolled in the Atherosclerosis Risk in Communities (ARIC) study, a prospective study that assessed atherosclerotic disease and its clinical consequences in a cohort of approximately 16,000 US adults.
Subjects underwent carotid ultrasound to evaluate carotid intima-medial thickness, a surrogate of atherosclerotic progression. Assessments were made at baseline and at a follow-up visit 3 years later. All participants completed self-administered questionnaires based upon which they were classified as current smokers, ex-smokers, nonsmokers, and exposed to environmental tobacco smoke.
Current smokers demonstrated the highest rate of atherosclerotic progression (41 µm per 3 years). Rates of progression followed, in descending order, ex-smokers with environmental tobacco smoke exposure, nonsmokers with environmental tobacco smoke exposure, ex-smokers without environmental tobacco smoke exposure, followed by nonsmokers without environmental tobacco smoke exposure, 39.6 µm, 33.2 µm,32.5 µm; and 27.0 µm, respectively.
The authors therefore concluded that both active smoking and environmental tobacco smoke exposure are associated with increased progression of carotid atherosclerosis.
25.9
μm/3年
不吸烟者且无被动吸烟b
不吸烟者但有被动吸烟b
戒烟者且无被动吸烟b
戒烟者有被动吸烟b
吸烟者
aAdjusted for demographic characteristics, cardiovascular risk factors, and lifestyle variables (risk factor model and Keys score, education, leisure activity, body mass index, and alcohol use). bTo environmental tobacco smoke. Howard et al. JAMA. 1998;279(2):
Reference
Howard G, Wagenknecht LE, Burke GL, et al; the ARIC Investigators.. Cigarette smoking and progression of atherosclerosis: the Atherosclerosis Risk in Communities (ARIC) Study. JAMA. 1998;279(2):

28. 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％
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 ( ).
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 ( ) to 2.9 ( ) to 3.8 ( ) 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):
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):

29. 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)
总出血性脑卒中
脑内出血
蛛网膜下腔出血
2.06
3.43
2.39
2.89
1.74
4.04
相对风险
可信区间
95％
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 ( ) 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.
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:
Reference
Kurth T, Kase CS, Berger K, Gaziano JM, Cook NR, Buring JE. Smoking and risk of hemorrhagic stroke in women. Stroke. 2003;34:

30. 吸烟增加脑卒中死亡风险 15-24 1-15 ≥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.
aTwenty-year age-adjusted mortality per 10,000 person-years for men. P<.014 for trend. Hart et al. Stroke. 1999;30:
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:

31. 吸烟与外周血管疾病 (PVD)

32. 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:

33. 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:
Wilmink TB, J Vasc Surg 1999; 30:

34. 戒烟对心血管的益处

35. 戒烟对心血管益处的病理生理机制

36. 戒烟使纤维蛋白原下降 长期吸烟者戒烟2周后，纤维蛋白原浓度和纤维蛋白原的合成速率均明显减低 P<.001 P<.001 3.06
纤维蛋白原绝对合成速率
3.06
血浆纤维蛋白原浓度
24.1
2.49
16.1
Key Point
After 2 weeks of cessation by formerly chronic smokers, both fibrinogen concentration and the rate of fibrinogen synthesis are reduced.
Elevated plasma fibrinogen is an independent risk factor for cardiovascular disease. Hunt et al sought to elucidate the relationship between smoking and hyperfibrinoginemia. The authors performed 2 studies, reported in the cited article. Data in the above slide is derived from the second study in which 11 male chronic smokers were evaluated before and after a 2-week trial of smoking abstinence. Serum levels of fibrinogen, fibrinogen synthesis, albumin, albumin synthesis and C-reactive protein were evaluated before and after abstention. Compliance with the nonsmoking regimen was assessed by measuring urinary cotinine concentration on 2 separate occasions during the study period.
All subjects demonstrated a reduction in plasma fibrinogen concentration. Mean fibrinogen concentration while smoking was 3.060.11 g/L, which decreased approximately 19% to 2.490.14 g/L after abstention (P<.001).
Absolute rate of fibrinogen synthesis (ASR) was calculated as the product of the percentage of the intravascular fibrinogen pool synthesized per day and intravascular fibrinogen mass (fibrinogen concentration × plasma volume). Fibrinogen ASR decreased from a mean value of 24.11.7 mg/kg per day while smoking to 16.1± 1.0 mg/kg per day after abstention (P<.001). Fibrinogen ASR decreased approximately 33% after cessation.
（ASR)
g/L 吸烟
戒烟a 吸烟
戒烟a
mg/kg
ASR=absolute rate of fibrinogen synthesis. aAbstention period of 2 weeks.
Hunter et al. Clin Sci (Lond). 2001;100(4):
Reference
Hunter KA, Garlick PJ, Broom I, Anderson SE, McNurlan MA. Effects of smoking and abstention from smoking on fibrinogen synthesis in humans. Clin Sci (Lond). 2001;100(4):

