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Official reprint from UpToDate®

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Cardiovascular risk of smoking and benefits of smoking cessation

Authors: Elizabeth Jackson, MD, MPH, Geoffrey Barnes, MD, MSc

Section Editor: Christopher P Cannon, MD
Deputy Editor: Brian C Downey, MD, FACC

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2018. | This topic last updated: Jun 19, 2018.

INTRODUCTION — As of 2015, an estimated 15.1 percent of adults ≥18 years of age (16.7 percent of
men and 13.7 percent of women) in the United States smoke [1]. Globally, an estimated 1.3 billion
people smoke, the majority of whom reside in developing countries where smoking rates are
estimated to be as high as 50 percent for men. Smoking rates are higher among those with lower
education and income levels. The majority of smokers start smoking before the age of 18 years, most
commonly around age 14 to 15 years. Approximately 16 percent of students grades 9 through 12
report smoking cigarettes.

The facts regarding the impact of cigarette smoking on the development of cardiovascular disease are
well known to both the medical profession and the public [2-6]. 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 [7]. (See "Overview of established risk factors for cardiovascular disease".)

The relationship between smoking and cardiovascular disease, the effects of smoking on the
atherosclerosis process, and the beneficial effects of smoking cessation will be reviewed here [2,8].
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

Cigarette smoking and CVD — With respect to cardiovascular disease (CVD), the following
observations have been made regarding a major role for cigarette smoking:

● Smoking is an independent major risk factor for total atherosclerotic CVD, coronary heart disease
(CHD), cerebrovascular disease, heart failure, and all-cause mortality, with an apparent dose-
dependent relationship [9-12]. (See 'Dose and duration of smoking exposure' below.)

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● The incidence of myocardial infarction (MI) is increased sixfold in women and threefold in men
who smoke at least 20 cigarettes per day, when compared with subjects who never smoked
[13,14]. In the worldwide INTERHEART study of patients from 52 countries, smoking accounted
for 36 percent of the population-attributable risk of a first MI [15]. (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
CHD and adjusted for the effects of other known CHD risk factors (over 2.4 million persons with
over 44,000 CHD events), female smokers were 25 percent more likely than male smokers to
develop CHD (relative risk ratio 1.25, 95% CI 1.12-1.39) [16]. Female sex is also associated with
more adverse events after acute coronary syndrome [17].

● 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 [12].

● Patients who continue to smoke in the presence of established CHD have an increased risk of
repeat MI and an increased risk of death, including sudden cardiac death [18-21]. Among
smokers who quit after MI, risk for recurrent events declines over time [22].

● 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 [23].

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 CHD and
approximately 25 percent increased risk for stroke [24]. With increases in the number of cigarettes
smoked per day, increased risk for CVD has been observed in several studies [12,24-29]. As
examples:

● 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 CHD compared with a non-smoker
[25]. For those who smoked less than 15 cigarettes per day, the risk of CHD was near double that
of a non-smoker.

● 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 [28]. The odds of having an MI was 1.056 for

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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 CHD 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 [26]. The highest CHD 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 CHD events, with a longer duration
and higher number of cigarettes yielding a greater risk. Increasing risk for CHD 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) [30].

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 non-smokers [31]. 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 [32-36].

• 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 non-smokers
[33].

• 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 non-smokers, advanced atherosclerotic
lesions were significantly more common among smokers compared with non-smokers (31
versus 14 percent), and the number of advanced atherosclerotic lesions was also greater in
smokers [34].

Non-cigarette smoking and CVD — With respect to the risk of CVD associated with non-cigarette
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

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disease, cigars are generally perceived as being safer than cigarettes. Moreover, data about the role
of cigar smoking and the risk of cardiovascular disease are 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 men who were followed for 14 years, those who smoked cigars were
at a greater risk for developing CHD (relative risk 1.3 compared with non-smokers); 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) [37].

● In a cohort study of 121,278 men ≥30 years of age, current cigar smokers ≤75 years of age had
an increased risk of death from CHD (adjusted rate ratio 1.3), while there was no increased risk in
those >75 years of age or former cigar smokers of any age [38].

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 non-smokers, which is still lower than that of cigarette smokers,
while others observed no increase in CVD risk [26,39-41]. In total, however, the evidence seems to
suggest pipe smoking increases the risk for CVD events [30,40].

● 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 non-smokers [40].

● Among a longitudinal cohort of 293,000 US veterans followed for 16 years, all-cause mortality for
pure pipe smokers was increased compared with non-smokers [26].

● Among 16,932 Norwegian men 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) [39].

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 [30].

Secondhand smoke — Exposure to secondhand smoke increases non-smokers' risk of

cardiovascular disease. While the risk estimates for secondhand smoke and CHD 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 [42-45]. 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 non-smokers.

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● In one case-control study of 687 men (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 non-smoking regular
snuff users and those who never used any tobacco products (adjusted odds ratio [OR] 0.96) [43].

● 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 [45]. For men 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) [44].

Electronic cigarettes — There are currently no data on the relationship between electronic
cigarette (e-cigarette) use and its impact on CVD outcomes. E-cigarettes are discussed in detail
separately. (See "E-cigarettes".)

