Review

Cardiovascular risks associated with smoking:

a review for clinicians
Serena Tonstada and J. Andrew Johnstonb
a

Department of Preventive Cardiology, Ulleval University Hospital, Oslo, Norway and bInnovaa Research,
Chapel Hill, North Carolina, USA.

Received 25 May 2005 Accepted 21 January 2006

The cardiovascular consequences of cigarette smoking may not be as readily recognized as the adverse respiratory
consequences. Smoking results in sudden death, myocardial infarction, coronary heart disease, worsened outcomes after
angioplasty or bypass surgery, cerebrovascular disease, aortic aneurysm, peripheral vascular disease, increased risk of
complications of hypertension and impotence. Physicians should encourage and help all their smoking patients to quit.
Pharmacotherapy for smoking cessation is one of the most cost-effective healthcare interventions and should be offered to
all dependent smokers. Both nicotine replacement and bupropion have been shown to be well tolerated in populations with
c 2006 The European Society of Cardiology
cardiovascular disease. Eur J Cardiovasc Prev Rehabil 13:507514
European Journal of Cardiovascular Prevention and Rehabilitation 2006, 13:507514
Keywords: cardiovascular morbidity and mortality, smoking, risk, treatments, smoking cessation
Conflict of interest: S.T. has obtained support for congresses, honoraria for lectures and consulted for GlaxoSmithKline, Novartis, and Pfizer which produce aids for
smoking cessation. J.A.J. was previously employed by GlaxoSmithKline, and has consulted for GlaxoSmithKline, Sanofi-Synthelabo, and Pfizer. GlaxoSmithKline provided
support to J.A.J. to help facilitate preparation of this manuscript.

Introduction
The number of cigarette smokers in the world is
estimated at 1.3 billion and this figure is expected to rise
to 1.7 billion by 2025 [1]. The morbidity and mortality
resulting from smoking have been extensively documented. Smoking harms nearly every organ of the body,
causing many diseases and reducing the health of smokers
in general [2]. Every second a smoker will die of a
tobacco-caused disease [1]. Because the smoke and
constituents from cigarettes are inhaled and immediately
reach the lung tissue and vasculature, patients, as well as
physicians, more readily recognize and accept the
pulmonary consequences of smoking, but do not readily
recognize the cardiovascular risks of smoking. As an
example, coronary heart disease is responsible for higher
excess mortality in smokers aged under 45 years compared with any other tobacco-related disease [3].
Extensive reviews on the cardiovascular risks of smoking
and the benefits of quitting are available [29]. It should
Correspondence and requests for reprints to Serena Tonstad, Department of
Preventative Cardiology, Ulleval University Hospital, N-0407, Oslo, Norway.
Tel: + 47 22 11 79 39; fax: + 47 22 11 99 75;
e-mail: serena.tonstad@ulleval.no

be emphasized that smoking is one of a number of risk

factors for cardiovascular disease (CVD) and all contributory factors should be addressed. Accordingly the SCORE
project developed a scoring system for risk management
which provides an estimation of 10-year risk for fatal CVD
in Europeans [10]. These risk scores may easily be used to
calculate the absolute effect of stopping smoking on CVD
risk. The number needed to treat for smoking cessation is
very favorable. On average, among 20 people with a risk
score of 10% that stop smoking and reduce their risk by
50%, one case of CVD is avoided. Among approximately
seven people with a risk score of 30% that stop smoking,
one case of CVD is avoided. The SCORE model further
shows that quitting smoking would move many individuals
from a risk category requiring pharmacological therapy for
reducing serum cholesterol, as an example, to a lower risk
category not requiring drug therapy. The results of the
initial five statin trials confirm this expectation. The event
rate among current smokers on active treatment was nearly
identical to the event rate among never and ex-smokers on
placebo [11].
The purpose of this manuscript is to provide clinicians
with a clinically useful review of the cardiovascular risks

c 2006 The European Society of Cardiology

1741-8267

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508 European Journal of Cardiovascular Prevention and Rehabilitation 2006, Vol 13 No 4

associated with smoking, the cardiovascular benefits of

stopping smoking and to also provide a review of available
treatments to help physicians assist their patients in
smoking cessation.