37. 戒烟使白细胞计数明显降低 戒烟a 吸烟 P<.026 白细胞计数 109/L
Key Point
Smoking cessation is associated with a significant reduction in white blood cells (WBC).
In an effort to evaluate the effect of smoking reduction and cessation on cardiovascular risk factors, Eliasson et al evaluated 58 current smokers (15 cigarettes/day for 3 years) in Göteborg, Sweden, and followed them up for a total of 12 months. The study consisted of 2 phases. During the initial phase (weeks 1-9), subjects reduced their daily cigarette smoking by a minimum of 50%. During the second phase (to week 17), subjects were required to completely abstain from smoking. All subjects were prescribed nicotine nasal spray, to be used as needed.
At 17 weeks, 33 subjects (57.8%) were abstinent. Smoking cessation was associated with significant reduction in WBC from 7.00.4(× 109) to 6.10.3 (× 109), P=.026.
aAbstention period of 17 weeks.
Eliasson et al. Nicotine Tob Res. 2001;3(3):
Reference
Eliasson B, Hjalmarson A, Kruse E, Landfeldt B, Westin A. Effect of smoking reduction and cessation on cardiovascular risk factors. Nicotine Tob Res. 2001;3(3):

38. 戒烟使血小板聚集率下降 腺苷二磷酸（ADP）=5.0 µmol/L A组a B组b 血小板聚集 (%) 20 60 100 40 8020 60
100 40 80
时间（天） 7 14 21 28 NS
P<.01
Key Point
Smoking abstinence is associated with reduced platelet aggregability.
In an attempt to evaluate the impact of smoking cessation on intracellular oxidative stress and platelet aggregability in long-term smokers, Morita et al evaluated 27 male smokers. Subjects smoked a minimum of 15 cigarettes per day for more than 5 years.
Participants were divided into 2 groups: group A abstained from smoking for 28 days, and group B abstained from smoking initially, but resumed smoking after 14 days. Bloodwork was assessed at baseline followed by days 7, 14, 21, and 28. Adenosine diphosphate (ADP) and collagen-induced platelet aggregation were assessed by adding ADP and collagen to washed platelet suspensions and light transmission was monitored using a platelet aggregometer.
Agonist (ADP or collagen)-induced platelet aggregations were similar between the 2 groups at baseline. In group A, agonist-induced platelet aggregations were significantly reduced throughout the period of abstinence. In group B, agonist-induced platelet aggregation significantly decreased through day 14; however, aggregability rapidly returned to baseline with reinitiation of smoking.
aQuit smoking for 28 days. bResumed smoking after quitting for 14 days.
ADP=adenosine diphosphate. ADP is a platelet aggregation agonist.
Morita et al. J Am Coll Cardiol. 2005;45:
Reference
Morita JH, Ikeda H, Haramaki N, Eguchi H, Imasizumi T. Only two-week smoking cessation improves platelet aggregability and intraplatelet redox imbalance of long-term smokers. J Am Coll Cardiol. 2005;45:

39. 戒烟使血脂改善 戒烟可改善脂蛋白构成，包括高密度脂蛋白升高，低密度脂蛋白降低 P<.015 P<.001 P<.001
高密度脂蛋白 (mmol/L) 吸烟
戒烟a
P<.015 吸烟
戒烟a
低密度脂蛋白 (mmol/L)
Key Point
Smoking cessation is associated with a significant increase in HDL, HDL/LDL ratio, and reduction in LDL.
In an effort to evaluate the effect of smoking reduction and cessation on cardiovascular risk factors, Eliasson et al evaluated 58 current smokers (15 cigarettes/day for 3 years) in Göteborg, Sweden, and followed up for a total of 12 months. The study consisted of 2 phases. During the initial phase (weeks 1-9), subjects reduced their daily cigarette smoking by a minimum of 50%. During the second phase (to week 17), subjects were required to completely abstain from smoking. All subjects were prescribed nicotine nasal spray, to be used as needed.
At 17 weeks, 33 subjects (57.8%) were abstinent. Smoking cessation was associated with significant increases in HDL concentration from 1.160.06 mmol/L to 1.320.06 mmol/L (P<.001), and in HDL/LDL ratio from 0.330.03 to 0.420.03 (P<.001) as well as a significant reduction in LDL concentration from 3.780.16 to 3.520.17 (P=.015).
HDL/LDL 比值
P<.001 吸烟
戒烟a
HDL=high-density lipoprotein;
LDL=low-density lipoprotein. aAbstention period of 17 weeks. Eliasson et al. Nicotine Tob Res. 2001;3(3):
Reference
Eliasson B, Hjalmarson A, Kruse E, Landfeldt B, Westin A. Effect of smoking reduction and cessation on cardiovascular risk factors. Nicotine Tob Res. 2001;3(3):

40. 戒烟使动脉顺应性改善 振荡顺应性 (mL/mm Hg × 100)a P<.01 吸烟 戒烟c P<.05 63.1 50.6
增强指数 (%)b
Key Point
Smoking cessation is associated with an improvement in hemodynamic parameters.
Oren et al performed an open-label study in which 60 chronic smokers (20 cigarettes a day for more than 10 years) were treated for 2 months with bupropion (300 mg/day) and participated in behavioral therapy. Complete physical exam was performed at baseline.
Arterial compliance was evaluated based upon noninvasive radial artery waveforms recorded from subjects while in the supine position. Computer analysis of waveforms and diastolic decay provided information regarding capacitive compliance and small artery reflective or oscillatory compliance. Augmentation index is the ratio of recorded augmentation pressure and pulse pressure. Augmentation index provides a measure of systolic arterial stiffness.
At the 6-month follow-up, 23 participants remained nonsmokers. Repeat physical exam demonstrated significant reduction in mean arterial pressure and heart rate, as well as improvement in oscillatory compliance from 5.12.3 to 6.33 (P<.01) and reduction in augmentation index from 63.122 to 50.617 (P<.05). 吸烟
戒烟c
aProvides an assessment of small arteriolar compliance. bThe amplitude of the reflected wave depends on the stiffness of the small vessels and large arteries and thus provides a measure of systolic arterial stiffness.cAbstention period of 6 months.
Oren et al. Angiology. 2006;57(5):
Reference
Oren S, Isakov I, Golzman B, et al. The influence of smoking cessation on hemodynamics and arterial compliance. Angiology. 2006;57(5):

