Version August 2025
INTRODUCTION —
The facts regarding the impact of cigarette smoking on the development of cardiovascular disease (CVD) are well known to both the medical profession and the public [1-5]. In spite of the extensive data and efforts to educate the public, many smokers do not believe that smoking is harmful for them (or for those around them via secondhand smoke exposure). As an example, in one study of 737 active smokers, over 60 percent of did not believe that they were at an increased risk for a myocardial infarction (MI) [6]. (See "Overview of established risk factors for cardiovascular disease".)
The relationship between smoking and CVD, the effects of smoking on the atherosclerotic process, and the beneficial effects of smoking cessation will be reviewed here [1,7]. The therapeutic approach to smoking cessation is presented separately. (See "Overview of smoking cessation management in adults" and "Pharmacotherapy for smoking cessation in adults" and "Behavioral approaches to smoking cessation".)
EPIDEMIOLOGY
Prevalence of smoking — Globally, an estimated 933.1 million people smoke, the majority of whom are male. The majority of smokers reside in low- to middle-income countries. As of 2022, an estimated 11.5 percent of adults ≥18 years of age (13.1 percent of male and 10.1 percent of female adults) in the United States report smoking cigarettes on a regular basis [8,9]. In the United States, the majority of smokers start smoking before the age of 25 years. An estimated 33.9 percent of high school students report consuming tobacco products, of which 1.6 percent report using smokeless tobacco products [8-10]. An estimated 28.9 percent of high school students report the use of e-cigarettes in the past 30 days [9].
The prevalence of cigarette smoking has decreased among American adults over the past several decades. However, the number of Americans who reported electronic cigarette (e-cigarette) use has increased, with the greatest increases among middle-aged adults, female adults, and former smokers [9].
●United States regional differences – Rates of smoking vary by region in the United States, with the highest number of current smokers residing in the Midwest (14.0 percent) and South (12.4 percent) [11]. West Virginia has the highest prevalence of current smokers at 23.6 percent, while Utah has the lowest (7.2 percent) [9,12].
●Sex and race/ethnic differences – Smoking rates are higher among male individuals and some Native American groups [13] compared with other racial/ethnic groups. An estimated 11.7 percent of non-Hispanic White Americans report current smoking, while 11.7 percent of non-Hispanic Black Americans, 5.4 percent of non-Hispanic Asian Americans, and 7.7 percent of Hispanic Americans report smoking [9,11].
●Sexual orientation – Rates of smoking are higher among lesbian/gay/bisexual adults than in heterosexual or straight adults (15.3 versus 11.4 percent).
●Socioeconomic status differences – Smoking rates are higher among those with lower education and income levels [8].
●Psychiatric comorbidities – Among smokers, rates of psychiatric disorders, including depression, are common [14].
Cigarette smoking and CVD — With respect to CVD, the following observations have been made regarding a major role for cigarette smoking:
●In a cohort of over 550,000 adults, all-cause mortality was significantly associated with current smoking (hazard ratio [HR] 2.8, 95% CI 2.73-2.88), with similar risk observed for males and females. Higher mortality risk was observed for non-Hispanic Black adults, non-Hispanic White adults, and Hispanic adults compared with other race/ethnic groups [15].
●The incidence of MI is increased sixfold in female adults and threefold in male adults who smoke at least 20 cigarettes per day compared with subjects who never smoked [16,17]. In the worldwide INTERHEART study of patients from 52 countries, smoking accounted for 36 percent of the population-attributable risk of a first MI [18]. (See "Overview of established risk factors for cardiovascular disease", section on 'Cigarette smoking'.)
●In a systematic review and meta-analysis of 75 cohorts that evaluated the risks of smoking on coronary artery disease (CAD) and adjusted for the effects of other known CAD risk factors (over 2.4 million persons with over 44,000 CAD events), female smokers were 25 percent more likely than male smokers to develop CAD (relative risk ratio 1.25, 95% CI 1.12-1.39) [19]. In a study of over 3000 patients recently hospitalized with an acute coronary event, female sex was associated with a higher risk for recurrent cardiac events in the six months after discharge [20].
●Among a cohort of 4129 Black participants in the Jackson Heart Study without a history of heart failure who were followed for a median of eight years, there was a significantly higher risk of developing heart failure among current cigarette smokers (hazard ratio [HR] 2.8, 95% CI 1.7-4.6) and former smokers with greater than 15 pack-year history (HR 2.1, 95% CI 1.3-3.3) compared with those who never smoked [21].