Cardiovascular diseases caused by smoking

Before reviewing the cardiovascular diseases caused by
smoking, the responsible pathology should be identified.
Three constituents of cigarette smoke, nicotine, carbon
monoxide, and oxidant gases, are the major contributors
to cardiovascular disease [4]. Nicotine affects hemodynamic parameters of the heart increasing heart rate, blood
pressure and thereby myocardial work. In some patients
with coronary heart disease there is evidence that
smoking may cause vasoconstriction and decrease coronary blood flow [12]. In addition, the exposure to carbon
monoxide and increase in carboxyhemoglobin levels
reduce the oxygen-carrying capacity and lead to an
increase in red cell mass. Other adverse effects
include
reduced
exercise
tolerance,
increased
exercise-induced ventricular dysfunction and ventricular
arrhythmias [4].
Smoking results in injury and dysfunction in the
endothelium in both peripheral and coronary arteries.
Endothelial damage may result in atherogenesis as well as
acute cardiovascular events [4]. These toxic effects are
thought to be primarily the result of oxidant chemicals
[4,13] that antagonize the actions of nitric oxide, which is
primarily responsible for the vasodilatory function of the
endothelium. Nitric oxide also helps regulate inflammation, leukocyte adhesion, platelet activation and thrombosis. Accordingly, the oxidant chemicals from smoking
may contribute to the hypercoagulable state seen in
smokers. Furthermore, smoking increases the chances of
plaque rupture. Smoking even one cigarette may cause
short-term increases in arterial wall stiffness that may
increase the risk for plaque rupture [14]. These
observations are consistent with epidemiological evidence that show smoking increases the risk of acute
myocardial infarction and sudden death more than it
increases the risk of angina pectoris. Smokers have a
greater thrombotic burden due to the effects of smoking
but less extensive atherosclerosis [15].
Coronary artery disease

Smoking predisposes individuals to several clinical

atherosclerotic syndromes, including myocardial infarction and other acute coronary syndromes, stable angina
and sudden death. Risks are greatest in smokers with
heavier smoking levels and with longer durations of
smoking behavior. The relative risk of coronary heart
disease is higher in smokers compared with non-smokers
regardless of age, but the relative risk decreases with
advancing age as the natural prevalence of coronary artery
disease increases with age [3]. The relative risk of sudden

death is two to four times greater for a smoker relative to

a non-smoker [3,5]. Increased risk is also noted in women
and in smokers without a history of coronary heart disease
[3,16]. The relative risk of death from coronary heart
disease in a smoker is 70% higher than for non-smokers.
This relative risk is even higher (200%) in heavy smokers
(greater than two packs per day) [5]. The risk is
furthermore increased in smokers with other concurrent
risk factors [3,5]. More recent data indicate that smoking
causes myocardial infarction across various racial and
ethnic groups [17]. Further, smoking has been identified
as a strong risk factor for myocardial infarction in younger
women [18,19]. Recently the World Health Organization
MONICA project showed that as many as 81% of men
and 77% of women aged 3539 years who experienced
non-fatal myocardial infarction smoked, giving an attributable risk of well over one-half [20]. Furthermore
smoking increases cardiovascular morbidity and mortality
among participants in trials using medications known to
reduce cardiovascular events [21]. Cigarette smoking has
also been shown to be a risk factor for congestive heart
failure [22]. The increased risk of congestive heart failure
from smoking is probably mediated, however, through
coronary heart disease, which is the underlying cause of
the majority (65%) of congestive heart failure cases [2].
Lastly, morbidity and mortality after percutaneous
coronary intervention is significantly increased in smoking patients [23].
Cerebrovascular disease

Studies conducted in the 1950s described the increased

mortality from strokes in smokers compared with nonsmokers [2,3]. Smoking has been shown to be associated
with an increase in incidence and mortality from both
main subtypes of stroke, ischemic stroke and subarachnoid hemorrhage [2]. An estimated overall relative risk of
stroke, from a 32-study meta-analysis, was found to be 1.5
in smokers versus non-smokers [24]. The risk was slightly
higher in women than in men, 1.7 and 1.4, respectively.
Further, an effect of age was noted with decreasing risk
with advancing age [24].
Abdominal aortic aneurysm

Smoking causes atherosclerosis and it has been documented that smokers have more atherosclerosis in the
abdominal aorta. As a consequence of this and possibly
other mechanisms, the relative risk of abdominal aortic
aneurysm is increased [2,3]. A doseresponse relationship
has also been shown with an odds ratio of 2.75 for 119
pack years up to an odds ratio of 9.55 for 50 or more pack
years [25].
Peripheral vascular disease

Cigarette smoking approximately doubles the risk of

intermittent claudication for both men and women.
There is a clear doseresponse relationship. In smokers
over the age of 45 and smoking in excess of 15 cigarettes a

