Smoking Cessation After Acute Myocardial Infarction

Division of Clinical Pharmacology and Experimental Therapeutics, the Departments of Medicine and Bioengineering & Therapeutic Sciences, University of California, San Francisco, California. Electronic address: .
Journal of the American College of Cardiology (Impact Factor: 16.5). 02/2013; 61(5):533-535. DOI: 10.1016/j.jacc.2012.11.017
Source: PubMed


Available from: Judith J Prochaska, Nov 09, 2015
Smoking Cessation After
Acute Myocardial Infarction*
Neal L. Benowitz, MD,†
Judith J. Prochaska, P
San Francisco and Stanford, California
Cigarette smoking produces endothelial dysfunction, con-
stricts blood vessels, activates platelets, creates a chronic
inflammatory state, and causes dyslipidemia (1). These
effects accelerate atherosclerosis, destabilize coronary artery
plaques, and precipitate acute coronary events and sudden
death. Smoking cessation substantially reduces the likeli-
hood of recurrent myocardial infarction, stent or graft
thrombosis, need for revascularization, and cardiovascular
death. Smoking cessation is probably the most important
thing a smoker with acute myocardial infarction can do to
improve future health.
See page 524
Hospitalization for an acute cardiovascular event provides
an important opportunity for quitting smoking. Smokers are
often strongly motivated to quit because the risks of smok-
ing are now personal. Furthermore, most hospitals are
smoke-free, requiring smokers to stop smoking at least
temporarily. The 2008 U.S. Clinical Practice Guidelines for
Treating Tobacco Use and Dependence recommend coun-
seling and medications to help all hospitalized tobacco users
maintain abstinence and to treat withdrawal symptoms (2).
However, smoking-cessation therapy in hospitalized pa-
tients offers a number of challenges. Many patients have
used tobacco for many years and have continued to smoke
despite having cardiovascular risk factors and being coun-
seled to quit, indicating a high level of dependence. The
duration of hospitalization for acute myocardial infarction is
usually brief and the hospital stay is busy, so it is difficult to
gain the patient’s full attention for smoking-cessation coun-
seling. Post-hospitalization, continuity of care for tobacco
treatment, and patient adherence can be challenging, requir-
ing coordination between inpatient and outpatient providers
and facilities.
A 2012 Cochrane review of 50 tobacco treatment trials
for hospitalized patients found that intensive counseling,
initiated during hospitalization with follow-up for at least 1
month after hospital discharge, significantly increased quit
rates (relative risk: 1.37; 95% CI: 1.27 to 1.48; 25 trials) (3).
The Cochrane analysis did not find a significant benefit for less
intensive counseling. Adding nicotine replacement therapy to
intensive counseling increased quitting compared with coun-
seling alone (relative risk: 1.54; 95% CI: 1.34 to 1.79; 6 trials).
Neither bupropion nor varenicline increased quit rates com-
pared with counseling alone, although the number of trials was
small (3 and 2, respectively), so statistical power was limited.
Some clinicians are hesitant to add a smoking-cessation
medication on top of a number of other medications that
have been initiated or continued in the context of myocar-
dial infarction and other medical conditions. In the trial by
Eisenberg et al. (4) in this issue of the Journal, for example,
a majority of the sample was prescribed 6 different heart-
related medications at hospital discharge. Clinicians also
may be concerned about the safety of smoking-cessation
medications in patients with heart disease. Nicotine medi-
cations increase heart rate, blood pressure, and myocardial
contractility and have the potential to cause endothelial
dysfunction and coronary vasoconstriction (1). Bupropion
also has sympathomimetic activity and in higher doses can
increase heart rate and blood pressure. Varenicline is a
relatively selective nicotinic receptor agonist. It acts on the
nicotinic cholinergic receptor, which is thought to be
most important in addiction, and has a lower affinity for the
receptor, which mediates cardiovascular effects. There is
little evidence in animal or human experimental studies that
varenicline has cardiovascular effects. However, a number of
cases of cardiovascular events, such as myocardial infarction,
arrhythmia, and syncope, in people taking varenicline have
been reported to regulatory authorities. One meta-analysis of
cardiovascular serious adverse events found a small but signif-
icant increase with varenicline versus placebo (5), whereas a
subsequent larger meta-analysis found no significantly in-
creased risk (6).
The study by Eisenberg et al. (4) is the first published trial
of pharmacotherapy for smoking cessation in a population
composed entirely of patients hospitalized with acute myo-
cardial infarction. This was a multicenter trial involving 392
smokers, two thirds from Canada and the remainder from
Iran and India. Subjects received bupropion in standard
doses or placebo, along with modest behavioral counseling.
