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Review |

Mortality Risk Reduction Associated With Smoking Cessation in Patients With Coronary Heart Disease:  A Systematic Review FREE

Julia A. Critchley, MSc, DPhil; Simon Capewell, MD, FRCPE
[+] Author Affiliations

Author Affiliations: Department of Public Health, University of Liverpool, Liverpool, England.


JAMA. 2003;290(1):86-97. doi:10.1001/jama.290.1.86.
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Published online

Context As more interventions become available for the treatment of coronary heart disease (CHD), policy makers and health practitioners need to understand the benefits of each intervention, to better determine where to focus resources. This is particularly true when a patient with CHD quits smoking.

Objective To conduct a systematic review to determine the magnitude of risk reduction achieved by smoking cessation in patients with CHD.

Data Sources Nine electronic databases were searched from start of database to April 2003, supplemented by cross-checking references, contact with experts, and with large international cohort studies (identified by the Prospective Studies Collaboration).

Study Selection Prospective cohort studies of patients who were diagnosed with CHD were included if they reported all-cause mortality and had at least 2 years of follow-up. Smoking status had to be measured after CHD diagnosis to ascertain quitting.

Data Extraction Two reviewers independently assessed studies to determine eligibility, quality assessment of studies, and results, and independently carried out data extraction using a prepiloted, standardized form.

Data Synthesis From the literature search, 665 publications were screened and 20 studies were included. Results showed a 36% reduction in crude relative risk (RR) of mortality for patients with CHD who quit compared with those who continued smoking (RR, 0.64; 95% confidence interval [CI], 0.58-0.71). Results from individual studies did not vary greatly despite many differences in patient characteristics, such as age, sex, type of CHD, and the years in which studies took place. Adjusted risk estimates did not differ substantially from crude estimates. Many studies did not adequately address quality issues, such as control of confounding, and misclassification of smoking status. However, restriction to 6 higher-quality studies had little effect on the estimate (RR, 0.71; 95% CI, 0.65-0.77). Few studies included large numbers of elderly persons, women, ethnic minorities, or patients from developing countries.

Conclusions Quitting smoking is associated with a substantial reduction in risk of all-cause mortality among patients with CHD. This risk reduction appears to be consistent regardless of age, sex, index cardiac event, country, and year of study commencement.

Figures in this Article

The causative relationship between smoking and coronary heart disease (CHD) is well established, with relative risks (RRs) or odds ratios (ORs) estimated between 1.5 to 3 or higher.15 Observational studies have estimated that smoking cessation reduces the risk of subsequent mortality and further cardiac events among patients with CHD by as much as 50%.69 Stopping smoking therefore may have a greater effect on reducing the risk of mortality among patients with CHD who smoke than the effect of any other intervention or treatment. Simulation models in the United States have demonstrated that quitting smoking has short-term economic as well as health benefits.10

However, the speed and magnitude of risk reduction of mortality when a smoker quits have been debated.11 Some authors suggest that risk can decline to that of a lifelong nonsmoker,12,13 and others maintain some "remnant risk" always remains.14 Moreover, some studies have found large reductions in risk after only 2 to 3 years.9,10,12 Other studies estimate that risk is still higher than that in lifelong nonsmokers even 20 years after quitting.14,15 The British Regional Heart Study found essentially no reduction in risk for ex-smokers after 7 years.16 However, at 18 years, the Whitehall cohort showed no increase risk of mortality among ex-cigarette smokers (≤20 cigarettes/d) compared with never smokers.17

A number of possible explanations for disagreement between studies exist. The relationship between smoking cessation and mortality may depend on many other factors, such as age, sex, baseline risk from other CHD risk factors, and severity of disease. Survival is generally higher for patients with angina18,19 than for those after myocardial infarction (MI)19,20 or heart failure.2123 Furthermore, smoking may be a more powerful risk factor for patients with MI than for those with angina pectoris.24,25

Differences in the accuracy of measurement of exposure status also may account for some uncertainty in the evaluation of risk of mortality. Prospective cohort studies may underestimate the risk reduction associated with stopping smoking, as an unknown proportion of quitters may start again, hence becoming misclassified as ex-smokers.14,15,26 Furthermore, some patients originally classified as smokers will subsequently stop. Case-control studies may equally be subject to a number of additional biases, particularly for selection and recall. Other aspects of study quality, particularly the degree of control of confounding variables, or differences in the baseline risk among quitters and those who continue to smoke, also may be important.