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Cardiovascular risks associated with smoking Tonstad and Johnston 509

day, the relative risk is up to nine times that of nonsmokers. Additionally, cigarette smoking has been linked
to progression of peripheral vascular disease [3,8,26].
Impotence

Impotence is associated with smoking, which is the most

common arterial risk factor in patients presenting with
impotence [27]. Penile blood pressure is lower among
patients who smoke than non-smokers [28]. Furthermore,
smoking has been demonstrated to be an independent
risk factor and predisposes smokers to impotence due to
atherosclerotic changes in the hypogastriccavernous
arterial bed [29].
Complications of hypertension

Though smokers in epidemiological studies have lower

levels of blood pressure than non-smokers, blood pressure
measured by ambulatory monitoring is reduced after
smoking cessation [30,31]. The risks of chronic hypertension include both stroke and renal complications.
Pharmacologic treatment in mildly hypertensive smokers
is much less effective in reducing the incidence of stroke
than in mildly hypertensive non-smokers. The relative
risk of stroke among hypertensive smokers is five times
that among normotensive smokers, but 20 times that of
normotensive non-smokers [32,33].

Effect of smoking cessation on risk

Not only are the harmful effects of cigarette smoking well
documented, but the beneficial effects of smoking
cessation are also well documented. The effects of
smoking are mediated by multiple mechanisms, some of
which are reversible within days or weeks of stopping
smoking. Examples of rapidly reversible effects include
platelet activation, clotting factors and carboxyhemoglobin [8]. Recently smoking cessation was shown to be
associated with a decreased inflammatory response [34].
Further data have indicated that smoking cessation leads
to a rapid restoration of the level of circulating
endothelial progenitor cells [35]. Other effects may not
be as readily reversible, such as atherosclerosis and lipid
deposition in the arterial intima [8]. Regardless of
reversibility, stopping smoking at a minimum prevents
the smoking-mediated progression of cardiovascular
disease. Therefore, stopping smoking results in beneficial
effects for all smoking-induced CVD. It must be
recognized that the decrease in risk for CVD is not
immediate, but decreases with time as is discussed below.
Furthermore, observational data suggest that smoking
reduction in contrast to quitting does not seem to lead to
a reduction in myocardial infarction [36].
Effect of smoking cessation on total mortality

Data on the mortality benefits of smoking cessation is

based primarily on observational epidemiological data.
These studies have consistently indicated that the death

rates of former cigarette smokers are lower than those of

current smokers, and that the former smoker death rates
converge toward those of never smokers the longer the
former smokers have not smoked. This decline begins
during the first 5 years after quitting and continues for at
least 1015 years [37]. Results of the seminal studies
done among British male physicians showed that those
who stopped smoking before age 35 years subsequently
avoided almost all of the excess risk that they would
otherwise have experienced [38]. In absolute terms, of
five smokers that quit before middle age, one avoids
premature death.
There have been two randomized controlled trials of
smoking cessation. In the Whitehall Civil Servants Study
the total mortality was reduced by 7% during 20 years of
follow-up [39]. In the Lung Health Study conducted in
subjects with airway obstruction all cause mortality was
significantly lower (8.83 per 100 personyears) in the
special smoking intervention group compared with the
control group (10.38 per 1000 personyears) after up to
14.5 years of follow-up [40].
Effect of smoking cessation on cardiovascular disease
in healthy smokers

In general, large cohort studies have shown that the

excess risk of coronary heart disease mortality among
former smokers drops substantially in the first 23 years.
Thereafter, the rate of decline decreases so that it may
take up to 1015 years for former smokers to reach the
same risk level as that of persons who have never smoked.
Likewise, the risk of first myocardial infarction after
smoking cessation declines quickly. This risk reaches the
levels of persons who have never smoked by the third or
fourth year [8,41,42]. In California, a large and aggressive
tobacco-control program was associated with a prompt
reduction in deaths from heart disease [43].
Effect of smoking cessation in smokers with
cardiovascular disease

A meta-analysis by van Berkel et al. [44] found that the

odds ratio for mortality or non-fatal myocardial infarction
was almost halved in patients with coronary heart disease
who stopped smoking compared with continuing smokers
in the course of 113 years of follow-up. Similarly, Wilson
et al. [45] reported that the odds ratio for death after
myocardial infarction was halved for smokers who quit. In
absolute terms, the 10-year risk for recurrent coronary
heart disease events in patients with established coronary
disease is about 30%. A 36% event reduction would
translate into one less myocardial infarction or death
during 10 years for every five smokers with coronary heart
disease that quit. In a later meta-analysis, a Cochrane
Review, the benefits of patients with coronary heart
disease stopping smoking were again demonstrated
with a 36% reduction in relative risk for mortality and a
32% reduction in relative risk for non-fatal myocardial