●Patients who continue to smoke in the presence of established CAD have an increased risk of repeat MI and an increased risk of death, including sudden cardiac death [22-25]. Furthermore, smoking multiplies the risk of CVD when other risk factors such as diabetes mellitus are present [26,27]. Among smokers who quit after MI, risk for recurrent events declines over time [28].
●Patients who continue to smoke following revascularization (either percutaneous coronary intervention or coronary artery bypass grafting) have significantly higher mortality compared with those who quit smoking. (See 'Surgical revascularization' below.)
●Smokers are at high risk for peripheral arterial disease (PAD). Among a cohort of 22,203 patients with PAD, including 1995 patients who smoke, almost 50 percent of smokers were hospitalized over a one-year follow-up period, significantly higher than PAD patients who do not smoke [29].
Dose and duration of smoking exposure — The risk of CVD related to cigarette smoking is present for even very low doses (ie, number of cigarettes), with smokers who consume less than five cigarettes per day having an increased risk for CVD events such as acute MI. Smoking even one cigarette per day is associated with approximately 50 percent increased risk for CAD and approximately 25 percent increased risk for stroke [30]. With increases in the number of cigarettes smoked per day, increased risk for CVD has been observed in several studies [21,30-35]. As examples:
●Data from the National Health Interview Survey from 329,035 United States adults observed a significant increase in all-cause mortality among those who smoked one to two cigarettes per day (HR 1.93, 95% CI 1.73-2.16) and three to five cigarettes per day (HR 1.99, 95% CI 1.83-2.17) compared with never smokers and after adjustment for demographic, clinical, and lifestyle factors [36]. Death due to CVD was also increased for those smoking one to two cigarettes per day (HR 1.92, 95% CI 1.58-2.36) and three to five cigarettes per day (HR 1.96, 95% CI 1.63-2.35).
●In the Pooling Project on Diet and Coronary Heart Disease study, which pooled data from eight prospective studies including 266,787 adults ages 40 to 89 years who were enrolled between 1974 and 1996 and followed for an average of up to eight years, current smokers who smoked 15 or more cigarettes per day had almost 2.5 times the risk of CAD compared with a nonsmoker [31]. For those who smoked less than 15 cigarettes per day, the risk of CAD was near double that of a nonsmoker.
●In a case-control study using 27,089 participants from the INTERHEART study (12,461 cases with acute MI, 14,637 controls), there was a clear dose-response between the number of cigarettes smoked per day and risk for acute MI [34]. The odds of having an MI was 1.056 for each additional cigarette smoked. The odds of an MI were ninefold higher among those who smoked 40 or more cigarettes per day compared with never-smokers.
●In the US Veterans study, the risk for CAD among current smokers ranged from 1.24 for those who smoked <10 cigarettes per day to 1.56 for those who smoked 10 to 20 cigarettes per day, and 1.76 for those who smoked between 20 and 40 cigarettes per day [32]. The highest CAD risk of 1.94 was observed for those who smoked 40 or more cigarettes per day.
The cumulative duration of smoking is also associated with risk for CAD events, with a longer duration and higher number of cigarettes yielding a greater risk. Increasing risk for CAD death was observed with increasing duration of smoking at every level of daily smoking (from 1 to 19 cigarettes per day to 40 or more cigarettes per day) [37].
Cigarette smoking and atherosclerosis — The direct effect of smoking on the development of atherosclerosis has been documented in numerous studies, including studies of living patients using surrogate markers (ie, intima-medial thickness) and autopsy studies with direct pathologic demonstration of atherosclerotic plaques.
●In the ARIC (Atherosclerosis Risk in Communities) study, which enrolled 10,914 patients and measured intima-medial thickness of the carotid artery by ultrasound over a three-year period, current smoking was associated with a 50 percent increase in the progression of atherosclerosis versus nonsmokers [38]. Additionally, patients with environmental tobacco smoke exposure (ie, secondhand smoke) had a 20 percent greater rate of atherosclerosis progression compared with patients without secondhand smoke exposure.
●Several large autopsy studies have noted an association between cigarette smoking and atherosclerosis in the major coronary arteries [39-43].