As more interventions become available for the treatment of CHD, it is increasingly important to quantify the risk reduction associated with each. Policy makers need a better understanding of the costs and benefits of each intervention, to better determine where to focus efforts and scarce resources. Therefore, we conducted a systematic review of the benefits of smoking cessation in patients with CHD.

Participants

Studies that had patients diagnosed with CHD (ie, previous MI or stable or unstable angina) were included. Ideally, CHD in the included studies should be defined according to the guidelines by the World Health Organization,27 but we did include studies that gave no explicit definition of CHD. Smokers ideally should be defined in the article, such as those who smoke regularly (eg, smoking at least on average 1 cigarette/d during the preceding year). Not all studies reported precise definitions of smoking or even smoking cessation.

Studies

Any prospective cohort study was included if (1) the cohort included current smokers at baseline; (2) smoking status was measured to ascertain which smokers had quit; (3) the cohort was followed-up for at least 2 years; and (4) the study reported all-cause mortality as an outcome measure.

Outcome Measures

The primary outcome was total mortality rate for each group. Secondary outcomes included any further cardiovascular event, either fatal or nonfatal; CHD; or stroke, which ideally should be defined according to the International Classification of Disease, Ninth Edition28 (eg, codes 410-414).

Data Sources

The databases searched to obtain the articles included MEDLINE (1966 to February 2003), EMBASE (1980 to February 2003), Science Citation Index (April 26, 2003), Cochrane Controlled Trial Register (Issue 2 of 2003), CINAHL (1982 to April 2003), PsychLit (1971 to April 2003), Dissertation Abstracts (1861 to March 2003), BIDS ISI (Bath Information and Data Services-Index to Scientific and Technical Proceedings) (1982 to June 29, 2000), and the United Kingdom National Research Register (CD-ROM version, Issue 1 of 2003) (the information is available in appendix 1 from the authors' Web site at: http://www.liv.ac.uk/PublicHealth/sc/jama_article_appendices.html). The search was not restricted by language of articles. The search strategy used both key words and MeSH term searches and took the form of (CHD or synonyms) and (smoking cessation or smoking or synonyms) and ((mortality or synonyms) OR (Cochrane RCT filter)).

Reference lists of retrieved articles were inspected (the information is available in appendix 2 from the authors' Web site). Sixty-one large cohort studies concerned with cardiovascular risk were identified from a log maintained by the Prospective Studies Collaboration29 and from any relevant publications. Authors of these studies were contacted to assess whether any relevant research had been carried out (see appendix 3, authors' Web site).

Study Selection and Data Extraction

Based on brief study details (eg, title, abstract) of identified articles, studies were excluded if they were not relevant. Two reviewers (J.A.C. and S.C.) independently assessed studies to determine eligibility and independently carried out data extraction using a prepiloted, standardized form. Any disagreement was resolved by discussion. Several authors were contacted to clarify details or provide additional information.

Criteria Used to Assess Quality

Unlike randomized controlled trials, no generally accepted lists of appropriate quality criteria for observational studies are available.3032 Rather than producing a simple quality score, which might be arbitrary, specific aspects of quality, such as control of confounding, minimization of selection biases, and sample size were used to assess the studies.

Data Synthesis

All analyses were carried out using RevMan 4.1 software33 or STATA.34 Studies were pooled using the DerSimonian and Laird random-effects model.35

Description of Studies

Of the 665 articles screened, 90 were considered in depth for inclusion, but 70 were excluded because they did not meet inclusion criteria or were duplicate publications (Figure 1) (see appendix 4, authors' Web site). Twenty studies7,8,19,3652 met all inclusion criteria and had sufficient data available (see appendix 4, authors' Web site). Agreement between the 2 reviewers for study eligibility was very high (weighted κ = 0.9). These studies had a total sample size of 12 603 smokers at baseline, of whom 5659 ceased smoking and 6944 continued to smoke.

