Review article

Smoking cessation is a cheap and effective way to reduce cardiovascular risk

Smoking, smoking cessation and cardiovascular risk

DOI: https://doi.org/10.4414/cvm.21.00588
Publication Date: 14.11.2018
Cardiovasc Med. 2018;21(11):00588

Isabella Sudano, Jens Barthelmes, Brigitt Kubli

University Heart Centre, University Hospital Zurich and University of Zurich, Switzerland

Summary

Smoking is a widely-recognised risk factor for several diseases, including cardiovascular disease, pulmonary disease and cancer at several sites, and is a primary cause of premature morbidity and mortality.

As early as 1964, the first report of the US Surgeon General pointed out that cigarette smoking has detrimental health effects, summarising studies from the United Kingdom and the United States.

Following those initial efforts, a vast body of research grew across all fields of medicine, surgery and public health, focusing on the role of tobacco as cardiovascular risk factor, the danger of active and passive smoking, and the health effects of smoking cessation.

This review aims to summarise the available evidence on the effect of tobacco on cardiovascular morbidity and mortality and the effect of smoking cessation on cardiovascular risk and disease.

Key words: tobacco; smoking; smoking cessation; cardiovascular risk

Introduction

Smoking is a widely-recognised risk factor for several diseases, including cardiovascular disease, pulmonary disease and cancer at several sites [1], and as such is a major cause of premature morbidity and mortality worldwide [2].

The first report of the US Surgeon General in the 1960s described the detrimental health effect of cigarette smoking [3]; it marked a turning point in the public recognition of the harms and hazards of smoking, as well as of cigarette consumption per capita in the US [1].

Following these initial efforts, mainly based on studies conducted in England and USA, considerable research has expanded the concept from cigarettes to the effects of smoked and smokeless tobacco on health [4, 5], and the role of active and passive smoking as cardiovascular risk factors [6–8].

Moreover, observational and interventional trials have assessed the health effects of smoking cessation achieved with behavioural and pharmacological approaches [9–15].

Tobacco as cardiovascular risk factor

Data reported in the 1950s by Doll and Peto [16] showed that smoking increased death rates due to coronary heart disease (CHD) in British physicians and underlined that smokers had a highly elevated relative risk for dying from CHD. This effect was significant at all ages and was particularly strong in adults younger than 45 years of age.

Further studies have consistently shown that the number of cigarettes smoked on a regular basis strongly correlates with the risk of myocardial infarction in both sexes [17]. Epidemiological data [18] and randomised studies have been summarised in systematical reviews [19, 20]. Pipe and cigar smoking were also clearly shown to increase death rates from several forms of cancer, especially in the oropharynx, and the CHD risk [21–24].

Passive or involuntary smoking occurs when nonsmokers breathe “side-stream” smoke produced by burning tobacco, or “main-stream” smoke exhaled by smokers. In the Nord-Trøndelag Health Survey 2 (HUNT2), which was conducted in 1995–1997 and included 65 229 participants aged 20 years or older, exposure to passive smoking increased lung cancer risk approximately 1.50 times [25]; prospective study results suggest that the relative risk of CHD is also raised appreciably [26–28].

More recently, the INTERHEART Study [6] confirmed that no tobacco product may be considered as “safe” for the cardiovascular system. Data from patients recruited in 52 different countries showed that smoked as well as smokeless tobacco was associated with an increased risk of myocardial infarction.

Tobacco affects the cardiovascular system directly and indirectly through unfavourable effects on a large variety of CHD risk factors. Although average smokers are leaner that nonsmokers, oxidation of lipids [29, 30] and lower high-density lipoprotein cholesterol were found more often in smokers than nonsmokers [31, 32]. Regular tobacco users have higher fasting blood glucose due to reduced insulin sensitivity [33–36] and typically have higher blood pressures and heart rate than nonsmokers [33, 37–39].

Other mechanisms by which smoking exerts its negative cardiovascular effects include a hypercoagulable [40, 41] and proinflammatory [42–44] state, characterised by increased fibrinogen levels, greater thromboxane A2, increased platelet activation, increased isoprostanes, and increased C-reactive protein. Smoking increases carbon monoxide in the body, and reduces oxygen delivery to vital tissues [45–47], activating the sympathetic nervous system and causing vasoconstriction beyond the direct vascular effects of nicotine (fig. 1) [48–52].

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Figure 1: Known mechanisms linking tobacco smoking and cardiovascular diseases.

Second hand smoking and cardiovascular risk

The negative effects of tobacco on the cardiovascular system are not limited to active users. People who are not using tobacco but are exposed to other’s tobacco smoke have been shown to have an increased risk of CHD.

Second-hand smoke, involuntary or passive smoking are defined as passive inhalation of a smoke mixture comprising 15% mainstream smoke (inhaled and exhaled by the smoker) and 85% side-stream or tertiary smoke (which is released from the burning tip of a cigarette between puffs). Tertiary smoke results from burning tobacco at a much higher temperature and with less available oxygen, and so toxic substances such as carbon monoxide, methane, cyanides and carcinogenic benzene are found in greater amounts than in mainstream smoke (nicotine 2:1, benzene 10:1, nitrosamines 100:1) [53].