41. 戒烟使血液动力学改善 P<.05 平均动脉压 (mm Hg) 吸烟 戒烟a P<.05 心率 (Beats/min) 吸烟
Key Point
Smoking cessation is associated with an improvement in hemodynamic parameters.
Oren et al performed an open-label study in which 60 chronic smokers (20 cigarettes a day for more than 10 years) were treated for 2 months with bupropion (300 mg/d) and participated in behavioral therapy. Complete physical exam was performed at baseline.
At the 6-month follow-up, 23 participants remained nonsmokers. Repeat physical exam demonstrated significant reductions in mean arterial pressure from 9010.7 to 8711.6 mm Hg (P<.05), and in heart rate from 7610 to 7210 (P<.05), as well as improvement in arterial compliance (as demonstrated in the next slide). 吸烟
戒烟a
a Abstention period of 6 months.
Oren et al. Angiology. 2006;57(5):
Reference
Oren S, Isakov I, Golzman B, et al. The influence of smoking cessation on hemodynamics and arterial compliance. Angiology. 2006;57(5):

42. 戒烟对心血管益处的流行病学

43. 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Ca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Ca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. Accessed on April 15, 2006.
2. American Cancer Society. Guide to Quitting Smoking. Available at: 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 Available at: 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 American Cancer Society. Guide to Quitting Smoking2006

44. 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 4 2 1 吸烟者 >1-3 >3-5
比值比
可信区间
95％ 2
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. 1
吸烟者
>1-3
>3-5
>5-10
>10-15
>15-20
20
戒烟者 (戒烟年数)
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:
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:

45. 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, ). 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):
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):

46. 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 (%)
戒烟者
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 Baseline smoking history was obtained at the time of surgery. Patients were followed up for a median of 20 years (range: 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, ) and of cardiac death, (RR, 1.75; 95% CI, ) 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%). 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):
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):

47. 戒烟使心律失常死亡风险减少 对于心梗后左心室功能异常的患者，戒烟可使心律失常造成死亡风险降低 20 40 60 80 100 P=.04020 40 60 80
100
P=.040
生存率％
Key Point
Cessation of cigarette smoking is associated with a reduction in arrhythmic death for patients with post-myocardial infarction (MI) left ventricular dysfunction.
Peters et al sought to evaluate the effect of smoking cessation on overall mortality and the incidence of arrhythmic death in participants of the Cardiac Arrhythmia Suppression Trial (CAST). There were 2 components to the CAST trial: CAST I and CAST II. Subjects in CAST I were treated with ecainide, flecainide, and moricizine between June 1987 and April Subjects in CAST II were treated with 3 doses of moricizine between April 1989 and August The CAST trials were multicenter, double-blind, placebo-controlled studies the objective of which was to determine whether suppression of ventricular ectopic activity, by means of antiarrhythmic therapy in patients with left ventricular dysfunction after acute MI, would reduce the incidence of arrhythmic death.
Ex-smokers were defined as patients who stopped smoking between the time of their index myocardial infarction and their 4-month follow-up visit. Current smokers were defined as those who continued to smoke until that time.
Of 2752 patients in the CAST trial, 1026 were smoking at the time of baseline examination and are the subjects of the Peters et al study. Of the 1026 current smokers, 517 stopped smoking between the time of the index MI and the 4-month follow-up. Ex-smokers had 17 arrhythmic deaths and 32 deaths overall, whereas current smokers had 30 arrhythmic deaths and 45 total deaths. The graph depicts the survival curves for smokers and ex-smokers and demonstrates that there was significantly reduced survival rates in smokers when compared with ex-smokers, P=.04. 吸烟
戒烟者 2 3 1
生存时间（年）
Peters et al. J Am Coll Cardiol. 1995;26(5):
Reference
Peters RW, Brooks MM, Todd L, Liebson PR, Wilhelmsen L; the Cardiac Arrhythmia Suppression Trial (CAST) Investigators. Smoking cessation and arrhythmic death: The CAST experience. J Am Coll Cardiol. 1995;26(5):

48. 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 2015
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:
Reference
Hallstrom AP, Cobb LA, Ray R. Smoking as a risk factor for recurrence of sudden cardiac arrest. N Engl J Med. 1986;314:

49. 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:
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:

50. 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 不吸烟者 戒烟者 吸烟者 (<20支/日)
吸烟者 (≥20 支/日）
P <.0001(趋势)
相对风险
可信区间
95％
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, ) than physicians currently smoking less than 20 and more than 20 cigarettes daily, (2.0, 95% CI, ) and (2.5, 95% CI, ), respectively.
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):
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):

51. 戒烟、降压、降胆固醇 对无CVD史者死亡的影响
全因死亡
戒烟1
全因死亡降低约15-20%
降压2
降胆固醇l3
CVD死亡
戒烟1
CVD死亡降低约25-35%
Blood pressure and cholesterol medications commonly considered to have a beneficial effect in reducing risk of death in a population of individuals without previous history of cardiovascular disease.
In subjects with no history of CVD, smoking cessation, blood pressure treatment and cholesterol treatment all reduce risk of death, both all cause and mortality due to CVD, to a comparable degree.
References
Kawachi, I. Smoking Cessation in Relation to Total Mortality Rates in Women. Ann Internal Med, 1993;119:
Lievre, M. Efficacy of Diuretics and beta-Blockers in Diabetic Hypertensive Patients. Diabetes Care, 2000;23(2):B65-B71.
Vrecer, M. Use of Statins in Primary and Secondary Prevention of Coronary Heart Disease and Ischemic Stroke. International Journal of Clinical Pharmacology and Therapeutics, 2003;41:
降压2
降胆固醇3 . 1 . 4 . 7 1 . 1 . 3 1 . 6 1 . 9
1。Kawachi, Lievre, Vrcer, 2003

52. 戒烟、降压、降胆固醇 对有CVD史者死亡的影响
全因死亡
戒烟1
全因死亡降低约12-35%
戒烟所致的风险降低最大
降压2a
降压2b
降胆固醇3
For those with a previous history of CVD, smoking cessation provides the greatest reduction in risk of death (all cause mortality) compared with different interventions controlling blood pressure and cholesterol.
References
Critchley, JA. Mortality Risk Reduction Associated with Smoking Cessation in Patients with Coronary Heart Disease. JAMA, 2003;290(1):86-97.
Blood Pressure Lowering Treatment Trialists’ Collaboration. Effects of different blood-pressure-lowering regimens on major cardiovascular events: results of prospectively-designed overviews of randomised trials. Lancet, 2003; 362: 1527–35.
Vrecer, M. Use of Statins in Primary and Secondary Prevention of Coronary Heart Disease and Ischemic Stroke. International Journal of Clinical Pharmacology and Therapeutics, 2003;41:
Cholesterol Treatment Trialists’ (CTT) Collaborators. Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from participants in 14 randomised trials of statins. Lancet, 2005; 366: 1267–78.
降胆固醇4 . 1 . 4 . 7 1 . 1 . 3 1 . 6 1 . 9
1. Critchley, BPLTTC, Vrercer, CTT, 2005