Figure 1. Flow Chart of the Study Selection Process
Graphic Jump Location

The majority of studies commenced data collection in the late 1960s or in the 1970s (Table 1). Most were conducted in Western countries, with 1 from Poland36 and 1 from India.37 Women were underrepresented (20% of cases). Six studies included only men8,36,38,41,43,45 and 1 small study was limited to women.7 In most of the studies, the mean age of smokers was approximately 55 years, which was younger than the mean age of the general population of patients with CHD.20 Reported cessation rates varied from 28% to 77% in the primary studies, with a mean of 45% (see appendix 5, authors' Web site).

Table Graphic Jump LocationTable 1a. Characteristics of the Studies Included

Not all studies clearly stated when smoking cessation occurred. Some studies reported that patients who quit did so quickly after their CHD diagnosis or event.19,41,45,47 However, some studies only reported changes in smoking status at later follow-up appointments (generally at 3, 6, or 12 months after the CHD event).36,38,42,43,50,52 Evidence from some of the primary studies,19,41 and other studies not included in this review,18 suggested that patients who are likely to quit do so rapidly after their CHD diagnosis, as this is the main motivator for stopping.53

Mean length of follow-up ranged from 2 years38 to 26 years,39 with a mean of 5 years. The majority of studies included followed-up hospital case series. Most well-known, prospective, general-population CHD cohorts (such as the Whitehall17 or the British Regional Heart Study16) (see appendix 3, authors' Web site) cannot address whether there was a reduction in mortality when a patient with CHD quits smoking. Ususally this is because they are unable to ascertain whether ex-smokers quit before or after experiencing a cardiac event. These studies therefore have not been included. Thirteen studies7,8,19,36,38,41,45,4752 followed up patients with MI only, and 4 studies39,40,42,44 included patients in which some underwent coronary artery bypass graft (CABG) surgery or angioplasty. Of the 4 studies, 1 was a large (N = 4165) and relatively high-quality study (see "Sensitivity Analyses" for evaluation of quality).40 The other 3 studies included patients with MI and with other coronary diseases.37,43,46

Quality Assessment of Included Studies

Quality assessment criteria (Table 2) included the sample size, clear definitions of the cardiac events, smoking and smoking cessation, whether smoking status was confirmed during follow-up or validated, the adequacy of control of confounding, and minimization of selection biases.

Table Graphic Jump LocationTable 2a. Quality Assessments of Studies Included in the Systematic Review

The number of smokers at baseline in the primary studies varied from 77 to 4165. Most studies had small sample sizes and only 8 contained more than 500 smokers at baseline.19,36,3842,45 The Coronary Artery Surgery Study included a large sample (N = 4165) of patients with angiographically proved coronary artery disease who underwent CABG surgery.40 The other larger studies contained more than 900 smokers who were male patients after MI from Gothenburg, Sweden, from 1968 to 197741; male patients after MI in the UK Diet and Reinfarction Trial, from the mid-1980s38; male patients with a first MI between 1968 and 1975 from Poland36; and male patients undergoing angioplasty at the Mayo clinic between 1979 and 1995.42

Minimization of Selection Biases

Losses to follow-up for mortality were generally small (Table 2). Most studies, however, recruited patients some weeks after their first cardiac event and frequently did not report how many smokers and nonsmokers died before entry into the study. The pooled RR in this review is therefore best regarded as an estimate of the reduction in risk for quitters who survived the initial cardiac event. A sensitivity analysis was carried out including only those studies that were able to ascertain smoking status rapidly (within 1 month) of the initial cardiac event.19,41,45,47 The risk reduction estimated by this analysis (RR, 0.63; 95% CI, 0.53-0.74) and the analysis including all 20 studies (RR, 0.64; 95% CI, 0.58-0.71) did not differ significantly.