A meta-analysis of 10 prospective cohort studies and 8 case-control studies [54] showed that second-hand smoke increases the relative risk of cardiovascular morbidity and mortality by 25% among nonsmokers. Passive smoking was consistently associated with an increased relative risk of coronary heart disease in men and in women, as well as in those exposed to smoking at home or in the workplace. The meta-analysis by He and colleagues [54] identified a significant dose-response relationship, with relative risks of 1.23 and 1.31 for nonsmokers who were exposed to the smoke of 1 to 19 cigarettes per day and 20 or more cigarettes per day, respectively, as compared with nonsmokers not exposed to smoke (p = 0.006 for linear trend).

The Auckland stroke study [55] pointed out that the risk of acute stroke was also increased. Exposure to environmental tobacco smoke was associated with an increased risk for stroke in men (odds ratio [OR] 2.06; 95% confidence interval [CI] 1.34–3.17) and women (OR 1.50; 95% CI 1.01–2.21). After adjustment for age and sex, exposure to environmental tobacco smoke was associated with an overall increased risk of stroke (OR 1.74; 95% CI 1.31–2.32).

The CARDIO2000 case-control study [56] investigated the association between environmental tobacco smoke exposure (at least 30 minutes a day) and the risk of developing acute coronary syndromes. The results of this study showed that, in a follow-up of 20 years, the risk of ischaemic heart disease in people without preexisting cardiovascular damage was increased by 1.61 in the group with high exposure (cotinine level 2.8–14 ng/ml).

The INTERHEART study showed that in subjects who had never smoked cigarettes, passive smoking accounted for 10.8 and 18.6% of all myocardial infarctions in women and men, respectively [6].

More recently, an analysis of 24 968 men and women followed up for 11 years in the Tromsø Study [57] showed that the risk of myocardial infarction increased linearly for both active and passive smoking in both sexes, but rather consistently more strongly for women than for men. Restricting the analysis to never-smokers’ passive smoking was found to be an independent risk factor for myocardial infarction in never-smoking women.

The cardiovascular risk associated with environmental tobacco smoke is rapidly reversible, as multiple studies performed all around the world have documented a rapid decline in hospital admissions for myocardial infarction after the adoption of smoking bans [58–63].

Smoking cessation and cardiovascular risk and diseases

Ceasing to smoke is not an easy challenge: people who try to stop smoking without additional aids face a high relapse risk. Individuals may have moderately high success in the short term with this approach, but the results at 12 months are generally not very encouraging (1–5% are still nonsmokers) [64].

The smoking cessation issue is complex and depends on individual factors, as well as factors that are prevalent in the society where the smoker lives.

Determinants of smoking cessation have been studied in the 1999–2001 follow-up of the European Community Respiratory Health Survey (ECRHS) [65]. Data from 9053 adults from 14 countries were collected. Overall, 28.8% of the participants stopped smoking during the follow-up; older age, and higher education level and social status were positively associated with a higher cessation rate.

In a longitudinal study of 2564 middle-aged smokers, nearly 40% quit smoking during an approximate 10-year study period [66]. The authors found an association between smoking cessation and fewer smoking years, as well as a high level of education. Neither presence of airway disease nor the known cardiovascular risk factors hypertension and diabetes seemed to predict smoking cessation. This was true also for those who developed airway disease, diabetes or hypertension during the study period. Known heart disease at baseline did not predict smoking cessation, but an acute episode of ischaemic heart disease during the study period was associated with a four-fold increase in the chance of smoking cessation. Other studies have shown that the presence of tobacco-related disease was a positive predictor for smoking cessation [67].

When smokers are able to stop, and remain nonsmokers, the rates of new cardiovascular events decrease significantly a few years after smoking cessation. In the Multiple Risk Factor Intervention Trial [68], the men who stopped smoking during the first 3 years of the study experienced a relative risk for CHD of 0.38 compared with those who had continued to smoke during the 10.5 years of follow-up. Moreover, Critchley and Capewell [69] showed that the mortality risk in patients with coronary heart disease was significantly reduced by smoking cessation.

Weight gain after smoking cessation, even though with wide variation, has been well documented [70] and remains an issue because it may deter smokers from quit attempts and women are probably less likely to respond to nicotine replacement therapy [71]. In combination with other cardiovascular risk factors, weight gain may subtract slightly from the health benefits of cessation [72] and ought to be counteracted by dietary and exercise counselling in the outpatient setting or during rehabilitation.