53. 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

54. 戒烟给心血管系统带来的益处（总结） 短期益处 长期益处 减少下列风险 卒中 重复冠脉搭桥术 心梗后反复发生冠脉事件 心梗后心律失常所致猝死
 纤维蛋白原浓度下降
 纤维蛋白原合成速率减低
 白细胞计数下降
高密度/低密度脂蛋白比例改善
 卒中风险降低
 高密度脂蛋白增加
 低密度脂蛋白下降
动脉压
 心率下降
动脉顺应性改善
 心梗后心律失常所致猝死风险减低
 血小板体积减小
血小板环磷酸腺苷反应增强，促使前列腺素E1 发生腺苷酸环化
 吸烟导致的血小板聚集减少
长期益处
减少下列风险 卒中
重复冠脉搭桥术
心梗后反复发生冠脉事件
心梗后心律失常所致猝死
继发心血管疾病
冠脉搭桥术后血运重建术 减少
冠脉搭桥术后的死亡率
经皮冠状动脉成形术后死亡率
与心血管疾病进展相关的炎症标志分子水平(C反应蛋白, 白细胞, 纤维蛋白原)
Smoking cessation is associated with multiple short- and long-term cardiovascular benefits.
Twardella D, Kupper-Nybelen J, Rothenbacher D, Hahmann H, Wusten B, Brenner H. Short-term benefit of smoking cessation in patients with coronary heart disease: estimates based on self-reported smoking data and serum cotinine measurements. Eur Heart J. 2004;25(23):
Morita J, Ikeda H, Haramaki N, Eguchi H, Imasizumi T. Only two-week smoking cessation improves platelet aggregability and intraplatelet redox imbalance of long-term smokers. J Am Coll Cardiol. 2005;45(4):
Oren S, Isakov I, Golzman B, et al. The influence of smoking cessation on hemodynamics and arterial compliance. Angiology. 2006;57(5):
Terres W, Becker P, Rosenberg A. Changed in cardiovascular risk profile during the cessation of smoking. Am J Med. 1994;97:
Nilsson P, Lundgren H, Söderström M, Fagerström K-O, Nilsson-Ehle P. Effects of smoking cessation on insulin and cardiovascular risk factors—a controlled study of 4 months' duration. J Intern Med. 1996;240(4):
Peters R, Brooks M, Todd L, Liebson P, Wilhelmsen L; The Cardiac Arrhythmia Suppression Trial (CAST) Investigators. Smoking cessation and arrhythmic death: the CAST experience. J Am Coll Cardiol. 1995;26:
Rea TD, Heckbert SP, Kaplan RC, Smith NL, Lemaitre RN, Psaty BM. Smoking status and risk for recurrent events after myocardial infarction. Ann Intern Med. 2002;137:
Hasdai D, Garratt K, Grill D, Lerman A, Holmes D. Effect of smoking status on the long-term outcome after successful percutaneous coronary revascularization. N Engl J Med. 1997;336:
van Domburg RT, Meeter K, van Berkel DFM, Veldkamp RF, van Herwerden LA, Bogers JAJC. Smoking cessation reduces mortality after coronary artery bypass surgery: a 20-year follow-up study. J Am Coll Cardiol. 2000;36:
Bakhru A, Erlinger TP. Smoking cessation and cardiovascular disease risk factors: results from the Third National Health and Nutrition Examination Survey. PLos Med. 2005;2(6, e160):
Eliasson B, Hjalmarson A, Kruse E, Landfeldt B, Westin A. Effect of smoking reduction and cessation on cardiovascular risk factors. Nicotine Tob Res. 2001;3(3):
Hunter KA, Garlick PJ, Broom I, Anderson SE, McNurlan MA. Effects of smoking and abstention from smoking on fibrinogen synthesis in humans. Clin Sci (Lond). 2001;100(4):
Wannamethee G, Shaper AG, Whincup PW, Walker M. Smoking cessation and the risk of stroke in middle-aged men. JAMA. 1995;274:
Twardella et al. Eur Heart J. 2004;25: ; Morita et al. J Am Coll Cardiol. 2005;45: ; Oren et al. Angiology. 2006;57: ; Terres et al. Am J Med. 1994; 97: ; Nilsson et al. J Int Med. 1996; 240: ; Peters et al. J Am Coll Cardiol. 1995;26: ; Rea et al. Ann Intern Med. 2002;137: ; Hasdai et al. N Engl J Med. 1997;336: ; van Domburg et al. J Am Coll Cardiol. 2000; 36: ; Bakhru et al. PLoS Med. 2005;2:e160; Eliasson et al. Nicotine Tob Res. 2001;3 : ; Hunter et al . Clin Sci. 2001;100 : ; Wannamethee et al. JAMA. 1995;274:

56. Thank You !