Definitions of Events and Smoking Status

Most studies defined the index cardiac event, but they did not clearly define who was considered a current smoker or a quitter (Table 2). Eleven7,8,41,4350 of the 20 studies attempted to verify smoking status during the follow-up time period (ie, whether or not the authors contacted patients during the follow-up period to check their smoking status. Mostly this was by self-report); only 2 attempted to assess smoking status biochemically.41,43

Control of Confounding

Assessing control of confounding was carried out independently by 2 reviewers using prespecified criteria. These criteria included age, sex, socioeconomic status, education, secondary prevention drug treatments, measurement and levels of other CHD risk factors, history of previous MI or angina, comorbidities, severity of the initial cardiac event (ie, measures reported in the individual studies, eg, severity of infarct, presence of left ventricular function) or any prognostic indices (see appendix 6, author's Web site). Control of confounding was classified as poor if little or no attempt was made to measure or control for known basic confounders such as age and sex (Table 2). Adequate control considered at least these basic confounders, and good control considered the majority of the clinical variables previously listed. Most of the studies were old, so little information on modern secondary preventive therapies, such as prescribing β-blockers, was reported. Only 1 study included any information on psychosocial outcomes.19

Reviewer agreement was good (weighted κ = 0.72). Control of confounding was poor in 9 studies (Table 2).38,43,4652 Only 5 studies were classified as good.7,19,40,41,44 Many of the studies provided only crude estimates of the reduction in mortality (Table 3).

Table Graphic Jump LocationTable 3a. Summary of Principle Results
Total Mortality

A random-effects meta-analysis was carried out, and the pooled RR for all 20 studies was 0.64 (95% CI, 0.58-0.71) (Figure 2). Although all 95% CIs for the primary studies overlapped, some heterogeneity was observed (χ2 for heterogeneity, P = .009), hence the need for the random-effects meta-analysis. The pooled estimate was dominated by the 3 larger CABG studies39,40,44 which together provided about half the total patients. However, the results did not differ when the analysis was limited to 13 studies, including only patients after having an MI (RR, 0.63; 95% CI, 0.56-0.72).7,8,19,36,7,8,19,36,38,41,45,4752

Figure 2. Pooled Relative Risks of Mortality Reduction When Patients With CHD Stop Smoking: Random-Effects Meta-analysis of All 20 Studies
Graphic Jump Location
CHD indicates coronary heart disease; RR, relative risk. χ2 for heterogeneity, P = .009.

A Begg funnel plot was created to compare the log OR with the SE of the log OR of the 20 studies, revealing possible publication bias. Larger, more precise studies with smaller SEs tended to find smaller reductions in risk of mortality on quitting smoking than did smaller studies with fewer deaths, and therefore larger SEs (P = .006) (Figure 3).

Figure 3. Begg Funnel Plot
Graphic Jump Location
Log odds ratio vs SE of the log odds ratio for each study are presented. The horizontal solid line indicates the log odds ratio of the pooled estimate; the sloping dashed lines are expected 95% confidence intervals. The funnel plot appears asymmetric and shows that larger, more precise studies with smaller SEs tended to find smaller reductions in risk of mortality on quitting smoking than smaller studies with fewer deaths (P = .006).
Sensitivity Analyses

Sensitivity analyses were carried out, as planned, using the following 3 criteria: (1) an initial sample size of at least 500 smokers at baseline; (2) at least 85% of the initial case series included in the analyses; and (3) adequate or good control of confounding. Only 6 of the 20 studies met all these criteria.36,3942,45 However, the pooled RR for these 6 studies (RR, 0.71; 95% CI, 0.65-0.77) was essentially the same as for all 20 (RR, 0.64; 95% CI, 0.58-0.71).

Morbidity Outcomes

Nonfatal Myocardial Reinfarctions. Eight studies presented information on nonfatal myocardial reinfarctions(Table 3; Figure 4; see appendix 5, authors' Web site).7,8,40,41,44,47,48,50 The pooled RR for nonfatal reinfarctions was 0.68 (95% CI, 0.57-0.82). Ideally, we would analyze a combined outcome of cardiac deaths and nonfatal reinfarction, but it was not possible to extract this information as reinfarctions were mostly reported as total events rather than for individuals.

Figure 4. Pooled Relative Risks of Reduction in Nonfatal Myocardial Reinfarction When Patients With CHD Stop Smoking: Random-Effects Meta-analysis of 8 Studies
Graphic Jump Location
CHD indicates coronary heart disease; RR, relative risk.

Other Outcomes. A few studies reported other cardiovascular outcomes, such as other cardiovascular disease (unspecified), new angina cases, or stroke/transient ischemic attack (see appendix 5, authors' Web site).