All smoking cessation interventions, such as personal advice from medical personnel [73–75] or via media/Internet [76, 77] and the use of nicotine replacement therapy [78], bupropion [79, 80] or and varenicline [79, 81] ­increase the rate of smoking cessation [82], are very cost-effective [83] and do not have any negative effect on cardiovascular risk [84, 85]. Swiss data [86] demonstrate the effectiveness of a counselling intervention in the setting of hospitalisation for an acute coronary syndrome hospitalisation in inducing patients to take up further counselling. Public policy interventions are beyond the scope of this review, but multinational evidence seems clearly in favour of public smoking bans as a means to reduce cardiovascular and respiratory disease burden [60, 87, 88].

However, smoking cessation receives generally less attention than counselling and pharmaceutical therapy for other classic cardiovascular risk factors such as hypertension, possibly because of physicians’ concerns that the intervention may take an excessive amount of time with limited reimbursement. It has been shown [89] that approximately 3 minutes of a general practitioner’s consultation time is enough to effectively initiate and even maintain cessation effects by following the 5A mnemonic: “(1) ask the patient if he or she uses tobacco, (2) advise him or her to quit, (3) assess willingness to make a quit attempt, (4) assist those who are willing to make a quit attempt, and (5) arrange for follow-up contact to prevent relapse” [89].

Vaporisers and heat-not-burn devices either heat a liquid with or without nicotine or heat an amalgam of tobacco to a lower temperature than a burning cigarette does. In 2016, an updated Cochrane review on whether these “e-cigarettes” have a place as aides in smoking cessation was published [90]; it summarised 24 studies of which only 2 were eligible randomised controlled trials, including 662 patients. The sparse data from randomised controlled trials is the most pressing problem as it has been and persists to be in other areas of research on harm by tobacco. Aside from the question of the safety of such devices in comparison with tobacco or in their own right, we fully endorse the conclusion 17–10 from the 2018 National Academies of Sciences consensus report: “Overall, there is limited evidence that e-cigarettes may be effective aids to promote smoking cessation” [91].

Conclusion

Smoking cessation is a cheap way to prevent cardiovascular disease and reduces the associated morbidity and mortality. Informing people who use tobacco regularly that quiting smoking may rapidly reduce the risk of future cardiovascular events may be highly motivating. Despite unequivocal evidence, tobacco is often a forgotten cardiac risk factor, receiving less attention than treating hypertension, hyperlipidaemia or diabetes.

Routine identification of smoking status, advising cessation and referring to counselling resources should be standard practice. Moreover, it is important that communication to people using tobacco and to the general population should include information about second-hand smoke as a risk factor for cardiovascular disease.

Disclosure statement

No financial support and no other potential conflict of interest ­relevant to this article was reported.

Credits

Header image: ID 7253322 © Suljo | Dreamstime.com

Correspondence

Correspondence:
Isabella Sudano, MD
University Heart Center, Cardiology
University Hospital Zurich
Rämistrasse 100
CH-8091 Zurich
isabella.sudano[at]usz.ch

References

 1 The Health Consequences of Smoking-50 Years of Progress: A Report of the Surgeon General. Reports of the Surgeon General. Atlanta (GA) 2014.

 2 Reitsma MB, Fullman N, Ng M, Salama JS, Abajobir A, Abate KH, et al.; GBD 2015 Tobacco Collaborators. Smoking prevalence and attributable disease burden in 195 countries and territories, 1990-2015: a systematic analysis from the Global Burden of Disease Study 2015. Lancet. 2017;389(10082):1885–906. doi:https://doi.org/10.1016/S0140-6736(17)30819-X.

 3 Health UDoHaHSSa. Report of the Advisory Committee to the Surgeon General of the Public Health Service. Washington, DC; 1964.

 4 Doll R, Peto R, Boreham J, Sutherland I. Mortality in relation to smoking: 50 years’ observations on male British doctors. BMJ. 2004;328(7455):1519. doi:https://doi.org/10.1136/bmj.38142.554479.AE.

 5 Peto R, Darby S, Deo H, Silcocks P, Whitley E, Doll R. Smoking, smoking cessation, and lung cancer in the UK since 1950: combination of national statistics with two case-control studies. BMJ. 2000;321(7257):323–9. doi:https://doi.org/10.1136/bmj.321.7257.323.

 6 Teo KK, Ounpuu S, Hawken S, Pandey MR, Valentin V, Hunt D, et al.; INTERHEART Study Investigators. Tobacco use and risk of myocardial infarction in 52 countries in the INTERHEART study: a case-control study. Lancet. 2006;368(9536):647–58. doi:https://doi.org/10.1016/S0140-6736(06)69249-0.

 7 Jiang F, Wang J, Zhang R, Chen M, Peng D, Sun X, et al. Effects of active and passive smoking on the development of cardiovascular disease as assessed by a carotid intima-media thickness examination in patients with type 2 diabetes mellitus. Clin Exp Pharmacol Physiol. 2015;42(5):444–50. doi:https://doi.org/10.1111/1440-1681.12379.