•Using autopsy data from 93 children and young adults (age range from 2 to 39 years) enrolled in the Bogalusa Heart Study who had died principally from trauma and for whom data on risk factors were available, cigarette smoking increased the number of fatty streaks and fibrous plaques (the beginnings of atherosclerotic plaques) compared with nonsmokers [40].
•In the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study, a multicenter study that included trauma victims between the ages of 15 and 34 years and compared findings from coronary arteries in 50 smokers and 50 nonsmokers, advanced atherosclerotic lesions were significantly more common among smokers compared with nonsmokers (31 versus 14 percent), and the number of advanced atherosclerotic lesions was also greater in smokers [41].
Noncigarette smoking and CVD — With respect to the risk of CVD associated with noncigarette smoking (eg, pipe or cigar smoking, smokeless tobacco, etc), the data are somewhat less clear regarding the risks. Many studies have shown an increased CVD risk associated with pipe or cigar smoking, but others have not shown this increased CVD risk.
Cigar smoking — Although there is an established association between cigar smoking and cancer of the upper respiratory, lungs, and gastrointestinal tract and the risk of chronic obstructive lung disease, data on the risk of CVD for cigars are less robust than for cigarettes. Moreover, data about the role of cigar smoking and the risk of CVD remain limited. Cigar smoke contains many of the same toxic and carcinogenic compounds that are found in cigarette smoke, and subjects who smoke four or more cigars per day are exposed to an amount of smoke equivalent to 10 cigarettes; even those who do not inhale are exposed to their own environmental smoke.
●In a cohort study of 17,774 male adults who were followed for 14 years, those who smoked cigars were at a greater risk for developing CAD (relative risk 1.3 compared with nonsmokers); there was a dose-response relationship for those who smoked less than or greater than five cigars per day (relative risk 1.2 and 1.6, respectively) [44].
●In a cohort study of 121,278 male adults ≥30 years of age, current cigar smokers ≤75 years of age had an increased risk of death from CAD (adjusted risk ratio 1.3), while there was no increased risk in those >75 years of age or former cigar smokers of any age [45].
●In a pooled cohort study of 103,642 participants, cigar smoking was associated with an increased risk of stroke (hazard ratio [HR] 1.25; 95% CI 1.01-1.55), atrial fibrillation (HR 1.32; 95% CI 1.13-1.53), and heart failure (HR 1.29; 95% CI 1.10-1.41) compared with never using cigars [46].
Pipe smoking — Data specifically related to the risk of CV events from pipe smoking are limited compared with the wealth of data available regarding cigarette smoking. Some studies suggest increased CVD risk compared with nonsmokers, which is still lower than that of cigarette smokers, while others observed no increase in CVD risk [32,47-49]. In total, however, the evidence seems to suggest pipe smoking increases the risk for CVD events [37,48].
●In early data derived from over 5000 participants in the Framingham Heart Study, the risks of MI and death due to heart disease were not significantly different between pipe and cigar smokers and nonsmokers [48].
●Among a longitudinal cohort of 293,000 US veterans followed for 16 years, all-cause mortality for pure pipe smokers was increased compared with nonsmokers [32].
●Among 16,932 Norwegian male adults ages 20 to 49 years who were screened in the mid-1970s and again between 3 to 13 years later, then followed through 2007, pipe smoking was associated with increased total mortality (adjusted RR 2.0, 95% CI 1.7-2.3) [47].
●In a pooled cohort study of 103,642 participants, pipe smoking was associated with an increased risk of heart failure (HR 1.23; 95% CI 1.01-1.49) compared with never using a pipe [46]. For pipe-smoking patients who did not also use cigarettes, pipe smoking was associated with an increased risk of myocardial infarction (HR 1.43; 95% CI 1.17-1.74).
Although study results have varied, differences in data collection regarding pipe smoking and combinations of pipe, cigar, and cigarette smoking in addition to variation in duration of follow-up may at least partially explain the heterogeneity. For the studies that suggest a lower CV risk related to pipe smoking (relative to cigarette smoking), reduced inhalation of smoke has been thought to be a reason for the lower risk [37].
Secondhand smoke — Exposure to secondhand smoke increases nonsmokers' risk of CVD. While the risk estimates for secondhand smoke and CAD outcomes vary, most studies show modest increases in risk. The impact of secondhand smoke on the cardiovascular system is discussed separately. (See "Secondhand smoke exposure: Effects in adults", section on 'Cardiovascular disease and stroke'.)