This systematic review strongly suggests that quitting smoking is associated with reduced risk of total mortality. The pooled crude RR was 0.64 (95% CI, 0.58-0.71). This 36% reduction appears at least as great as other secondary preventive therapies, such as use of statins for lowering cholesterol levels (a 29% reduction),54 aspirin (15%),55 β-blockers (23%),56 or angiotenin-converting enzyme inhibitors (23%),57 which have received greater attention in recent years. Moreover, evidence from the United States and the United Kingdom has shown that quitting smoking has considerable short-term economic as well as health benefits because of reductions in hospitalizations for MI and stroke.10,58

This review was not able to assess how quickly the risk of mortality was reduced. Only 20 studies were included, and most of these had a mean length of follow-up between 3 and 7 years.7,8,19,36,43,4549 One possible implication is that the risk reduction occurs relatively quickly after stopping smoking, as early as 2 years (the minimum follow-up period for the review), and hence greater risk reductions over time are not observed. Another possibility is increasing misclassification with time, as discussed below.

The risk reduction associated with quitting smoking appears relatively consistent, regardless of the type of index cardiac event or years in which the study was conducted. Other measured features of the studies, such as the age, population, or aspects of quality, did not appear to influence the results. However, relatively few studies have included many women, ethnic minorities, or older patients. The majority of studies were also conducted in Western countries. The generalizability to these groups is therefore uncertain.

Limitations of Review

Observational Data. This review has a number of limitations. First, we are considering observational data. Smokers who quit after MI may well differ from those who continue to smoke in a number of ways, including their age, sex, socioeconomic status, psychological characteristics, and other factors. However the direction of this potential difference is not obvious. Some studies found that subsequent mortality risk in quitters was higher,19,41 lower,8,46,50 or showed little difference from those who continued to smoke.37,39,42,47,49 The one study that considered psychosocial factors in detail found these factors had little influence on rates of quitting smoking, or mortality.19

Second, meta-analysis was carried out using crude estimates. The 10 studies that presented adjusted outcome measures for total mortality used markedly different adjustment methods (some used Cox hazards regression models and others used Mantel-Haenszel stratification or logistic regression) to consider different covariates and were measured in varying ways.7,8,19,37,3942,44,45 However, results of these 10 studies found surprisingly small differences between adjusted and crude estimates (Table 3) (table of confounders are in appendix 6, authors' Web site). If anything, the risk reduction appeared greater after adjustment in most studies, suggesting our estimates may slightly underestimate the true risk reduction associated with smoking cessation in patients with CHD.

Misclassification. A further limitation is the potential for bias from misclassification of smoking status. Patients who continued to smoke may have falsely claimed cessation. Only 2 studies attempted to validate self-reported smoking status biochemically and only then on a subset of patients.41,43 Although self-reporting appears generally accurate when compared with biochemical markers of tobacco inhalation,59 it may be less accurate for patients with CHD.60,61

Not all the primary studies clearly stated when smoking cessation occurred among smokers who quit. However, the magnitude of risk reduction among studies able to report that quitting took place rapidly after the cardiac event (RR, 0.63; 95% CI, 0.53-0.74) compared with that from all studies (RR, 0.64; 95% CI, 0.58-0.71) was the same. This suggests that most smokers who quit do so quickly after their CHD diagnosis.

A further potential for misclassification arises over time. Many studies relied on baseline assessments of smoking status only. Clearly, some patients who had reported quitting might have started again.9,62 Conversely, patients who had not initially stopped smoking might have quit later on, and thus be erroneously regarded as continuers. Such nondifferential misclassification may dilute the differences between the 2 groups and therefore underestimate the true RR. Only 3 of the studies incorporated more than 1 follow-up and excluded patients who reported mixed smoking histories (ie, those who quit smoking after their cardiac event but then started smoking again later on, or those who quit did not quit initially, but did later on).41,45,52 The risk reduction in these 3 studies was not statistically significantly different from that in all 20 studies (RR, 0.73; 95% CI, 0.63-0.86).

Our analyses were repeated assuming that an arbitrary 10% of those who reported to have ceased smoking actually had continued. In this case, the pooled crude RR would be reduced slightly to 0.61 (95% CI, 0.54-0.68).

As with any systematic review, there is always a possibility of publication bias, as suggested by the funnel plot (Figure 3).63 However, exclusion of the smaller studies in a sensitivity analysis made essentially no difference to the pooled RR.

