European Heart Journal Advance Access originally published online on June 12, 2008
European Heart Journal 2008 29(16):1932-1933; doi:10.1093/eurheartj/ehn275
Smokers paradox or not in heart failure. Just quit
1 Department of Medicine (Cardiology) and Department of Epidemiology and Biostatistics, London Health Sciences Centre/University of Western Ontario, 339 Windermere Rd, London, Ontario N6A 5A5, Canada
2 Faculty of Medicine, University of Ottawa, Ottawa, Canada
3 Division of Prevention and Rehabilitation, University of Ottawa Heart Institute, 40 Ruskin Street, Ottawa, Ontario, K1Y 4W7, Canada
4 Department of Psychology, University of Western Ontario, Ontario, Canada
5 Cardiac Rehabilitation and Secondary Prevention Program, London Health Sciences Centre, Ontario, Canada
* Corresponding author. Tel: +1 519 663 3488, Fax: +1 519 663 3583, Email: nsuskin{at}uwo.ca
This editorial refers to ‘A smoker's paradox in patients hospitalized for heart failure: findings from OPTIMIZE-HF’
by G.C. Fonarow et al., on page 1983
Footnotes
The opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology.
Fonarow et al. have explored the ‘smoker's paradox’ in a novel inception cohort of hospitalized heart failure patients included in the OPTIMIZE-HF registry, by determining the impact of current or recent smoking on outcomes during hospitalization and in the first 60–90 day period following hospital discharge.1 Adjustments for known important potential confounders were performed. Smokers were more likely to have left ventricular systolic dysfunction (59 vs. 51%), were more likely to be male (61 vs. 46%), and had higher B-type natriuretic peptide (BNP) levels (895 vs. 789 pg/mL). However, smokers were much younger (63 vs. 75 years of age), were less likely to have a previous history of heart failure admission (84 vs. 89%), and were less likely to have a diagnosis of diabetes requiring insulin therapy (14 vs. 17%). Despite this, when compared with non-smokers, the risk of in-hospital mortality was 
30% lower for current or recent smokers, while the risk for re-hospitalization or post-discharge mortality was similar between the two groups.
How could this be? Assuming the authors appropriately assembled an inception cohort, correctly classified smokers, and appropriately adjusted for important potential confounders, only one of two conclusions can be drawn: either smoking is somehow ‘protective’ in heart failure patients; or a substantial component of the adverse effects of smoking in heart failure is reversible and has a short half-life (i.e. days) so that ‘enforced’ in-hospital smoking cessation led to an imbalance of beneficial therapies in the smokers (usual therapy plus smoking cessation) compared with their non-smoking cohorts (usual therapies only). The former hypothesis (that smoking is protective) can probably be refuted immediately. There is overwhelming evidence that smoking increases the incidence of heart failure,2 as well as heart failure morbidity and mortality (including sudden death) for those who have heart failure.3,4
It can be argued that there is substantially more merit in the second argument. Constituents of inhaled tobacco damage the cardiovascular system in numerous ways: producing endothelial and platelet dysfunction; enhancing coagulation; increasing heart rate and blood pressure; increasing myocardial oxygen demand and consumption; and inducing vasoconstriction.5,6 Cigarette smoking also significantly increases carboxyhaemoglobin production, impairing oxygen carriage and release, which has a negative inotropic effect, increasing left ventricular end-diastolic pressure.6 Thus the abrupt removal of these deleterious effects of cigarette smoking following hospital admission and enforced smoking cessation, in addition to the provision of the usual heart failure therapies in smokers, might well be expected to ‘outstrip’ the impact of usual therapies alone in non-smokers.