Smokeless tobacco — The cardiovascular health hazards of smokeless tobacco are not well established, with mixed results in different studies [50-53]. However, the evidence seems to suggest that the risk for CVD events is lower than the risk in smokers but higher than the risk in nonsmokers.
●In one case-control study of 687 male adults (ages 24 to 64 years) with a first-time MI and 687 matched controls, there was no significant difference in the incidence of MI between nonsmoking regular snuff users and those who never used any tobacco products (adjusted odds ratio [OR] 0.96) [51].
●In contrast, in a much larger study of over 135,000 male construction industry employees from Sweden, including over 6000 smokeless tobacco users, the age-adjusted relative risk of cardiovascular mortality was 1.4 for smokeless tobacco users [53]. For male adults aged 35 through 54 at the start of follow-up, the relative risk was 2.1.
●Among a cohort of 2474 Swedish smokeless tobacco users treated for MI between 2005 and 2009 who were followed for an average of 2.1 years, patients who quit using snuff following their MI had a significant reduction in mortality compared with those who continued to use snuff (HR 0.55, 95% CI 0.21-0.99) [52].
●In a pooled cohort study of 103,642 participants, smokeless tobacco use was associated with an increased risk of coronary artery disease mortality (HR 1.31; 95% CI 1.08-1.59) and myocardial infarction (HR 1.20; 95% CI 1.03-1.39) compared with never using smokeless tobacco [46].
Electronic cigarettes — Data on the relationship between electronic cigarette (e-cigarette) use and its impact on CVD outcomes are limited. However, of concern are the rates of new smokers who report initially starting e-cigarette use before starting to smoke cigarettes [54]. Furthermore, in a study of 449,092 participants, those who reported the dual use of e-cigarettes and combustible traditional cigarettes had a higher odds for CVD (OR 1.36, 95% CI 1.18-1.56) compared with those who reported smoking combustible cigarettes alone [55]. E-cigarettes have been associated with higher levels of inflammatory biomarkers and vascular dysfunction, both associated with an increased risk for CVD [9,55,56].
E-cigarettes are discussed in detail separately. (See "Vaping and e-cigarettes".)
PATHOGENESIS —
Although the relationship between CAD and smoking, even when passive, appears clear, the mechanism by which it occurs is incompletely understood. Multiple factors are likely involved since smoking has a variety of effects that may contribute to atherogenesis [1,57].
●Smoking is associated with an adverse effect on serum lipids (elevated low-density lipoproteins and triglycerides and reduced high-density lipoproteins) and with insulin resistance [58-60]. In addition, free radicals in cigarette smoke damage lipids, resulting in the formation of proatherogenic oxidized particles, specifically oxidized low-density lipoprotein cholesterol [61-63]. A similar effect is seen with acute secondhand smoke exposure [64]. (See "Lipoprotein classification, metabolism, and role in atherosclerosis", section on 'Lipoproteins and atherosclerosis'.)
●Cigarette smoking activates the sympathetic nervous system, producing an increase in heart rate and blood pressure, and cutaneous and perhaps coronary vasoconstriction [5,65-67].
●Cigarette smoke contains carbon monoxide, which when inhaled results in higher levels of carboxyhemoglobin. This does not appear to directly cause atherosclerosis or CVD, but may have adverse effects for patients with established CVD. (See 'Role of carbon monoxide' below.)
●Smoking is associated with increased inflammation (as measured by C-reactive protein) and enhances the prothrombotic state via inhibition of tissue plasminogen activator release from the endothelium, elevation in the blood fibrinogen concentration, increased platelet activity (possibly due to enhanced sympathetic activity), increased expression of tissue factor, and, in patients with advanced lung disease, elevated whole blood viscosity due to secondary polycythemia [5,68-74]. (See "C-reactive protein in cardiovascular disease", section on 'Possible pathogenic role of CRP'.)
●Smoking can damage the vascular wall, possibly leading to impaired prostacyclin production and enhanced platelet-vessel wall interactions [75]. This can reduce the elastic properties of the aorta, resulting in stiffening of and trauma to the wall [76].