Statistical pooling of RR for observational data is itself controversial because of the many biases that can arise in observational studies, compared with those in randomized controlled trials.63 It has been argued that presenting a single pooled estimate without additional detail may give a simple statistic that could be misleading.63 However, a single summary statistic is highly appealing for clinicians and other health care professionals working with cardiac patients. Furthermore, these studies showed relatively little heterogeneity, particularly for the sensitivity analysis of the 6 higher-quality studies (χ2 for heterogeneity, P = .51). The implication is that the risk reduction associated with quitting smoking in these studies is essentially the same, regardless of the differences between these studies in terms of factors, such as the type of index cardiac event (MI, CABG, angioplasty, or other) and the time period during which patients were recruited.

Given the overwhelming evidence of the benefits of stopping smoking and the growing evidence of the best methods of helping patients to achieve this goal, it is unlikely that substantial further work exploring the magnitude or speed of effect of smoking cessation is needed. People who stop smoking following onset of CHD or after undergoing revascularization have a considerably lower risk of death. Advice and support for smoking cessation should be provided routinely to all patients with a diagnosis of CHD.

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van Domburg RT, van Berkel TFM, Meeter K, Veldkamp RF, van Herwerden LA, Bogers AJJC. Smoking cessation reduces mortality after coronary artery bypass surgery: a 20-year follow-up study.  J Am Coll Cardiol.2000;36:878-883.
PubMed
Vlietstra RE, Kronmal RA, Oberman A, Frye RL, Killip T. Effect of cigarette smoking on survival of patients with angiographically documented coronary artery disease: report from the CASS registry.  JAMA.1986;255:1023-1027.
PubMed
Aberg A, Bergstrand R, Johansson S.  et al.  Cessation of smoking after myocardial-infarction—effects on mortality after 10 years.  Br Heart J.1983;49:416-422.
PubMed
Hasdai D, Garratt KN, Grill DE, Lerman A, Holmes-DR J. Effect of smoking status on the long-term outcome after successful percutaneous coronary revascularization.  N Engl J Med.1997;336:755-761.
PubMed
Daly LE, Mulcahy R, Graham IM, Hickey N. Long term effect on mortality of stopping smoking after unstable angina and myocardial infarction.  BMJ Clin Res Ed.1983;287:324-326.
Voors AA, van Brussel BL, Plokker HW.  et al.  Smoking and cardiac events after venous coronary bypass surgery: a 15-year follow-up study.  Circulation.1996;93:42-47.
PubMed
Salonen JT. Stopping smoking and long-term mortality after acute myocardial infarction.  Br Heart J.1980;43:463-469.
PubMed
Hallstrom AP, Cobb LA, Ray R. Smoking as a risk factor for recurrence of sudden cardiac arrest.  N Engl J Med.1986;314:271-275.
PubMed
Perkins J, Dick TB. Smoking and myocardial infarction: secondary prevention.  Postgrad Med J.1985;61:295-300.
PubMed
Sparrow D, Dawber TR. The influence of cigarette smoking on prognosis after a first myocardial infarction: a report from the Framingham Study.  J Chronic Dis.1978;31:425-432.
PubMed
Tofler GH, Muller JE, Stone PH, Davies G, Davis VG, Braunwald E. Comparison of long-term outcome after acute myocardial infarction in patients never graduated from high school with that in more educated patients: Multicenter Investigation of the Limitation of Infarct Size (MILIS).  Am J Cardiol.1993;71:1031-1035.
PubMed
Herlitz J, Bengtson A, Hjalmarson A, Karlson BW. Smoking habits in consecutive patients with acute myocardial infarction: prognosis in relation to other risk indicators and to whether or not they quit smoking.  Cardiology.1995;86:496-502.
PubMed
Baughman KL, Hutter-AM J, DeSanctis RW, Kallman CH. Early discharge following acute myocardial infarction: long-term follow-up of randomized patients.  Arch Intern Med.1982;142:875-878.
PubMed
Hedback B, Perk J, Wodlin P. Long-term reduction of cardiac mortality after myocardial infarction: 10-year results of a comprehensive rehabilitation programme.  Eur Heart J.1993;14:831-835.
PubMed
Hajek P, Taylor TZ, Mills P. Preventing relapse to smoking in cardiac rehabilitation patients—a controlled trial of brief intervention by cardiac rehab nurses.  BMJ.2002;324:87-89.
PubMed
Pignone M, Phillips C, Mulrow C. Use of lipid lowering drugs for primary prevention of coronary heart disease: meta-analysis of randomised trials.  BMJ.2000;321:983-986.
PubMed
 Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients  BMJ.2002;324:71-86.
PubMed
Freemantle N, Cleland J, Young P, Mason J, Harrison J. beta Blockade after myocardial infarction: systematic review and meta regression analysis.  BMJ.1999;318:1730-1737.
PubMed
Flather MD, Yusuf S, Kober L.  et al.  Long-term ACE-inhibitor therapy in patients with heart failure or left-ventricular dysfunction: a systematic overview of data from individual patients: ACE-Inhibitor Myocardial Infarction Collaborative Group.  Lancet.2000;355:1575-1581.
PubMed
Naidoo B, Stevens W, McPherson K. Modelling the short term consequences of smoking cessation in England on the hospitalisation rates for acute myocardial infarction and stroke.  Tob Control.2000;9:397-400.
PubMed
Patrick DL, Cheadle A, Thompson DC, Diehr P, Koepsell T, Kinne S. The validity of self-reported smoking: a review and meta-analysis.  Am J Public Health.1994;84:1086-1093.
PubMed
Woodward M, Tunstall-Pedoe H. Biochemical evidence of persistent heavy smoking after a coronary diagnosis despite self-reported reduction: analysis from the Scottish Heart Health Study.  Eur Heart J.1992;13:160-165.
PubMed
Wilcox RG, Hughes J, Roland J. Verification of smoking history in patients after infarction using urinary nicotine and cotinine measurements.  BMJ.1979;2:1026-1028.
PubMed
Skaar KL, Tsho JY, McClure JB.  et al.  Smoking cessation 1: an overview of research.  Behav Med.1997;23:5-13.
PubMed
Egger M, Schneider M, Davey-Smith G. Spurious precision? meta-analysis of observational studies.  BMJ.1998;316:140-144.
PubMed