 8 Lee W, Hwang SH, Choi H, Kim H. The association between smoking or passive smoking and cardiovascular diseases using a Bayesian hierarchical model: based on the 2008-2013 Korea Community Health Survey. Epidemiol Health. 2017;39:e2017026. doi:https://doi.org/10.4178/epih.e2017026.

 9 Eddy DM, Peskin B, Shcheprov A, Pawlson G, Shih S, Schaaf D. Effect of smoking cessation advice on cardiovascular disease. Am J Med Qual. 2009;24(3):241–9. doi:https://doi.org/10.1177/1062860609332509.

10 Mallaina P, Lionis C, Rol H, Imperiali R, Burgess A, Nixon M, et al. Smoking cessation and the risk of cardiovascular disease outcomes predicted from established risk scores: results of the Cardiovascular Risk Assessment among Smokers in Primary Care in Europe (CV-ASPIRE) study. BMC Public Health. 2013;13(1):362. doi:https://doi.org/10.1186/1471-2458-13-362.

11 Mohiuddin SM, Mooss AN, Hunter CB, Grollmes TL, Cloutier DA, Hilleman DE. Intensive smoking cessation intervention reduces mortality in high-risk smokers with cardiovascular disease. Chest. 2007;131(2):446–52. doi:https://doi.org/10.1378/chest.06-1587.

12 Mons U, Müezzinler A, Gellert C, Schöttker B, Abnet CC, Bobak M, et al.; CHANCES Consortium. Impact of smoking and smoking cessation on cardiovascular events and mortality among older adults: meta-analysis of individual participant data from prospective cohort studies of the CHANCES consortium. BMJ. 2015;350(apr20 2):h1551. doi:https://doi.org/10.1136/bmj.h1551.

13 Pipe AL. Network meta-analysis demonstrates the safety of pharmacotherapy for smoking cessation in cardiovascular patients. Evid Based Med. 2014;19(5):193. doi:https://doi.org/10.1136/eb-2014-110030.

14 Prochaska JJ, Benowitz NL. Smoking cessation and the cardiovascular patient. Curr Opin Cardiol. 2015;30(5):506–11. doi:https://doi.org/10.1097/HCO.0000000000000204.

15 Wilson PW. Smoking, smoking cessation, and risk of cardiovascular disease. Curr Treat Options Cardiovasc Med. 2006;8(4):276–81. doi:https://doi.org/10.1007/s11936-006-0048-0.

16 Doll R, Peto R. Mortality in relation to smoking: 20 years’ observations on male British doctors. BMJ. 1976;2(6051):1525–36. doi:https://doi.org/10.1136/bmj.2.6051.1525.

17 Cupples LA, D’Agostino RB. The Framingham Study. An Epidemiological Investigation of Cardiovascular Disease. Section 34: Some Risk Factors Related to the Annual Incidence of Cardiovascular Disease and Death Using Pooled Repeated Biennial Measurements: Framingham Heart Study, 30-year Follow-up. Springfield, VA; 1987.

18 Stallones RA. The association between tobacco smoking and coronary heart disease. Int J Epidemiol. 2015;44(3):735–43. doi:https://doi.org/10.1093/ije/dyv124.

19 Franck C, Filion KB, Eisenberg MJ. Smoking cessation in patients with acute coronary syndrome. Am J Cardiol. 2018;121(9):1105–11. doi:https://doi.org/10.1016/j.amjcard.2018.01.017.

20 Snaterse M, Deckers JW, Lenzen MJ, Jorstad HT, De Bacquer D, Peters RJG, et al.; EUROASPIRE Investigators. Smoking cessation in European patients with coronary heart disease. Results from the EUROASPIRE IV survey: A registry from the European Society of Cardiology. Int J Cardiol. 2018;258:1–6. doi:https://doi.org/10.1016/j.ijcard.2018.01.064.

21 Malhotra J, Borron C, Freedman ND, Abnet CC, van den Brandt PA, White E, et al. Association between Cigar or Pipe Smoking and Cancer Risk in Men: A Pooled Analysis of Five Cohort Studies. Cancer Prev Res (Phila). 2017;10(12):704–9. doi:https://doi.org/10.1158/1940-6207.CAPR-17-0084.

22 McCormack VA, Agudo A, Dahm CC, Overvad K, Olsen A, Tjonneland A, et al. Cigar and pipe smoking and cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC). Int J Cancer. 2010;127(10):2402–11. doi:https://doi.org/10.1002/ijc.25252.

23 Shaper AG, Wannamethee SG, Walker M. Pipe and cigar smoking and major cardiovascular events, cancer incidence and all-cause mortality in middle-aged British men. Int J Epidemiol. 2003;32(5):802–8. doi:https://doi.org/10.1093/ije/dyg206.

24 Wyss A, Hashibe M, Chuang SC, Lee YC, Zhang ZF, Yu GP, et al. Cigarette, cigar, and pipe smoking and the risk of head and neck cancers: pooled analysis in the International Head and Neck Cancer Epidemiology Consortium. Am J Epidemiol. 2013;178(5):679–90. doi:https://doi.org/10.1093/aje/kwt029.