In examining the assumptions mentioned above, it is important to note that the authors classified smokers as ‘having smoked anytime during the previous year’—according to convention set by the Joint Commission.7 This classification has the potential to categorize individuals who were actively smoking on the day of admission and those who had not smoked for 364 days as ‘smokers’. Those who had not been active smokers for many months would not have been able to experience the benefit of enforced in-hospital smoking cessation, yet they were still younger than their non-smoking cohorts, and thus would have been predicted to enjoy the prognostic benefits from being almost a decade younger. The problems associated with the misclassification of smoking status in cohort studies have been noted before. The lack of validated smoking status at follow-up raises the potential for misclassification. The inability to quantify previous smoking exposure (cigarettes per day, pack-years, etc.) also clouds the current analysis. Although we do not know the proportion of individuals classified as smokers who quit within the year prior to admission, the fact that the 60–90 day post-discharge event rate was similar between individuals classified as smokers compared with non-smokers supports the notion that the short-term beneficial effects of enforced in-hospital smoking cessation had run their course, with those who benefitted from it having done so already (and expressed as lower incidence of death or shorter hospital stay), leaving the remaining smokers (some of whom might have resumed smoking post-discharge) and the non-smokers with similar benefits from ‘usual therapies’. Conversely, the decade younger age of smokers was not able to account for a continued benefit on outcome (compared with non-smokers) once the acute benefits of smoking cessation had worn off. More importantly, post-index hospitalization follow-up was only possible in the 35% of the cohort who provided appropriate consent. It is therefore extremely challenging to generalize from these results, particularly given that post-discharge smoking status was not available.
Although the authors adhered to accepted statistical methods in adjusting for potential confounders and covariates, this may not have been sufficient. For example, in the CHARM programme,8 increasing age [hazard ratio (HR) 1.73 per decade over 60 years of age] was a more powerful predictor of death than decreasing ejection fraction (HR 1.13 per 5% decrease below 45); yet both appear to be similarly weighted as continuous predictor variables in the current study. It is possible that using additional procedures to account for the differences in covariates such as propensity matching9 might have accounted for the differences in outcomes between smokers and non-smokers, but this remains unclear.
It could be argued that the main ‘take home’ message from this study is that while smoking is associated with earlier onset and more severe symptoms of heart failure, smoking cessation at the time of hospitalization for heart failure probably has a powerful beneficial effect on heart failure outcomes while in hospital, and thus systematic efforts should be made while patients are in hospital to identify smokers and begin cessation counselling immediately. While smoking cessation is recommended by national organizations involved in the care of cardiac patients,10–12 these guidelines do not specifically address the issues related to smoking cessation for patients hospitalized for acute heart failure. In general, it has been noted that the cardiovascular community has been slow to adopt integrated, systematized approaches to smoking cessation.13,14 The systematic identification and treatment of all admitted patients according to an established protocol offers promise in enhancing the quality of care provided to cardiac patients. One such model with demonstrated efficacy is the ‘Ottawa Model’.15 The Ottawa model, which ensures the identification and documentation of the smoking status of all admitted patients, also mandates the provision of counselling, pharmacotherapy where appropriate, and a 6-month post-discharge follow-up using sophisticated telephone technology; it has been associated with a 15% absolute increase in self-reported cessation 6 and 12 months post-discharge. Systematic approaches to cessation in an acute coronary syndrome population have been associated with a >40% decrease in subsequent re-hospitalization and a 70% reduction in all-cause mortality.16 The benefits of smoking cessation in the treatment of heart failure are clear.4,8 The provision of smoking cessation treatment to all of our cardiac patients in a systematic, organized manner at the time of their admission is long overdue.
Conflict of interest: none declared.
Footnotes
The opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology.
doi:10.1093/eurheartj/ehn210 
References
- Fonarow GC, Abraham WT, Albert NM, Stough WG, Gheorghiade M, Greenberg BH, O'Connor CM, Nunez E, Yancy CW, Young JB. A smoker's paradox in patients hospitalized for heart failure: findings from OPTIMIZE-HF. Eur Heart J (2008) 29:1983–1991. First published on May 15, 2008. doi:10.1093/eurheartj/ehn210.
[Abstract/Free Full Text] - Eriksson H, Svardsudd K, Larsson B, Ohlson LO, Tibblin G, Welin L, Wilhelmsen L. Risk factors for heart failure in the general population: the study of men born in 1913. Eur Heart J (1989) 10:647–656.
[Abstract/Free Full Text] - Kannel WB, Plehn JF, Cupples LA. Cardiac failure and sudden death in the Framingham Study. Am Heart J (1988) 115:869–875.[CrossRef][Web of Science][Medline]
- Suskin N, Sheth T, Negassa A, Yusuf S. Relationship of current and past smoking to mortality and morbidity in patients with left ventricular dysfunction. J Am Coll Cardiol (2001) 37:1677–1682.