The 7-day point prevalence smoking-cessation rates at 1
year were 37.2% for bupropion versus 32% for placebo (p
0.33). The authors concluded that bupropion is ineffective
for smoking cessation in patients after myocardial infarc-
*Editorials published in the Journal of the American College of Cardiology reflect the
views of the authors and do not necessarily represent the views of JACC or the
American College of Cardiology.
From the †Division of Clinical Pharmacology and Experimental Therapeutics, the
Departments of Medicine and Bioengineering & Therapeutic Sciences, University of
California, San Francisco, California; and the ‡Department of Medicine, Stanford
Prevention Research Center, Stanford University, Stanford, California. Dr. Benowitz
is a paid consultant to pharmaceutical companies that market smoking-cessation
medications, including Pfizer, GlaxoSmithKline, and McNeil; and has served as a
paid expert witness in litigation against tobacco companies. Dr. Prochaska is an ad hoc
advisory board member, grant reviewer, and principal investigator on an investigator-
initiated research award with Pfizer Inc.
Journal of the American College of Cardiology Vol. 61, No. 5, 2013
© 2013 by the American College of Cardiology Foundation ISSN 0735-1097/$36.00
Published by Elsevier Inc.
Page 1
tion. There were also no significant differences in cessation
rates when assessed at 3 or 6 months. The authors did find
that among persistent smokers cigarette consumption de-
creased substantially in both treatment groups, with a
decrease on average from 22.8 to 8.4 cigarettes per day. The
authors observed few cardiovascular events during the trial
with no difference by condition. The findings of the study
by Eisenberg et al. (4) are similar to those of the 2 other
published studies of smokers hospitalized for acute cardio-
vascular disease (CVD) treated with bupropion (7,8), both
of which reported fairly high quit rates in the placebo group
(21% and 33% at 1 year), with no significant difference by
condition. Small samples are common across these trials,
and the trial by Eisenberg and colleagues (4) also is limited
with regard to power. Eisenberg and colleagues’ trial
achieved 20% of its registered recruitment goal, so it likely
was underpowered for the intended evaluation of efficacy
and certainly underpowered for safety. Had the reported
cessation rates been observed with the intended sample size
of N 1,500, the treatment differences would have been
significant at p 0.05 at all time points. From a public
health perspective, a difference in quit rates of 5% at 1 year
is meaningful in a patient population at high risk for future
cardiovascular events associated with continued tobacco use.
The findings of the trial by Eisenberg et al. (4) and other
studies in hospitalized patients are in contrast to the results
of studies of bupropion and varenicline in outpatients with
stable CVD. Tonstad et al. (9) studied 629 patients with
stable CVD treated with bupropion for 7 weeks versus
placebo and found significantly higher quit rates with
bupropion (point prevalence abstinence 27% vs. 11%, con-
tinuous abstinence 22% vs. 9%, p 0.001 at 1 year). Rigotti
et al. (10) treated 714 smokers with stable CVD with
varenicline or placebo for 12 weeks and found significantly
higher quit rates with varenicline (7-day point prevalence
abstinence 28% vs. 16%; continuous abstinence of 19% vs.
7% at 1 year, both p 0.001).
When comparing abstinence rates, why is it that the
absolute differences in quit rates between bupropion (and
perhaps varenicline) and placebo seem to be less in patients
hospitalized with acute CVD compared with outpatients
with stable CVD? Several factors may be involved. First, as
Eisenberg et al. (4) acknowledged, having approximately
one third of patients taking placebo quit smoking at 1 year
is fairly high compared with many other trials, suggesting
that patients who entered this trial were highly motivated to
quit, and per study inclusion criteria, patients had to want to
quit smoking to be enrolled. The finding that those who
continued to smoke markedly reduced their cigarette con-
sumption is also suggestive of high motivation to reduce
health risks. It also may be that patients who experience a
life-threatening event such as a myocardial infarction, are
hospitalized, and are given a study medication are particu-
larly susceptible to placebo effects. On the other hand, the
observation that two thirds of the sample continued to
smoke after a myocardial infarction is discouraging. It may
be that the acute nature of the hospitalization was insuffi-
cient for maximizing the utility of bupropion (i.e., patients
were discharged before reaching therapeutic blood levels)
and cessation counseling. The patient population is varied,
with two thirds treated in Canada and one third treated in
Iran or India. We know relatively little about smoking
cessation in Iran and India, although the authors report that
the results of the trial were not different when controlling
for country site.