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510 European Journal of Cardiovascular Prevention and Rehabilitation 2006, Vol 13 No 4

infarction [6]. The benefits of cessation may even be

larger than suggested by these studies when corrected for
serum cotinine measurements [46].
Smoking cessation decreases the rate of restenosis after
percutaneous coronary intervention, recurrence of disease
in saphenous vein bypass grafts and death after coronary
artery bypass surgery [23,47,48]. Taira et al. [47] reported
that patients who continue to smoke after a percutaneous
coronary intervention receive about one-half the benefit
in terms of quality of life and functional status as those
who stop smoking (and only one-third the benefit as
those who never smoked).
Effect of smoking cessation on stroke and peripheral
vascular disease

For stroke, the excess risk in smokers decreases steadily

after cessation becoming indistinguishable in former
smokers from that of lifetime nonsmokers after 515 years
depending on the study [8]. One study found, however,
that the risk in light smokers decreased to that of never
smokers following cessation but a complete loss of risk
was not observed for heavy smokers following cessation
[49]. Patients with peripheral vascular disease who quit
smoking have increased exercise tolerance, decreased risk
of amputation following surgery, and increased overall
survival [8]. Current smokers with peripheral vascular
disease with intermittent claudication had decreased
time to claudication and increased pain compared with
similar patients who had quit smoking an average of
7 years prior [50]. Data on the risk of abdominal aortic
aneurysm indicate that the risk is lower, approximately
half, in former smokers compared with current smokers
[2,38].

Treatment of the tobacco-dependent patient

with cardiovascular disease
The presence of a cardiovascular illness provides strong
motivation for a patient to stop smoking. In fact, in an
observational study of smokers admitted to a coronary
care unit where no formal smoking cessation program was
offered, 32% of survivors were not smoking at the end of
6 months and 25% were not smoking at the end of 1 year
[51]. These results represent a significant change in
smoking behavior and compare very favorably with the
12-month quit rate of 3% seen in the overall population of
smokers using willpower alone [52]. Conversely, threequarters of these cardiovascularly ill patients were still
smoking at the end of 1 year thus highlighting the
difficulty in stopping smoking even under these serious
circumstances [51]. Further analysis revealed that lighter
smokers and those newly diagnosed with coronary heart
disease were the most likely to successfully quit. The
authors concluded that admission to a coronary care unit
may represent a time when smoking habits are particularly susceptible to intervention.

Interventions for smoking cessation in hospitalized

patients were reviewed by Munafo et al. who found in
the pooled data that intensive intervention (inpatient
contact with follow-up for at least 1 month) was
associated with higher quit rates (odds ratio 1.82)
compared with controls [53]. Contact during hospitalization without minimal follow-up was not associated with a
statistically significant increase in quit rate. Results from
two recent studies enrolling patients with CVD are
consistent with the above review. In the first study,
smokers hospitalized for coronary heart disease and given
inpatient intervention followed by monthly follow-up for
a minimum of 5 months had a 57% quit rate versus 37%
(P < 0.01) for a control group [54]. In the second study,
smokers admitted for myocardial infarction or for cardiac
bypass surgery were given brief inpatient intervention
(20 min) without post-hospitalization follow-up [55].
Compared with a control group given standard care
(verbal advice and a booklet) there was no significant
difference in quitting between the two groups (41 versus
37% at 12 months).
The above data strongly emphasize that hospitalized
smokers with CVD be given inpatient intervention with
follow-up upon discharge. On admission, the smoking
status of the patient should be ascertained and documented. For current smokers, tobacco use/dependence
should be included in the admission problem list and on
the discharge summary. Counseling and pharmacotherapy
should be offered to all patients [56]. Follow-up after
discharge is pivotal [53]. Most hospitals with cardiac care
units either have their own smoking cessation programs or
access to external programs. These programs provide a
range from minimal intervention (pamphlets on smoking
cessation) to maximum intervention (individual or
group counseling) [56]. Table 1 provides a summary of
treatment steps.
As an outpatient, the patient with CVD typically sees
their physician on a routine basis. This provides multiple
opportunities for intervention and encouragement. At
every patient visit smoking status should be obtained and
documented. This could be done by a clinic nurse or even
by the receptionist. The physician in turn should advise
every patient who smokes to quit and indicate they
should not wait to attempt quitting [56]. It has been
shown than brief advice from the physician to stop
smoking increases smoking cessation by around 50% [56].
Specific medical reasons (cardiovascular and other) as
well as personal reasons for quitting should be given to
each individual smoker in order to personalize the
message and, hopefully, increase the patients motivation
for quitting. This message should be given every time the
patient appears in the clinic. Although this could be
difficult in that patients not attempting to quit may feel
as though they are not meeting their physicians
expectations, this advice needs to be given and should