25 Sun YQ, Chen Y, Langhammer A, Skorpen F, Wu C, Mai XM. Passive smoking in relation to lung cancer incidence and histologic types in Norwegian adults: the HUNT study. Eur Respir J. 2017;50(4):1700824. doi:https://doi.org/10.1183/13993003.00824-2017.

26 Metsios GS, Flouris AD, Angioi M, Koutedakis Y. Passive smoking and the development of cardiovascular disease in children: a systematic review. Cardiol Res Pract. 2010;2011:587650. doi:http://dx.doi.org/10.4061/2011/587650.

27 Taylor BV, Oudit GY, Kalman PG, Liu P. Clinical and pathophysiological effects of active and passive smoking on the cardiovascular system. Can J Cardiol. 1998;14(9):1129–39.

28 Humble C, Croft J, Gerber A, Casper M, Hames CG, Tyroler HA. Passive smoking and 20-year cardiovascular disease mortality among nonsmoking wives, Evans County, Georgia. Am J Public Health. 1990;80(5):599–601. doi:https://doi.org/10.2105/AJPH.80.5.599.

29 Pilz H, Oguogho A, Chehne F, Lupattelli G, Palumbo B, Sinzinger H. Quitting cigarette smoking results in a fast improvement of in vivo oxidation injury (determined via plasma, serum and urinary isoprostane). Thromb Res. 2000;99(3):209–21. doi:https://doi.org/10.1016/S0049-3848(00)00249-8.

30 Mol MJ, de Rijke YB, Demacker PN, Stalenhoef AF. Plasma levels of lipid and cholesterol oxidation products and cytokines in diabetes mellitus and cigarette smoking: effects of vitamin E treatment. Atherosclerosis. 1997;129(2):169–76. doi:https://doi.org/10.1016/S0021-9150(96)06022-4.

31 Noh JM, Lee SH, Kim HW, Yang HS. Changes in the Serum Level of High Density Lipoprotein-cholesterol after Smoking Cessation among Adult Men. Korean J Fam Med. 2012;33(5):305–10. doi:https://doi.org/10.4082/kjfm.2012.33.5.305.

32 Lawlor DA, Song YM, Sung J, Ebrahim S, Smith GD. The association of smoking and cardiovascular disease in a population with low cholesterol levels: a study of 648,346 men from the Korean national health system prospective cohort study. Stroke. 2008;39(3):760–7. doi:https://doi.org/10.1161/STROKEAHA.107.494823.

33 Vazquez-Benitez G, Desai JR, Xu S, Goodrich GK, Schroeder EB, Nichols GA, et al. Preventable major cardiovascular events associated with uncontrolled glucose, blood pressure, and lipids and active smoking in adults with diabetes with and without cardiovascular disease: a contemporary analysis. Diabetes Care. 2015;38(5):905–12. doi:https://doi.org/10.2337/dc14-1877.

34 Odeberg J, Freitag M, Forssell H, Vaara I, Persson ML, Odeberg H, et al. The influence of smoking and impaired glucose homoeostasis on the outcome in patients presenting with an acute coronary ­syndrome: a cross-sectional study. BMJ Open. 2014;4(7):e005077. doi:https://doi.org/10.1136/bmjopen-2014-005077.

35 Gerber PA, Locher R, Schmid B, Spinas GA, Lehmann R. Smoking is associated with impaired long-term glucose metabolism in patients with type 1 diabetes mellitus. Nutr Metab Cardiovasc Dis. 2013;23(2):102–8. doi:https://doi.org/10.1016/j.numecd.2011.08.007.

36 Rafalson L, Donahue RP, Dmochowski J, Rejman K, Dorn J, Trevisan M. Cigarette smoking is associated with conversion from normoglycemia to impaired fasting glucose: the Western New York Health Study. Ann Epidemiol. 2009;19(6):365–71. doi:https://doi.org/10.1016/j.annepidem.2009.01.013.

37 Li G, Wang H, Wang K, Wang W, Dong F, Qian Y, et al. The association between smoking and blood pressure in men: a cross-sectional study. BMC Public Health. 2017;17(1):797. doi:https://doi.org/10.1186/s12889-017-4802-x.

38 Jamalizadeh A, Kamiab Z, Esmaeili Nadimi A, Nejadghaderi M, ­Saeidi A, Porkarami A. Prevalence of smoking and high blood ­pressure, two major risk factors for non-communicable diseases: the SuRF NCD (surveillance of risk factors of non-communicable disease) report 2012. J Cardiovasc Thorac Res. 2016;8(4):183–7. doi:https://doi.org/10.15171/jcvtr.2016.36.

39 Ohta Y, Kawano Y, Hayashi S, Iwashima Y, Yoshihara F, Nakamura S. Effects of cigarette smoking on ambulatory blood pressure, heart rate, and heart rate variability in treated hypertensive patients. Clin Exp Hypertens. 2016;38(6):510–3. doi:https://doi.org/10.3109/10641963.2016.1148161.