Given the current study’s findings and the extant litera-
ture, what then is the role of cessation pharmacotherapy in
hospitalized smokers? On the basis of the Cochrane 2012
review, there is evidence of benefit from nicotine replace-
ment therapy, but limited evidence to support the routine
prescription of bupropion or varenicline for smoking cessa-
tion in hospitalized smokers. An issue separate from phar-
macotherapy’s impact on long-term smoking cessation is
the use of nicotine medication in the hospital setting to
relieve withdrawal symptoms. Such treatment can reduce
discomfort and enhance compliance with medical treat-
ments and hospital-wide smoking bans. Further, and in
need of greater study, it may be that individualizing phar-
macotherapy according to patient preference and side effects
will enhance long-term cessation.
Given the significant health consequences of smoking
after myocardial infarction, we suggest a minimal goal of
achieving 50% of smokers quitting at long-term follow-up.
Our recommendations, based on available data and The
Joint Commission’s current recommended hospital-wide
standards, are as follows:
1. Effective counseling in the hospital for all smokers, and
not just the minority who are ready to quit. Hospital-
based cessation treatment needs to be proactive, tailored
to readiness to quit, progressive in use of nicotine
replacement for the management of withdrawal
symptoms, and focused on gaining buy-in and build-
ing rapport for continued treatment and patient
adherence post-hospitalization.
2. Effective transition from inpatient to outpatient smoking-
cessation treatment, with a minimum of 1-month follow-up
and preferably longer.
3. Personalized prescription of medication, intended to
relieve withdrawal symptoms in all patients and to sup-
port long-term cessation in patients motivated to quit.
4. Management of co-occurring mental health condi-
tions, such as depression, that are known to be triggers
to smoking relapse and predictive of mortality after
cardiovascular events. A prospective observational
study found that a majority of patients relapsed to
smoking within 6 months after hospitalization for
myocardial infarction (11). Patients treated at a hospital
without a smoking-cessation program (odds ratio [OR]:
1.71) who were not referred for cardiac rehabilitation
(OR: 1.80) and had greater depressive symptoms during
hospitalization (OR: 1.75) were more likely to relapse to
534 Benowitz and Prochaska
JACC Vol. 61, No. 5, 2013
Smoking Cessation After AMI
February 5, 2013:533–5
Page 2
tobacco. Treatments need to consider the holistic needs
of patients presenting with heart disease, including smok-
ing status, mental health, and other associated risk be-
haviors (sedentary, alcohol use).
Beyond short-term, acute-care measures, we support
smoking-cessation treatment consistent with a chronic dis-
ease model, similar to management of other diseases, such
as hypertension and diabetes. In this type of approach, all
patients are counseled with the expectation that sooner or
later they will quit smoking as an essential element of their
health care (12). Pharmacotherapy is prescribed in an individ-
ualized and flexible way to initiate and sustain abstinence, with
medications combined and/or doses adjusted to relieve with-
drawal symptoms and minimize urges to smoke. Relapse to
smoking is anticipated, and patients are counseled about
both relapse prevention and re-engagement in the quitting
process after relapse. The observation that cigarette con-
sumption was substantially reduced in the trial by Eisenberg
et al. (4) suggests that these smokers remained concerned
about smoking as a health risk and may have lowered their
level of tobacco dependence, making them more amenable
to later smoking cessation within a chronic disease–
management program.
A continuing care model for smoking-cessation interven-
tion for patients hospitalized with CVD has been described
in Canada, named the “Ottawa Model” (13). The Ottawa
Model intervention begins with customized counseling and
pharmacotherapy for all smokers while in the hospital.
Post-hospitalization follow-up is done using an interactive
voice-responsive telephone system, with automated phone
calls at frequent intervals for up to 180 days after discharge.
Relapse counseling is provided as needed. Counselors are
available to respond to particular patient needs. This ap-
proach is reported to result in 29% continuous abstinence at
6 months across institutions and as high as 44% at one
In conclusion, the standard of care for managing patients
after myocardial infarction should include not only blood
pressure and lipid management but also smoking cessation.
At present, the quit rates for smokers after myocardial
infarction are higher than those for the general population
of smokers, yet given the enormous health risks, still much
too low. Increasing quit rates will likely require a combina-
tion of counseling and personalized medications, with a
chronic disease management approach. Future studies of
smoking cessation in hospitalized patients should be con-
ducted to test the effectiveness of such multicomponent
Reprint requests and correspondence: Dr. Neal L. Benowitz,
Division of Clinical Pharmacology and Experimental Therapeutics,
University of California–San Francisco, Box 1220, San Francisco,
California 94143-1220. E-mail:
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Key Words: acute myocardial infarction y bupropion y randomized
controlled trial y smoking cessation.