Figures

Figure 1. Flow Chart of the Study Selection Process
Graphic Jump Location
Figure 2. Pooled Relative Risks of Mortality Reduction When Patients With CHD Stop Smoking: Random-Effects Meta-analysis of All 20 Studies
Graphic Jump Location
CHD indicates coronary heart disease; RR, relative risk. χ2 for heterogeneity, P = .009.
Figure 3. Begg Funnel Plot
Graphic Jump Location
Log odds ratio vs SE of the log odds ratio for each study are presented. The horizontal solid line indicates the log odds ratio of the pooled estimate; the sloping dashed lines are expected 95% confidence intervals. The funnel plot appears asymmetric and shows that larger, more precise studies with smaller SEs tended to find smaller reductions in risk of mortality on quitting smoking than smaller studies with fewer deaths (P = .006).
Figure 4. Pooled Relative Risks of Reduction in Nonfatal Myocardial Reinfarction When Patients With CHD Stop Smoking: Random-Effects Meta-analysis of 8 Studies
Graphic Jump Location
CHD indicates coronary heart disease; RR, relative risk.

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PubMed
van Domburg RT, van Berkel TFM, Meeter K, Veldkamp RF, van Herwerden LA, Bogers AJJC. Smoking cessation reduces mortality after coronary artery bypass surgery: a 20-year follow-up study.  J Am Coll Cardiol.2000;36:878-883.
PubMed
Vlietstra RE, Kronmal RA, Oberman A, Frye RL, Killip T. Effect of cigarette smoking on survival of patients with angiographically documented coronary artery disease: report from the CASS registry.  JAMA.1986;255:1023-1027.
PubMed
Aberg A, Bergstrand R, Johansson S.  et al.  Cessation of smoking after myocardial-infarction—effects on mortality after 10 years.  Br Heart J.1983;49:416-422.
PubMed
Hasdai D, Garratt KN, Grill DE, Lerman A, Holmes-DR J. Effect of smoking status on the long-term outcome after successful percutaneous coronary revascularization.  N Engl J Med.1997;336:755-761.
PubMed
Daly LE, Mulcahy R, Graham IM, Hickey N. Long term effect on mortality of stopping smoking after unstable angina and myocardial infarction.  BMJ Clin Res Ed.1983;287:324-326.
Voors AA, van Brussel BL, Plokker HW.  et al.  Smoking and cardiac events after venous coronary bypass surgery: a 15-year follow-up study.  Circulation.1996;93:42-47.
PubMed
Salonen JT. Stopping smoking and long-term mortality after acute myocardial infarction.  Br Heart J.1980;43:463-469.
PubMed
Hallstrom AP, Cobb LA, Ray R. Smoking as a risk factor for recurrence of sudden cardiac arrest.  N Engl J Med.1986;314:271-275.
PubMed
Perkins J, Dick TB. Smoking and myocardial infarction: secondary prevention.  Postgrad Med J.1985;61:295-300.
PubMed
Sparrow D, Dawber TR. The influence of cigarette smoking on prognosis after a first myocardial infarction: a report from the Framingham Study.  J Chronic Dis.1978;31:425-432.
PubMed