●Smoking, as well as passive exposure to smoke, impairs endothelium-dependent vasodilation of normal coronary arteries and reduces coronary flow reserve [77-82]. Smoking can also potentiate the endothelial dysfunction induced by hypercholesterolemia [62,79]. The effect on endothelial function results from oxidative stress with enhanced oxidation of LDL and from reduced generation of nitric oxide [72,78,81,83,84].
●Smoking, in addition to narrowing the lumen of epicardial coronary arteries and larger arterioles, causes microvascular constriction through a variety of biochemical, physiological, and metabolic factors [85]. Changes in endothelial and platelet function, and the adrenergic nervous system, in addition to changes in metabolic vasoregulation, may contribute to smoking-induced alterations in the coronary microcirculation and result in angina and/or cardiac dysfunction.
●Smoking has been correlated with elevations in serum homocysteine, which is thought to induce vascular injury by multiple mechanisms [73]. (See "Overview of homocysteine".)
●Nicotine in cigarette smoke plays a major role in the transient smoking-related increases in cardiac output, heart rate, and blood pressure. However, it is not clear if nicotine plays a direct role in the development of atherosclerosis [86-89]. (See "Cardiovascular effects of nicotine".)
Role of carbon monoxide — Carbon monoxide is inhaled in cigarette smoke. It binds more avidly than oxygen to hemoglobin, reducing the amount of hemoglobin available to carry oxygen and impeding oxygen release by hemoglobin that is not directly bound to carbon monoxide. This effect can be detected clinically by measuring carboxyhemoglobin levels, which average 5 to 10 percent higher in smokers than nonsmokers, in whom levels are less than 1 percent [90]. (See "Inhalation injury from heat, smoke, or chemical irritants".)
In healthy subjects, carbon monoxide administration, under conditions similar to cigarette smoking, does not affect blood pressure, plasma catecholamines, platelet aggregation, or serum C-reactive protein [91]. Since these parameters are changed with smoking, the observations suggest that something other than carbon monoxide is responsible. By comparison, carbon monoxide exposure in patients with CAD results in severe adverse effects. These include exercise-induced ischemia at a lower level of work, ventricular dysfunction, and increased number and complexity of ventricular arrhythmias [92,93].
SMOKING AND OUTCOMES AFTER REPERFUSION THERAPIES —
The relative outcomes of smokers compared with nonsmokers following reperfusion therapies have been evaluated across the spectrum of presentations of CAD.
After fibrinolytic therapy for STEMI — Despite the important role of cigarette smoking in the development of atherosclerosis, several studies have reported that smokers who receive a fibrinolytic agent for an acute MI have a better outcome than nonsmokers [94-101]. This phenomenon is called the "smoker's paradox." (See "Acute ST-elevation myocardial infarction: Management of fibrinolysis".)
As an example, GUSTO I, the largest trial to evaluate the impact of cigarette smoking on outcomes, included 11,975 nonsmokers, 11,117 ex-smokers, and 17,507 current smokers [96]. Nonsmokers had significantly higher in-hospital mortality (9.9 versus 3.7) and 30-day mortality (10.3 versus 4.0 percent).
The reason for the paradoxically better outcomes after fibrinolysis in smokers may be related to the following factors:
●Smokers have a higher hematocrit and baseline level of fibrinogen, suggesting a hypercoagulable state [97,98]. More active thrombogenic mechanisms may lead to a larger thrombus component that is more susceptible to fibrinolytic therapy, resulting in smokers having a higher patency rate and being more likely to have TIMI-3 flow in the infarct artery after fibrinolysis [97,98,102].
●Smokers have an otherwise better risk profile than nonsmokers; they tend to be significantly younger (mean 11 years in GUSTO I) and have a lower incidence of diabetes, hypertension, previous infarction, and severe coronary disease than nonsmokers [94-101]. Also, for unclear reasons, smokers are more likely to have an inferior rather than anterior wall infarction [97,98,101].
After adjustment for these clinical factors, some but not all studies reported that smoking history was of not an independent prognostic factor [96,97,99,101].
After revascularization with PCI or CABG — In contrast to the smoker’s paradox identified among patients receiving thrombolytic therapy for STEMI, patients who smoke and undergo revascularization with either percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) appear to have worse outcomes compared with nonsmokers [103,104].
●Among 6519 patients from three cohorts (EPIC, EPILOG, and EPISTENT), including 34 percent who smoked, smokers were more likely to experience death, MI, or urgent revascularization within 30 days following their initial PCI (adjusted OR 1.22, 95% CI 1.02-1.47) [104].