40 Pretorius E, Oberholzer HM, van der Spuy WJ, Meiring JH. Smoking and coagulation: the sticky fibrin phenomenon. Ultrastruct Pathol. 2010;34(4):236–9. doi:https://doi.org/10.3109/01913121003743716.

41 Billimoria JD, Pozner H, Metselaar B, Best FW, James DC. Effect of cigarette smoking on lipids, lipoproteins, blood coagulation, fibrinolysis and cellular components of human blood. Atherosclerosis. 1975;21(1):61–76. doi:https://doi.org/10.1016/0021-9150(75)90094-5.

42 Tibuakuu M, Kamimura D, Kianoush S, DeFilippis AP, Al Rifai M, Reynolds LM, et al. The association between cigarette smoking and inflammation: The Genetic Epidemiology Network of Arteriopathy (GENOA) study. PLoS One. 2017;12(9):e0184914. doi:https://doi.org/10.1371/journal.pone.0184914.

43 Kianoush S, Yakoob MY, Al-Rifai M, DeFilippis AP, Bittencourt MS, Duncan BB, et al. Associations of Cigarette Smoking With Subclinical Inflammation and Atherosclerosis: ELSA-Brasil (The Brazilian Longitudinal Study of Adult Health). J Am Heart Assoc. 2017;6(6):e005088. doi:https://doi.org/10.1161/JAHA.116.005088.

44 Attard R, Dingli P, Doggen CJM, Cassar K, Farrugia R, Wettinger SB. The impact of passive and active smoking on inflammation, lipid profile and the risk of myocardial infarction. Open Heart. 2017;4(2):e000620. doi:https://doi.org/10.1136/openhrt-2017-000620.

45 Sørhaug S, Steinshamn S, Nilsen OG, Waldum HL. Chronic inhalation of carbon monoxide: effects on the respiratory and cardiovascular system at doses corresponding to tobacco smoking. Toxicology. 2006;228(2-3):280–90. doi:https://doi.org/10.1016/j.tox.2006.09.008.

46 Zevin S, Saunders S, Gourlay SG, Jacob P, III, Benowitz NL. Cardiovascular effects of carbon monoxide and cigarette smoking. J Am Coll Cardiol. 2001;38(6):1633–8. doi:https://doi.org/10.1016/S0735-1097(01)01616-3.

47 Kjeldsen K. Smoking and carbon monoxide uptake as a risk factor in atherosclerotic cardiovascular disease. Adv Exp Med Biol. 1975;63:317–21. doi:https://doi.org/10.1007/978-1-4684-3258-9_22.

48 Speeckaert MM, Delanghe JR, Vanholder RC. Chronic nicotine exposure and acute kidney injury: new concepts and experimental evidence. Nephrol Dial Transplant. 2013;28(6):1329–31. doi:https://doi.org/10.1093/ndt/gft019.

49 Kurahashi K, Shirahase H, Nakamura S, Tarumi T, Koshino Y, Wang AM, et al. Nicotine-induced contraction in the rat coronary artery: possible involvement of the endothelium, reactive oxygen species and COX-1 metabolites. J Cardiovasc Pharmacol. 2001;38(Suppl 1):S21–5. doi:https://doi.org/10.1097/00005344-200110001-00006.

50 Chalon S, Moreno H, Jr, Benowitz NL, Hoffman BB, Blaschke TF. Nicotine impairs endothelium-dependent dilatation in human veins in vivo. Clin Pharmacol Ther. 2000;67(4):391–7. doi:https://doi.org/10.1067/mcp.2000.105153.

51 Mayhan WG, Sharpe GM. Superoxide dismutase restores endothelium-dependent arteriolar dilatation during acute infusion of ­nicotine. J Appl Physiol (1985). 1998;85(4):1292–8. doi:https://doi.org/10.1152/jappl.1998.85.4.1292.

52 Mayhan WG, Patel KP. Effect of nicotine on endothelium-dependent arteriolar dilatation in vivo. Am J Physiol. 1997;272(5 Pt 2):H2337–42.

53 JH O. Focus on Smoking and Health Research. Hauppauge, NY; 2005.

54 He J, Vupputuri S, Allen K, Prerost MR, Hughes J, Whelton PK. Passive smoking and the risk of coronary heart disease – a meta-analysis of epidemiologic studies. N Engl J Med. 1999;340(12):920–6. doi:https://doi.org/10.1056/NEJM199903253401204.

55 Bonita R, Duncan J, Truelsen T, Jackson RT, Beaglehole R. Passive smoking as well as active smoking increases the risk of acute stroke. Tob Control. 1999;8(2):156–60. doi:https://doi.org/10.1136/tc.8.2.156.

56 Pitsavos C, Panagiotakos DB, Chrysohoou C, Skoumas J, Tzioumis K, Stefanadis C, et al. Association between exposure to environmental tobacco smoke and the development of acute coronary syndromes: the CARDIO2000 case-control study. Tob Control. 2002;11(3):220–5. doi:https://doi.org/10.1136/tc.11.3.220.