JACC Vol. 61, No. 5, 2013
Benowitz and Prochaska
February 5, 2013:533–5
Smoking Cessation After AMI
Page 3
  • Source
    • "Short inpatient education programs have not increased smoking cessation rates at one year and at five years [30] . More intensive behavioral interventions with at least one month of supportive contacts after hospital discharge increased cessation rates [31,32], as does add pharmacological management [30,33]. We observed lower mortality rates across intervention groups when data were analysed into two successive 45-month periods. "
    [Show abstract] [Hide abstract] ABSTRACT: Background Smoking is an undertreated risk factor for coronary artery disease (CAD) and is associated with adverse outcomes after myocardial infarction. Aims of our study were to determine if management of CAD by medical therapy (MT) alone or with coronary artery bypass grafting (CABG) or percutaneous coronary intervention (PCI) influence smoking status at one year following angiography and if a change in smoking status at one year influences long term survival. Methods Prospective cohort study using the APPROACH registry. Two cohorts were examined: (1) 11,334 patients who returned a one year follow-up questionnaire; (2) 4,246 patients propensity-matched based on their post-angiography treatment - MT or revascularization (RV). Multivariate modeling and survival analysis were used. Results In the propensity-matched cohort, quit rates at one year were greater among CABG patients (68%) than PCI (37%) or MT patients (47%). Smokers in the RV group, who self-reported quitting at one year, had a significantly reduced mortality compared to those who continued to smoke. Conclusions CABG patients were more likely to quit smoking than those treated with MT alone or PCI. Quitting smoking was associated with improved long-term survival; smoking remains a key risk factor for mortality in patients with CAD. These data underscore the importance of nicotine addiction management in patients with CAD and the need to emphasize cessation particularly in those patients undergoing MT or PCI.
    Full-text · Article · Oct 2014 · BMC Cardiovascular Disorders
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    [Show abstract] [Hide abstract] ABSTRACT: This cohort study examined the role of smoking during hospitalization, duration of cessation counseling, patient awareness of the hospital's smoke-free policy, belief that smoking is associated with a current symptom or disease, and the presence of withdrawal symptoms with 12-month smoking cessation among inpatients enrolled in a smoking cessation program. Inpatients in four community hospitals (N = 1,317) participated in a smoking cessation intervention consisting of face-to-face counseling at baseline and four follow-up counseling phone calls. Patients were classified as nonsmokers only if they reported not smoking at both the 6- and the 12-month interviews. All patients lost to follow-up were considered smokers. At 1 year the smoking cessation rate was 22.5%. Cessation was independently associated with reporting no smoking during hospitalization, noting no withdrawal symptoms at baseline, and believing that a current illness or symptom is related to smoking. Length of counseling interview and awareness of the hospital's smoke-free policy were not independently associated with cessation. CONCLUSIONS. Smoking cessation programs and hospital policies that decrease smoking during hospitalization, address withdrawal symptoms during hospitalization, and make clear the connection between a patient's health and cigarette smoking may increase the effectiveness of their smoking cessation efforts.
    Full-text · Article · Jul 2000 · Preventive Medicine
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    [Show abstract] [Hide abstract] ABSTRACT: Cigarette smoking is a risk factor for the formation and rupture of intracranial aneurysms. Few studies have examined predictors of resumption of cigarette smoking after a first episode of subarachnoid hemorrhage (SAH). Of 620 SAH patients treated between July 1996 and November 2002, we prospectively evaluated continued cigarette use in 152 smokers alive at 3 months. Univariate and multivariate logistic regression analyses were used to identify potential demographic, social, and clinical predictors of continued cigarette use, defined as smoking > or =1 cigarette per week in the month before follow-up. Thirty-seven percent (56 of 152) resumed smoking after their SAH. Patients who continued smoking were younger, were more often black, had begun smoking at an earlier age, and had a higher frequency of prior alcohol or cocaine use and self-reported depression or anxiety than those who quit (all P<0.05). Smoking at < or =16 years of age (odds ratio [OR], 5.88; 95% confidence interval [CI], 2.33 to 14.29), self-reported depression (OR, 5.29; 95% CI, 2.10 to 13.35), and prior alcohol use (OR, 4.51; 95% CI, 1.45 to 14.05) independently predicted continued cigarette use. Smokers had a functional outcome similar to that of nonsmokers at 3 months but were more likely to resume alcohol consumption (OR, 3.88; 95% CI, 1.91 to 7.88). More than one third of prior smokers continue to use nicotine after SAH. Young age at smoking onset and a history of depression or alcohol use are risk factors for continued cigarette use. Targeted smoking cessation programs are needed to reduce the high rate of smoking resumption after SAH.
    Full-text · Article · Sep 2003 · Stroke
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