●Among patients in the SYNTAX trial comparing PCI with drug-eluting stents and CABG, smoking was an independent predictor of death, MI, or stroke (HR 1.8, 95% CI 1.3-2.5) [103].
CARDIOVASCULAR BENEFITS OF SMOKING CESSATION
Overall cardiovascular benefits — The benefits of quitting cigarette smoking (and tobacco use of any variety) are firmly established but perhaps less well-known and accepted amongst the general public. Among subjects without known CAD, the reduction in cardiac event rate associated with smoking cessation ranges from 7 to 47 percent [105-108]. The cardiac risks associated with cigarette smoking diminish within a few years after smoking cessation and continue to fall with increasing length of time since quitting. Among 8770 participants in the original and offspring portions of the Framingham Heart Study, including 5308 "ever" smokers who were followed for a median of 26.4 years, the risk of a major adverse cardiovascular event (MACE; includes CVD death, MI, stroke, or heart failure) was significantly lower within five years of quitting smoking (HR 0.61, 95% CI 0.49-0.76 compared with active smokers) [109]. However, it takes at least 10, and perhaps as long as 15, years for MACE incidence rates of former smokers to approach those of "never" smokers [109]. More intensive smoking cessation efforts have been shown to be more successful in achieving sustained abstinence and lowering future CVD risks [110]. (See "Benefits and consequences of smoking cessation".)
Despite these facts, significant proportions of the adult population worldwide continue to smoke, and there has been little change in the prevalence of smoking since 1990 [111]. Smoking rates are higher in less educated and poorer segments of the population. Approximately 70 percent of cigarette smokers state that they would like to quit smoking. (See 'Introduction' above.)
Impact of public smoking bans — Changes in public policy have resulted in smoking bans in many communities, with subsequent research on the effects of smoking using communities as their own controls (ie, comparing disease rates before and after smoking bans). In a meta-analysis including 11 studies published between 2004 and 2009 that included data on acute MI rates and data on smoking bans, smoking bans were associated with a 17 percent decrease in acute MI risk (incident rate ratio 0.83, 95% CI 0.75-0.92) [112]. Reductions in hospital admissions for smoking-related diseases, including CAD, have also been reported following smoking bans, with the greatest reduction in hospital admissions noted for CAD admissions, which were reduced by 39 percent after one year and 47 percent by three years postimplementation [113].
Acute coronary syndromes — Smoking cessation improves outcomes in patients who have had an acute coronary syndrome [23,24,28,110,114,115]. In a meta-analysis of 20 prospective cohort studies (including patients with an MI, coronary artery bypass graft surgery [CABG], percutaneous coronary intervention [PCI], or known stable CAD and at least two years follow-up), which included 12,603 smokers, of whom 5659 ceased smoking and 6944 continued to smoke, the relative risk of mortality for smokers who quit compared with those who continued to smoke was 0.64 (95% CI 0.58-0.71). The benefit was not affected by age, sex, index cardiac event, country, or the year in which the study began [114]. Observations from the 1995 to 2015 Coronary Artery Risk Development in Young Adults (CARDIA) study showed a 46 percent reduction in the risk of incident CVD in participants living in areas with workplace smoke-free policies compared with those who resided in areas without such policies [116].
Health-related quality of life has been shown to improve significantly among patients who quit smoking after an acute MI [117]. Using data from two large US registries, smokers who did not quit had worse health-related quality of life metrics as compared with those who quit or never smoked.
Surgical revascularization — Smoking status following coronary revascularization, either coronary artery bypass graft (CABG) surgery or percutaneous coronary intervention (PCI), directly affects mortality.
●Persistent smokers after CABG have a greater relative risk of all-cause mortality (relative risk 1.7), cardiac death (relative risk 1.8), and need for repeat revascularization (relative risk 1.4) compared with those who stopped smoking for at least one year [118]. (See "Coronary artery bypass graft surgery: Graft choices".)
●Persistent smokers after PCI have a greater relative risk of death (1.8) and Q wave MI (2.1) compared with nonsmokers, and a higher relative risk of total and cardiac mortality (relative risk 1.4 and 1.5, respectively) when compared with those who quit smoking [119].