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Cardiovascular risks associated with smoking Tonstad and Johnston 511

Table 1

Treatment steps for clinical practice

Inpatient

Outpatient

Inpatient and outpatient

Establish smoking status on admission

For smokers, document smoking on the problem
list and include in the discharge summary
Use health crisis as opportunity for intervention.
Insist on immediate smoking cessation

Obtain smoking status at each visit

Provide brief advice to stop smoking at every visit

Relate current hospitalization to smoking and

recovery to smoking cessation
Enroll in smoking cessation program; program
should be intensive with follow-up after discharge

Educate on the benefits and increased odds of

quitting using support programs
Provide support material at a minimum and,
if patient is willing, refer to a smoking
cessation program
Help patient set a quit date

Use personalized message from both a medical

(e.g. cardiovascular disease) and personal
perspective (e.g. children in household)

Let the patient know you will help them stop smoking
Offer all patients pharmacotherapy, bupropion or
nicotine replacement therapy, unless contraindicated
Provide follow-up for all patients attempting to quit; this
is usually should be done at 1 week following the quit
date and at 1 month; thereafter, follow-up should be
based on patient-specific needs
For quitters during each follow-up contact, congratulate and reinforce continued cessation
Provide continual relapse prevention strategies; most
patients relapse within the first 3 months of quitting
Be aware of potential factors that may lead to relapse:
weight gain, prolonged withdrawal symptoms,
depression; provide intervention when needed
For non-quitters continue to offer help and encourage a
new quit attempt

Data from Fiore et al. [56] and West et al. [60].

Patients should be encouraged to take advantage of both

or either of supportive/behavioral help and pharmacotherapy. They should be informed of the low success rates
when using willpower alone [52]. Proactive telephone,
group and individual counseling have all been shown to
be effective, and when multiple formats are used, quit
rates are increased [56]. Three types of counseling and
behavioral therapy have been found to be especially
effective: provision of practical counseling, provision of
social support as part of treatment, and help in securing
social support outside of treatment [56]. Generally the
more intensive the smoking cessation program the greater
the chance of successful cessation [56].

works on both the noradrenergic and dopaminergic

pathways in the brain to help smokers stop smoking.
Similar to nicotine replacement, bupropion also decreases
craving and withdrawal upon cessation [57]. Nicotine
replacement is available in a number of formulations
including patch, gum, spray, inhaler, and lozenges/
sublingual tablets [56,5860]. The patch and gum are
the most widely used formulations. Table 2 summarizes
pertinent clinical information for the nicotine replacement products and bupropion. Choice of pharmacotherapy should be made jointly between the patient and
physician after discussing the relative advantages of each
therapy. All patients should be screened for any medical
contraindications [56,60]. Bupropion and NRT can also
be used in combination, but this should be reserved for
harder-to-treat smokers and, when using this combination, blood pressure should be monitored [61].

Pharmacotherapy should be offered to all smokers.

Currently, pharmacotherapy can be divided into two
classes, nicotine replacement therapy (NRT) and bupropion HCl sustained-release. Use of pharmacotherapy
approximately doubles a patients chance of quitting
compared with a placebo [56]. Supportive/behavioral help
should always be provided along with pharmacotherapy
[56]. Smoking cessation products typically come with a
supportive stop smoking program. Pharmacotherapy for
smoking cessation is considered to be among the most
cost-effective of all healthcare interventions [58]. The
estimated incremental cost per lifeyear saved is about
d10002400 for NRT and d6401500 for bupropion SR.
Even the higher range for both treatments provides
estimates of cost-effectiveness better than many other
medical interventions.