PATHOGENESIS — Although the relationship between coronary heart disease (CHD) 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 [2,46].

● 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 [47-49]. In
addition, free radicals in cigarette smoke damage lipids, resulting in the formation of
proatherogenic oxidized particles, specifically oxidized low-density lipoprotein cholesterol [50-52].
A similar effect is seen with acute secondhand smoke exposure [53]. (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 [6,54-56].

● Cigarette smoke contains carbon monoxide, which when inhaled results in higher levels of
carboxyhemoglobin. This does not appear to directly cause atherosclerosis or cardiovascular
disease (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 [6,57-63].
(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

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enhanced platelet-vessel wall interactions [64]. This can reduce the elastic properties of the aorta,
resulting in stiffening of and trauma to the wall [65].

● Smoking, as well as passive exposure to smoke, impairs endothelium-dependent vasodilation of

normal coronary arteries and reduces coronary flow reserve [66-71]. Smoking can also potentiate
the endothelial dysfunction induced by hypercholesterolemia [51,68]. The effect on endothelial
function results from oxidative stress with enhanced oxidation of LDL and from reduced
generation of nitric oxide [61,67,70,72,73].

● 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 [74]. 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 [62]. (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 [75-78]. (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 non-smokers, in whom levels are less than 1 percent [79]. (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 [80]. Since these parameters are changed with smoking, the observations suggest that some
factor other than carbon monoxide is responsible. By comparison, carbon monoxide exposure in
patients with CHD 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 [81,82].

SMOKING AND OUTCOMES AFTER REPERFUSION THERAPIES — The relative outcomes of

smokers compared with non-smokers following reperfusion therapies have been evaluated across the
spectrum of presentations of coronary heart disease.

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 myocardial infarction (MI) have a better outcome than non-smokers [83-90]. This
phenomenon is called the "smoker's paradox." (See "Fibrinolysis for acute ST elevation myocardial
infarction: Initiation of therapy".)

As an example, GUSTO I, the largest trial to evaluate the impact of cigarette smoking on outcomes,

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included 11,975 non-smokers, 11,117 ex-smokers, and 17,507 current smokers [85]. Non-smokers
had a 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 [86,87]. 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 [86,87,91].

● Smokers have an otherwise better risk profile than non-smokers; 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 non-smokers [83-90]. Also, for unclear
reasons, smokers are more likely to have an inferior rather than anterior wall infarction [86,87,90].

After adjustment for these clinical factors, some but not all studies reported that smoking history was
of not an independent prognostic factor [85,86,88,90].

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 non-smokers [92,93].

● 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) [93].

● 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) [92].

CARDIOVASCULAR 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. Among subjects without known coronary heart disease (CHD),
the reduction in cardiac event rate associated with smoking cessation ranges from 7 to 47 percent
[94-97]. The cardiac risks associated with cigarette smoking diminish relatively soon after smoking
cessation and continue to fall with increasing length of time since quitting [98]. More intensive smoking
cessation efforts have been shown to be more successful in achieving sustained abstinence and
lowering future cardiovascular disease (CVD) risks [99]. (See "Benefits and risks 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 [100]. In both genders, 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

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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 myocardial infarction (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) [101]. Reductions in hospital admissions for smoking-
related diseases, including CHD, have also been reported following smoking bans, with the greatest
reduction in hospital admissions noted for CHD admissions, which were reduced by 39 percent after
one year and 47 percent by three years post implementation [102].

Acute coronary syndromes — Smoking cessation improves outcomes in patients who have had an
acute coronary syndrome [19,20,22,99,103,104]. 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 CHD 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 [103].

Health-related quality of life has been shown to improve significantly among patients who quit smoking
after an acute MI [105]. 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 and never smokers.

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 [106]. (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 non-smokers, 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 [107].

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 [97].
(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 women, the excess risk among former smokers largely disappeared two to four years
after cessation [108]. (See "Overview of secondary prevention of ischemic stroke", section on
'Smoking'.)

Effect of age — The relative benefits of smoking cessation are equivalent in young and old patients

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[103,104]. In one study of 1893 patients with CHD 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) [104]. 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 [66,69]. The
impact of smoking cessation on endothelial function was studied prospectively in over 1500 smokers;
after one year, 36 percent had successfully quit smoking [71]. 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 coronary heart disease" and "Society guideline links: Secondary
prevention of coronary heart 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 (The Basics)" and "Patient education:
Heart attack recovery (The Basics)" and "Patient education: Recovery after coronary artery
bypass graft surgery (CABG) (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

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● Smoking is a leading preventable risk factor for cardiovascular disease (CVD), and is an
independent major risk factor for total atherosclerotic CVD, coronary heart disease (CHD),
cerebrovascular disease, and all-cause mortality, with an apparent dose-dependent relationship.
Similarly, among those 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.)

● With respect to the risk of CVD associated with non-cigarette 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 non-smokers' risk of
cardiovascular disease. (See 'Non-cigarette smoking and CVD' above.)