Sudden cardiac death — In Olmsted County, Minnesota, a community that instituted a smoke-free workplace law, the incidence of MI declined by 33 percent, and the incidence of sudden cardiac death declined by 17 percent (109.1 to 92.0 per 100,000 population) in the 18 months following implementation of the smoke-free workplace law compared with the 18 months before the law [108]. (See "Secondhand smoke exposure: Effects in adults" and "Control of secondhand smoke exposure", section on 'Public smoking bans'.)
Stroke — The risk of ischemic stroke also decreases over time after smoking cessation. In one series of middle-aged female adults, the excess risk among former smokers largely disappeared two to four years after cessation [120]. (See "Overview of secondary prevention of ischemic stroke", section on 'Smoking and tobacco use'.)
Effect of age — The relative benefits of smoking cessation are equivalent in young and old patients [114,115]. In one study of 1893 patients with CAD who were older than 55 years, the mortality after six-year follow-up was significantly higher among patients who continued to smoke compared with those who stopped (relative risk 1.7) [115]. The benefits were equivalent in those ages 55 to 64 and over age 65 and were the same as observed among comparable patients aged 34 to 54.
Improvement in endothelial function — As mentioned above, smoking impairs endothelium-dependent vasodilation of normal coronary arteries and reduces coronary flow reserve [77,80]. The impact of smoking cessation on endothelial function was studied prospectively in over 1500 smokers; after one year, 36 percent had successfully quit smoking [82]. Despite gaining an average of 5 kg, smokers who quit had significantly improved endothelial function compared with baseline, while endothelial function did not improve from baseline in those who continued to smoke. This improvement in endothelial function likely contributes to the reduction in mortality and other benefits associated with smoking cessation.
Methods of smoking cessation — There are a number of ways that clinicians can and should actively intervene against smoking in virtually all smokers (table 1). Behavioral therapy, nicotine replacement therapy, and the use of certain medications may each improve the quit rate. The approach to smoking cessation along with the available therapeutic options are discussed separately. (See "Overview of smoking cessation management in adults" and "Pharmacotherapy for smoking cessation in adults" and "Behavioral approaches to smoking cessation".)
SOCIETY GUIDELINE LINKS —
Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Primary prevention of cardiovascular disease" and "Society guideline links: Secondary prevention of cardiovascular disease".)
INFORMATION FOR PATIENTS —
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Quitting smoking for adults (The Basics)" and "Patient education: Heart attack – Discharge instructions (The Basics)" and "Patient education: Coronary artery bypass graft surgery – Discharge instructions (The Basics)")
●Beyond the Basics topics (see "Patient education: Quitting smoking (Beyond the Basics)" and "Patient education: Heart attack recovery (Beyond the Basics)" and "Patient education: Recovery after coronary artery bypass graft surgery (CABG) (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
●Smoking as primary CVD risk factor – Smoking is a leading preventable primary risk factor for cardiovascular disease (CVD); is an independent major risk factor for total atherosclerotic CVD, coronary artery disease (CAD), cerebrovascular disease, and all-cause mortality; and has an apparent dose-dependent relationship with CVD outcomes. (See 'Cigarette smoking and CVD' above.)
●Smoking as a secondary CVD risk factor – Among patients with established CVD, the risk of a recurrent event is increased among those who continue to smoke, compared with those who do not. (See 'Cigarette smoking and CVD' above and 'Smoking and outcomes after reperfusion therapies' above.)
●Non cigarette smoking – With respect to the risk of CVD associated with noncigarette smoking (eg, pipe or cigar smoking, smokeless tobacco, etc), the data are somewhat less clear regarding the risks. Many studies have shown an increased CVD risk associated with pipe or cigar smoking, but others have not shown this increased CVD risk. Exposure to secondhand smoke increases nonsmokers' risk of CVD. (See 'Noncigarette smoking and CVD' above.)
●Benefits of smoking cessation – The benefits of quitting cigarette smoking (and tobacco use of any variety) are firmly established but perhaps less well-known and accepted amongst the general public. The cardiac risks associated with cigarette smoking diminish within a few years after smoking cessation and continue to fall with increasing length of time since quitting. (See 'Cardiovascular benefits of smoking cessation' above.)
ACKNOWLEDGMENT — The editorial staff at UpToDate acknowledge Geoffrey Barnes, MD, MSc, who contributed to an earlier version of this topic review.
