(Circulation. 2002;105:e55.)
© 2002 American Heart Association, Inc.
Correspondence |
Paradoxical Clinical Value of Another Smoker’s Paradox
First Cardiac Department of Evaggelismos Hospital, Athens, Greece
Cardiac Department of 251 Hellenic Airforce Aviation Medical Center, Athens, Greece
Professor of Cardiology of Athens University, Director of Cardiac Department of Athens University, Hippokration Hospital, Athens, Greece
To the Editor:
Dr Cohen and coworkers, based on data derived from 9 multicenter trials, have recently reported in the Circulation that the rate of target lesion revascularization (TLR) in patients undergoing contemporary percutaneous coronary intervention (PCI) was significantly lower in smokers despite the lack of differences regarding angiographic restenosis.1 The subtitle of the article questions the possible existence of "another smoker’s paradox."
Indeed, the dissociation between clinical and angiographic restenosis could have been related to "reduced sensitivity" to restenosis by smokers as the authors hypothesized, but this phenomenon may be also mediated by uncontrolled factors, such as the imbalances in access to advanced medical care because of socioeconomic differences related to smoking status. But, whatever the underlying mechanisms, the existence of paradoxical effects related to smoking status is still questionable. Furthermore, although the authors do briefly discuss the clinical value of the observed adverse effects of smoking on mortality after PCI, regardless of the rate of TLR, the title, the abstract, and the main part of the manuscript may lead inexperienced readers to misunderstandings. Actually, the markedly increased multivariate relative risk of death at 1 year (RR=1.8, P=0.02) associated with smoking is not mentioned in the abstract and has not been extensively discussed by the authors, especially in relation to the need for TLR.
The term Smoker’s Paradox has been associated in the literature with the seemingly improved survival of smokers after acute myocardial infarction. However, the vast majority of these studies did not include appropriate adjustment for confounding factors and were based on secondary analyses of data derived in randomized trials, which had enrolled highly selected populations. The existence of the Smoker’s Paradox has been recently refuted in the study by Gottlieb et al2 and in our study.3 Both these studies were based on countrywide registries of consecutive, unselected patients with acute myocardial infarction and included multivariate analysis adjusting for the main confounding factors. Thus, the use of the term "smoker’s paradox" itself does not seem to be fully justified.
The study by Cohen and coworkers may unintentionally promote the misleading use of this term and most importantly might lead the public to misunderstandings. In the case of Smoker’s Paradox, our duty to clarify and emphasize the nonparadoxical effects of smoking on cardiovascular mortality and morbidity, including the effects of smoking on prognosis after percutaneous coronary interventions, keeps pace with respect for accurate terminology.
References
1.
Cohen DJ, Doucet M, Cutlip DE, et al. Impact of smoking on clinical and angiographic restenosis after percutaneous coronary intervention: another smoker’s paradox? Circulation. 2001; 104: 773–778.
2. Gottlieb S, Boyko V, Zahger D, et al. Smoking and prognosis after acute myocardial infarction in the thrombolytic era. J Am Coll Cardiol. 1996; 28: 1506–1513.[Abstract]
3.
Andrikopoulos GK, Richter DJ, Dilaveris PE, et al. In-hospital mortality of habitual cigarette smokers after acute myocardial infarction. The smoker’s paradox in a countrywide study. Eur Heart J. 2001; 22: 776–784.
Response
Harvard Clinical Research Institute, Harvard Medical School, Boston, Mass
Dr Andrikopoulos and colleagues are concerned that our title "Impact of smoking on clinical and angiographic restenosis: another smoker’s paradox?"1 may have been misleading to the uninitiated reader. As they correctly note, the original use of the term "smoker’s paradox" referred to the finding of reduced long-term mortality after acute myocardial infarction in smokers compared with nonsmokers, which was explained largely by confounding by age.2,3 In our study, the "other smoker’s paradox" to which we referred was the observation that smokers have a reduced incidence of clinical restenosis after percutaneous coronary revascularization. In this situation, simple statistical confounding did not explain this apparent "benefit" of smoking, which was explained by both reduced sensitivity to restenosis on the part of smokers and by the greater reluctance of smokers to seek medical attention when such signs and symptoms appear. Indeed, in the subset of our cohort who underwent protocol-mandated angiographic follow-up, there was no evidence of reduced angiographic restenosis among smokers (adjusted relative risk=0.91, 95% CI 0.75 to 1.11). Thus, the "smoker’s paradox" to which our title alludes is distinctly different from that seen after acute myocardial infarction and has a mechanism substantially more complex than simple statistical confounding. Although these important details were provided in an earlier version of the manuscript, they were later removed because of space constraints. Although the subtitle of our paper was intended to convey these important differences, we agree that if one only read the title and not the Results and Discussion, our findings could be easily misconstrued.
Finally, we agree fully with Dr Andrikopoulos that our study confirms the adverse consequences of smoking on long-term survival after percutaneous coronary intervention (PCI). Since this effect is well-recognized and has been previously described, it was not the focus of our article. Nonetheless, we emphasized this finding in our conclusion and, consequently, the importance of efforts to promote smoking cessation in all patients undergoing PCI.
References
1. Cohen DJ, Doucet M, Cutlip DE, et al. Impact of smoking on clinical and angiographic restenosis after percutaneous coronary intervention: another smoker’s paradox? Circulation. 2001; 104: 773–778.
2. Barbash GI, Reiner J, White HD, et al. Evaluation of paradoxic beneficial effects of smoking in patients receiving thrombolytic therapy for acute myocardial infarction: mechanism of the "smoker’s paradox" from the GUSTO-I trial, with angiographic insights. J Am Coll Cardiol. 1995; 26: 1222–1229.[Abstract]
3.
Grines CL, Topol EJ, O’Neill WW, et al. Effect of cigarette smoking on outcome after thrombolytic therapy for myocardial infarction. Circulation. 1995; 91: 298–303.
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