Tofler GH, Muller JE, Stone PH, Davies G, Davis VG, Braunwald E. Comparison of long-term outcome after acute myocardial infarction in patients never graduated from high school with that in more educated patients: Multicenter Investigation of the Limitation of Infarct Size (MILIS).  Am J Cardiol.1993;71:1031-1035.
PubMed
Herlitz J, Bengtson A, Hjalmarson A, Karlson BW. Smoking habits in consecutive patients with acute myocardial infarction: prognosis in relation to other risk indicators and to whether or not they quit smoking.  Cardiology.1995;86:496-502.
PubMed
Baughman KL, Hutter-AM J, DeSanctis RW, Kallman CH. Early discharge following acute myocardial infarction: long-term follow-up of randomized patients.  Arch Intern Med.1982;142:875-878.
PubMed
Hedback B, Perk J, Wodlin P. Long-term reduction of cardiac mortality after myocardial infarction: 10-year results of a comprehensive rehabilitation programme.  Eur Heart J.1993;14:831-835.
PubMed
Hajek P, Taylor TZ, Mills P. Preventing relapse to smoking in cardiac rehabilitation patients—a controlled trial of brief intervention by cardiac rehab nurses.  BMJ.2002;324:87-89.
PubMed
Pignone M, Phillips C, Mulrow C. Use of lipid lowering drugs for primary prevention of coronary heart disease: meta-analysis of randomised trials.  BMJ.2000;321:983-986.
PubMed
 Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients  BMJ.2002;324:71-86.
PubMed
Freemantle N, Cleland J, Young P, Mason J, Harrison J. beta Blockade after myocardial infarction: systematic review and meta regression analysis.  BMJ.1999;318:1730-1737.
PubMed
Flather MD, Yusuf S, Kober L.  et al.  Long-term ACE-inhibitor therapy in patients with heart failure or left-ventricular dysfunction: a systematic overview of data from individual patients: ACE-Inhibitor Myocardial Infarction Collaborative Group.  Lancet.2000;355:1575-1581.
PubMed
Naidoo B, Stevens W, McPherson K. Modelling the short term consequences of smoking cessation in England on the hospitalisation rates for acute myocardial infarction and stroke.  Tob Control.2000;9:397-400.
PubMed
Patrick DL, Cheadle A, Thompson DC, Diehr P, Koepsell T, Kinne S. The validity of self-reported smoking: a review and meta-analysis.  Am J Public Health.1994;84:1086-1093.
PubMed
Woodward M, Tunstall-Pedoe H. Biochemical evidence of persistent heavy smoking after a coronary diagnosis despite self-reported reduction: analysis from the Scottish Heart Health Study.  Eur Heart J.1992;13:160-165.
PubMed
Wilcox RG, Hughes J, Roland J. Verification of smoking history in patients after infarction using urinary nicotine and cotinine measurements.  BMJ.1979;2:1026-1028.
PubMed
Skaar KL, Tsho JY, McClure JB.  et al.  Smoking cessation 1: an overview of research.  Behav Med.1997;23:5-13.
PubMed
Egger M, Schneider M, Davey-Smith G. Spurious precision? meta-analysis of observational studies.  BMJ.1998;316:140-144.
PubMed
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