57 Iversen B, Jacobsen BK, Løchen ML. Active and passive smoking and the risk of myocardial infarction in 24,968 men and women during 11 year of follow-up: the Tromsø Study. Eur J Epidemiol. 2013;28(8):659–67. doi:https://doi.org/10.1007/s10654-013-9785-z.

58 Shiue I. Effect of smoking ban at home on adult cardiovascular health: Scottish Health Survey, 2012. Int J Cardiol. 2014;176(1):268–9. doi:https://doi.org/10.1016/j.ijcard.2014.06.097.

59 Sipilä JO, Gunn JM, Kauko T, Rautava P, Kytö V. Association of restaurant smoking ban and the incidence of acute myocardial infarction in Finland. BMJ Open. 2016;6(1):e009320. doi:https://doi.org/10.1136/bmjopen-2015-009320.

60 Di Valentino M, Muzzarelli S, Limoni C, Porretta AP, Rigoli A, Barazzoni F, et al. Reduction of ST-elevation myocardial infarction in Canton Ticino (Switzerland) after smoking bans in enclosed public places--No Smoke Pub Study. Eur J Public Health. 2015;25(2):195–9. doi:https://doi.org/10.1093/eurpub/cku067.

61 Hurt RD, Weston SA, Ebbert JO, McNallan SM, Croghan IT, Schroeder DR, et al. Myocardial infarction and sudden cardiac death in Olmsted County, Minnesota, before and after smoke-free workplace laws. Arch Intern Med. 2012;172(21):1635–41. doi:https://doi.org/10.1001/2013.jamainternmed.46.

62 Morito N, Miura SI, Yano M, Hitaka Y, Nishikawa H, Saku K. Association Between a Ban on Smoking in a Hospital and the In-Hospital Onset of Acute Myocardial Infarction. Cardiol Res. 2015;6(3):278–82. doi:https://doi.org/10.14740/cr404e.

63 Sebrié EM, Sandoya E, Bianco E, Hyland A, Cummings KM, Glantz SA. Hospital admissions for acute myocardial infarction before and after implementation of a comprehensive smoke-free policy in Uruguay: experience through 2010. Tob Control. 2014;23(6):471–2. doi:https://doi.org/10.1136/tobaccocontrol-2012-050954.

64 Clinical Practice Guideline Treating Tobacco Use and Dependence 2008 Update Panel, Liaisons, and Staff. A clinical practice guideline for treating tobacco use and dependence: 2008 update. A U.S. Public Health Service report. Am J Prev Med. 2008;35(2):158–76. doi:https://doi.org/10.1016/j.amepre.2008.04.009.

65 Janson C, Künzli N, de Marco R, Chinn S, Jarvis D, Svanes C, et al. Changes in active and passive smoking in the European Community Respiratory Health Survey. Eur Respir J. 2006;27(3):517–24. doi:https://doi.org/10.1183/09031936.06.00106605.

66 Holm M, Schiöler L, Andersson E, Forsberg B, Gislason T, Janson C, et al. Predictors of smoking cessation: A longitudinal study in a large cohort of smokers. Respir Med. 2017;132:164–9. doi:https://doi.org/10.1016/j.rmed.2017.10.013.

67 Kale D, Gilbert HM, Sutton S. Are predictors of making a quit attempt the same as predictors of 3-month abstinence from smoking? Findings from a sample of smokers recruited for a study of computer-tailored smoking cessation advice in primary care. Addiction. 2015;110(10):1653–64. doi:https://doi.org/10.1111/add.12972.

68 Ockene JK, Kuller LH, Svendsen KH, Meilahn E. The relationship of smoking cessation to coronary heart disease and lung cancer in the Multiple Risk Factor Intervention Trial (MRFIT). Am J Public Health. 1990;80(8):954–8. doi:https://doi.org/10.2105/AJPH.80.8.954.

69 Critchley JA, Capewell S. Mortality risk reduction associated with smoking cessation in patients with coronary heart disease: a systematic review. JAMA. 2003;290(1):86–97. doi:https://doi.org/10.1001/jama.290.1.86.

70 Aubin HJ, Farley A, Lycett D, Lahmek P, Aveyard P. Weight gain in smokers after quitting cigarettes: meta-analysis. BMJ. 2012;345(jul10 2):e4439. doi:https://doi.org/10.1136/bmj.e4439.

71 Perkins KA. Smoking cessation in women. Special considerations. CNS Drugs. 2001;15(5):391–411. doi:https://doi.org/10.2165/00023210-200115050-00005.

72 Luo J, Rossouw J, Margolis KL. Smoking cessation, weight change, and coronary heart disease among postmenopausal women with and without diabetes. JAMA. 2013;310(1):94–6. doi:https://doi.org/10.1001/jama.2013.6871.