● 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 relatively soon after smoking cessation and continue
to fall with increasing length of time since quitting. (See 'Cardiovascular benefits of smoking
cessation' above.)

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GRAPHICS

Five "A's" for assessing for tobacco use and addressing smoking cessation

Intervention Technique

Ask Implement an officewide system that ensures that, for every patient at every clinic visit,
tobacco-use status is queried and documented. Repeated assessment is not necessary
in the case of the adult who has never used tobacco or has not used tobacco for many
years, and for whom this information is clearly documented in the medical record.

Advise Strongly urge all tobacco users to quit in a clear, strong, personalized manner.

Advice should be:

Clear - "I think it is important for you to quit smoking now and I can help you." "Cutting down
while you are ill is not enough."

Strong - "As your clinician, I need you to know that quitting smoking is the most important
thing you can do to protect your health now and in the future. The clinic staff and I will help
you."

Personalized - Tie tobacco use to current health/illness and/or its social and economic costs,
motivation level/readiness to quit, and/or the impact of tobacco use on children and others in
the household.

Assess Determine the patient's willingness to quit smoking within the next 30 days:
If the patient is willing to make a quit attempt at this time, provide assistance.

If the patient will participate in an intensive treatment, deliver such a treatment or refer to an
intensive intervention.

If the patient clearly states he or she is unwilling to make a quit attempt at this time, provide
a motivational intervention.

If the patient is a member of a special population (eg, adolescent, pregnant smoker), provide
additional information specific to that population.

Assist Provide aid for the patient to quit. These actions are summarized in the accompanying
table.

Arrange Schedule follow-up contact, either in person or by telephone. Follow-up contact should
occur soon after the quit date, preferably during the first week. A second follow-up
contact is recommended within the first month. Schedule further follow-up contacts as
indicated.

Congratulate success during each follow-up. If tobacco use has occurred, review
circumstances and elicit recommitment to total abstinence. Remind the patient that a
lapse can be used as a learning experience. Identify problems already encountered and
anticipate challenges in the immediate future. Assess pharmacotherapy use and
problems. Consider use or referral to more intensive treatment.

Adapted from: Fiore MC, Jaen C, Baker T, et al. Treating tobacco use and dependence: 2008 update. Clinical
Practice Guideline. Rockville, MD: US Department of Health and Human Services. Public Health Service. 2008.

Graphic 74402 Version 11.0

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Contributor Disclosures
Elizabeth Jackson, MD, MPH Consultant/Advisory Boards: McKesson [CVD prevention]; Happify,
INC [General Wellness]. Employment: Am J of Medicine/Elsevier Publishing [COMPLETED 10/2016];
Circulation; Springer Science + Business Media. Other Financial Interest: Motley, Rice LLC [Expert
witness (CVD/smoking)]. Geoffrey Barnes, MD, MSc Grant/Research/Clinical Trial Support:
Pfizer/BMS [Anticoagulation (Apixaban)]; Janssen [Anticoagulation (Xarelto)]. Consultant/Advisory
Boards: Portola [Anticoagulation (BevyxXa)]; Pfizer/BMS [Anticoagulation (Apixaban); Janssen
[Anticoagulation (Xarelto)]. Christopher P Cannon, MD Grant/Research/Clinical Trial Support:
Amgen [Lipids (Evolocumab), heart failure (Ivabradine)]; Arisaph (Lipids); Boehringer-Ingelheim [AF
(Dabigatran), DM (Empaglifozin, Linagliptin)]; Bristol-Myers Squibb [AF (Apixaban)]; Daiichi Sankyo
[AF (Edoxaban)]; Janssen [AF (Rivaroxaban), DM (Canagliflozin)]; Merck [Lipids (Ezetimibe), DM
(Ertugliflozin, Sitaglipitin)]; Regeneron [Lipids (Alirocumab)]; Sanofi [Lipids (Alirocumab), ACS
(Clopidogrel)], diabetes (Lixisenatide, Sotagliflozin); Takeda [DM (Pioglitazone, Alogloptin)].
Consultant/Advisory Boards: Alnylam [Lipids (Inclisiran)]; Amarin [Lipids (Vascepa icosapent ethyl)];
Amgen [Lipids (Evolocumab), heart failure (Ivabradine)]; Arisaph [Lipids]; BI [AF (Dabigatran), DM
(Empaglifozin, Linagliptin)]; Bristol-Myers Squibb [AF (Apixaban)]; Eisai [Lipids/obesity (Locaserin)];
GlaxoSmithKline [Lipids]; Kowa [Lipids (Pitavastatin)]; Lipimedix [Lipids]; Merck [Lipids (Ezetimibe),
DM (Ertugliflozin, Sitaglipitin)]; Pfizer [AF (Apixaban), DM (Ertugliflozin), lipids (Atorvastatin)];
Regeneron [Lipids (Alirocumab)]; Sanofi [Lipids (Alirocumab), ACS (Clopidogrel)], diabetes
(Lixisenatide, Sotagliflozin); Takeda [DM (Pioglitazone, Alogloptin)]. Brian C Downey, MD,
FACC Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these
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