Potential issues concerning safety in cardiovascularly ill

patients arose following marketing of both the nicotine
patch and bupropion [62,63]. In the case of the nicotine
patch, relatively soon following marketing, media reports
of myocardial infarction in patients receiving the patch
while continuing to smoke appeared. A number of studies
have since evaluated the safety of NRT in patients with
cardiovascular illness and no evidence of cardiovascular
adverse effects were demonstrated [6466]. Although
nicotine has been implicated as a constituent in cigarette
smoke which contributes to cardiovascular illness, studies
have shown that the risk of smoking while using nicotine
replacement therapy is no greater than the risk of
smoking alone. This is due to the flat doseresponse
curve of nicotine and due to only a modestly increased
intake of nicotine compared to smoking alone [4,67].

NRT replaces, in part, the nicotine delivered by

cigarettes and allows the smoker to stop smoking without
experiencing the full withdrawal and craving that would
normally be present. Bupropion is an antidepressant that

Similarly, media reports about the safety of bupropion

arose in Europe concerning a number of adverse
cardiovascular events [62]. Evaluation of existing data,
however, and further study did not find evidence of

be done with understanding and patience. Throughout all

interactions with their patients who smoke, the physician
must remain aware that smoking is addictive [56,57].

Copyright European Society of Cardiology. Unauthorized reproduction of this article is prohibited.

Dependence potential in between

Delivery declines below 51C
nicotine therapies and cigarettes
Patients should not sniff, swallow
Eating and drinking (except
or inhale spray
water) should be avoided 15 min
before and during inhalation

increased risk for these cardiovascular effects and

concluded that the adverse event profile was accurately
represented in the product label. A prescription event
monitoring study in the United Kingdom involving over
11 000 patients was completed and concluded that the
adverse event profile of bupropion was, with few
exceptions, consistent with the previously known safety
profile [68]. In addition, two clinical studies in patients
with cardiovascular disease have been conducted and
demonstrated that bupropion is generally well tolerated
in patients with cardiovascular illness [69,70].
Conclusion

Special considerations

References
1

Chew slowly and then park

gum in cheek; repeat 37 times
Do not drink for 15 min before
and after gum

Screen smokers for predisposition to seizure

Allow at least 8 h between
doses
Second dose should not
be close to bedtime

Use 912 pieces/day

Apply patch to clean non-hairy

skin
If vivid dreams or insomnia
occur do not wear at night

Smoking can cause every major CVD. Regardless of age or

severity of cardiovascular illness, stopping smoking is
beneficial. Patients need to know that as long as they
smoke they are at increased risk, and they should not
delay attempting to quit. Maximal treatment should be
offered including supportive/behavioral help along with
pharmacotherapy. Inpatients should receive intensive
intervention with follow-up. Both nicotine replacement
therapy and bupropion are appropriate choices for the
cardiovascular patient. Patience and understanding of the
nature of tobacco dependence will help in dealing with
the cardiovascularly ill smoker. Repeated attempts to stop
may be required. These attempts need to be encouraged
and help provided on each quit attempt.

Data from Fiore et al. [56] and Shiffman et al. [59].

Local irritation in the mouth,

coughing, rhinitis
Nasal irritation, nasal congestion,
changes in taste and smell

Heartburn and indigestion

from too rapid use
Headache, cough, nausea
and hiccups
Use every 12 h for first 6 weeks,
then reduce
Suck on lozenge like hard
candy and move from side to side
Do not chew
Skin irritation, insomnia

Initiation of treat12 weeks before cessation

ment
attempt
Most common sideInsomnia, dry mouth
effects

Dose

Jaw soreness

Use 4 mg if time in morning to

smoking first cigarette is within
30 min and 2 mg if over 30 min
1 piece every 12 h; no more
than 24 pieces/day
Use 4 mg for heavy smokers

1 patch/day

Usually start with 21 mg but

lower strengths may be used with
lighter smokers
Lower strengths may be used
Maximum 40 doses/day
for tapering
Initiate at time of cessation attempt (patients should not smoke and use nicotine replacement at the same time)

Prescription
Prescription and over the counter
1 mg (0.5 mg delivery to each
4 mg cartridge (80 puffs or
nostril)
inhalations)
12 doses/hour initially increas- Self-titration using between 6
ing as needed
and 16 cartridges per day
Minimum 8 doses/day
Prescription and over the
2 and 4 mg
Prescription and over the
counter 7, 14, and 21 mg
Prescription and over the
counter 2 and 4 mg

Lozenge

Prescription
150 mg sustained-release
tablet
150 mg once daily increasing to 150 mg twice daily

Bupropion HCl sustained

release

Gum

Patch

Availability
Formulation

Table 2

Summary of bupropion and nicotine replacement therapy

Nicotine replacement therapy

Spray

Inhaler

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