73 Rice VH, Heath L, Livingstone-Banks J, Hartmann-Boyce J. Nursing interventions for smoking cessation. Cochrane Database Syst Rev. 2017;12:CD001188.

74 Lindson-Hawley N, Thompson TP, Begh R. Motivational interviewing for smoking cessation. Cochrane Database Syst Rev. 2015;(3):CD006936.

75 Stead LF, Buitrago D, Preciado N, Sanchez G, Hartmann-Boyce J, Lancaster T. Physician advice for smoking cessation. Cochrane ­Database Syst Rev. 2013;(5):CD000165.

76 Bala MM, Strzeszynski L, Topor-Madry R. Mass media interventions for smoking cessation in adults. Cochrane Database Syst Rev. 2017;11:CD004704.

77 Taylor GMJ, Dalili MN, Semwal M, Civljak M, Sheikh A, Car J. Internet-based interventions for smoking cessation. Cochrane Database Syst Rev. 2017;9:CD007078.

78 Stead LF, Perera R, Bullen C, Mant D, Hartmann-Boyce J, Cahill K, et al. Nicotine replacement therapy for smoking cessation. Cochrane Database Syst Rev. 2012;11:CD000146.

79 Anthenelli RM, Benowitz NL, West R, St Aubin L, McRae T, Lawrence D, et al. Neuropsychiatric safety and efficacy of varenicline, bupropion, and nicotine patch in smokers with and without psychiatric disorders (EAGLES): a double-blind, randomised, placebo-controlled clinical trial. Lancet. 2016;387(10037):2507–20. doi:https://doi.org/10.1016/S0140-6736(16)30272-0.

80 Grandi SM, Shimony A, Eisenberg MJ. Bupropion for smoking cessation in patients hospitalized with cardiovascular disease: a systematic review and meta-analysis of randomized controlled trials. Can J Cardiol. 2013;29(12):1704–11. doi:https://doi.org/10.1016/j.cjca.2013.09.014.

81 Cahill K, Lindson-Hawley N, Thomas KH, Fanshawe TR, Lancaster T. Nicotine receptor partial agonists for smoking cessation. Cochrane Database Syst Rev. 2016;(5):CD006103.

82 Hartmann-Boyce J, Stead LF, Cahill K, Lancaster T. Efficacy of interventions to combat tobacco addiction: Cochrane update of 2013 reviews. Addiction. 2014;109(9):1414–25. doi:https://doi.org/10.1111/add.12633.

83 Hagen G, Wisloff T, Klemp M. Cost-Effectiveness of Varenicline, Bupropion and Nicotine Replacement Therapy for Smoking Cessation. NIPH Systematic Reviews. Oslo, Norway2010.

84 Suissa K, Larivière J, Eisenberg MJ, Eberg M, Gore GC, Grad R, et al. Efficacy and Safety of Smoking Cessation Interventions in Patients With Cardiovascular Disease: A Network Meta-Analysis of Randomized Controlled Trials. Circ Cardiovasc Qual Outcomes. 2017;10(1):e002458. doi:https://doi.org/10.1161/CIRCOUTCOMES.115.002458.

85 Kittle J, Lopes RD, Huang M, Marquess ML, Wilson MD, Ascher J, et al. Cardiovascular adverse events in the drug-development program of bupropion for smoking cessation: A systematic retrospective adjudication effort. Clin Cardiol. 2017;40(10):899–906. doi:https://doi.org/10.1002/clc.22744.

86 Auer R, Gencer B, Tango R, Nanchen D, Matter CM, Lüscher TF, et al. Uptake and efficacy of a systematic intensive smoking cessation intervention using motivational interviewing for smokers hospitalised for an acute coronary syndrome: a multicentre before-after study with parallel group comparisons. BMJ Open. 2016;6(9):e011520. doi:https://doi.org/10.1136/bmjopen-2016-011520.

87 Bonetti PO, Trachsel LD, Kuhn MU, Schulzki T, Erne P, Radovanovic D, et al. Incidence of acute myocardial infarction after implementation of a public smoking ban in Graubünden, Switzerland: two year follow-up. Swiss Med Wkly. 2011;141:w13206.

88 Mackay D, Haw S, Ayres JG, Fischbacher C, Pell JP. Smoke-free legislation and hospitalizations for childhood asthma. N Engl J Med. 2010;363(12):1139–45. doi:https://doi.org/10.1056/NEJMoa1002861.

89 Stead LF, Bergson G, Lancaster T. Physician advice for smoking cessation. Cochrane Database Syst Rev. 2008;(2):CD000165.

90 Hartmann-Boyce J, McRobbie H, Bullen C, Begh R, Stead LF, Hajek P. Electronic cigarettes for smoking cessation. Cochrane Database Syst Rev. 2016;9:CD010216.

91 National Academies of Sciences E. Medicine. Public Health Consequences of E-Cigarettes. Stratton K, Kwan LY, Eaton DL, editors. Washington, DC: The National Academies Press; 2018. 774 p.

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