[Abstract/Free Full Text] - Nowak J, Murray JJ, Oates JA, FitzGerald GA. Biochemical evidence of a chronic abnormality in platelet and vascular function in healthy individuals who smoke cigarettes. Circulation (1987) 76:6–14.
[Abstract/Free Full Text] - Rabinowitz BD, Thorp K, Huber GL, Abelmann WH. Acute hemodynamic effects of cigarette smoking in man assessed by systolic time intervals and echocardiography. Circulation (1979) 60:752–760.
[Free Full Text] - Joint Commission on Accreditation of Healthcare Organizations. Joint Commission on Accreditation of Healthcare Organizations. Specification manual for national implementation of hospital core measures (2004) Oakbrook.
- Pocock SJ, Wang D, Pfeffer MA, Yusuf S, McMurray JJ, Swedberg KB, Ostergren J, Michelson EL, Pieper KS, Granger CB. Predictors of mortality and morbidity in patients with chronic heart failure. Eur Heart J (2006) 27:65–75.
[Abstract/Free Full Text] - Joffe MM, Rosenbaum PR. Invited commentary. Propensity scores. Am J Epidemiol (1999) 150:327–333.
[Abstract/Free Full Text] - Stone JA, Arthur HM. Canadian Guidelines for Cardiac Rehabilitation and Cardiovascular Disease Prevention, second edition, 2004: Executive summary. Can J Cardiol (2005) 21(Suppl D):3D–19D.[Medline]
- Arnold JMO, Howlett JG, Dorian P, Ducharme A, Giannetti N, Haddad H, Heckman GA, Ignaszewski A, Isaac D, Jong P, Liu P, Mann E, McKelvie RS, Moe GW, Parker JD, Svendsen AM, Tsuyuki RT, O'Halloran K, Ross HJ, Rao V, Sequeira EJ, White M. Canadian Cardiovascular Society Consensus Conference recommendations on heart failure update 2007: prevention, management during intercurrent illness or acute decompensation, and use of biomarkers. Can J Cardiol (2007) 23:21–45.[Medline]
- Swedberg K, Cleland J, Dargie H, Drexler H, Follath F, Komajda M, Tavazzi L, Smiseth OA, Gavazzi A, Haverich A, Hoes A, Jaarsma T, Korewicki J, Lévy S, Linde C, Lopez-Sendon JL, Nieminen MS, Piérard L, Remme WJ, Task Force for the Diagnosis and Treatment of Chronic Heart Failure of the European Society of Cardiology. Guidelines for the diagnosis and treatment of chronic heart failure: executive summary (update 2005): the Task Force for the Diagnosis and Treatment of Chronic Heart Failure of the European Society of Cardiology. Eur Heart J (2005) 26:1115–1140.
[Free Full Text] - Critchley JA, Capewell S. Mortality risk reduction associated with smoking cessation in patients with coronary heart disease: a systematic review. JAMA (2003) 290:86–97.
[Abstract/Free Full Text] - Lightwood J, Fleischmann KE, Glantz SA. Smoking cessation in heart failure: it is never too late. J Am Coll Cardiol (2001) 37:1683–1684.
[Free Full Text] - Reid RD, Pipe AL, Quinlan B. Promoting smoking cessation during hospitalization for coronary artery disease. Can J Cardiol (2006) 22:775–780.[Web of Science][Medline]
- Mohiuddin SM, Mooss AN, Hunter CB, Grollmes TL, Cloutier DA, Hilleman DE. Intensive smoking cessation intervention reduces mortality in high-risk smokers with cardiovascular disease. Chest (2007) 131:446–452.[CrossRef][Web of Science][Medline]
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Related articles in EHJ:
- A smoker's paradox in patients hospitalized for heart failure: findings from OPTIMIZE-HF
- Gregg C. Fonarow, William T. Abraham, Nancy M. Albert, Wendy Gattis Stough, Mihai Gheorghiade, Barry H. Greenberg, Christopher M. O'Connor, Eduardo Nunez, Clyde W. Yancy, and James B. Young
EHJ 2008 29: 1983-1991.[Abstract] [FREE Full Text]
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