Implications of cigarette smoking for the management of patients with acute coronary syndromes

https://doi.org/10.1016/S0033-0620(03)00075-6Get rights and content

Abstract

Smokers differ from nonsmokers in the way they present with acute coronary syndromes and in how they respond to treatment. Although smoking increases the risk of a coronary event and accelerates the progression of established atherosclerosis, paradoxically, smokers have better short-term survival after an acute myocardial infarction, mainly because they are younger and have more favorable coronary anatomy. Thrombolysis appears to be a better treatment in smokers than in nonsmokers, probably because thrombosis plays a more important role in the pathogenesis of acute coronary events in smokers. Patients who continue to smoke after angioplasty or bypass surgery have a worse outcome than nonsmokers or quitters. The 2.5- to 3-fold increase in risk for myocardial infarction or stroke in smokers compared with nonsmokers decreases exponentially after smoking cessation. By 4 years the risk is only slightly higher than the risk of a subject who never smoked.

Section snippets

Coronary anatomy and infarct location

The lower mortality rate in smokers compared with nonsmokers with acute MI can be explained in part by their less extensive coronary disease. Smokers have been shown to have a higher proportion of single vessel disease than nonsmokers. For example, among 41,021 patients with AMI who underwent thrombolysis in the GUSTO-1 trial, single vessel disease was more frequent in smokers than nonsmokers, 63% vs 55%.4

The location of the culprit artery causing AMI has also been found to be different in

Percutaneous coronary intervention

Among patients undergoing PCI in settings other than acute MI, smokers have increased mortality rates compared with nonsmokers. Cohen et al33 found that among patients without AMI who underwent PCI, smokers and nonsmokers had no difference in unadjusted mortality, but after multivariate adjustment, smokers were found to have a higher 1-year mortality than nonsmokers. An increased multivariate mortality rate in smokers was also found by Ashby et al34 among 5,592 patients without AMI who

Conclusions

The paradoxical decrease in mortality and morbidity rates among smokers with MI has been attributed to differences in age, gender, infarct location, and other clinical characteristics of smokers. However, in some studies, this “smokers’ paradox” persists after adjustment for these variables, including the presence of single vessel disease and preferential involvement of the right coronary artery and inferior wall in smokers. The unique pathology of acute MI in smokers may be the reason for the

References (55)

  • D. Hasdai et al.

    Smoking status and outcome after primary coronary angioplasty for acute myocardial infarction

    Am Heart J

    (1999)
  • D.T. Ashby et al.

    Comparison of one-year outcomes after percutaneous coronary intervention among current smokers, ex-smokers, and nonsmokers

    Am J Card

    (2002)
  • R.G. Macdonald et al.

    Patient-related variables and restenosis after percutaneous transluminal coronary angioplastya report from the M-HEART group

    Am J Cardiol

    (1990)
  • K.M. Galan et al.

    Increased frequency of restenosis in patients continuing to smoke cigarettes after percutaneous transluminal coronary angioplasty

    Am J Cardiol

    (1988)
  • J.B. Cavender et al.

    Effects of smoking on survival and morbidity in patients randomized to medical or surgical therapy in the Coronary Artery Surgery Study (CASS)10-year follow-up

    J Am Coll Cardiol

    (1992)
  • R.T. van Domburg et al.

    Smoking cessation reduces mortality after coronary artery bypass surgerya 20-year follow-up study

    J Am Coll Cardiol

    (2000)
  • M.J. Domanski et al.

    Prognostic factors for atherosclerosis progression in saphenous vein graftsthe Post-Coronary Artery Bypass Graft (Post-CABG) trial

    J Am Coll Cardiol

    (2000)
  • A. Dobson et al.

    How soon after quitting smoking does risk of heart attack decline?

    J Clin Epidemiol

    (1991)
  • N. Benowitz et al.

    Cardiovascular toxicity of nicotineimplications for nicotine replacement therapy

    J Am Coll Cardiol

    (1997)
  • T.L. Kelly et al.

    Smoking status at the time of acute myocardial infarction and subsequent prognosis

    Am Heart J

    (1985)
  • P. Molstad

    First myocardial infarction in smokers

    Eur Heart J

    (1991)
  • S. Thanavaro et al.

    Effect of infarct location on the in-hospital prognosis of patients with first transmural myocardial infarction

    Circulation

    (1982)
  • C.L. Grines et al.

    Effect of cigarette smoking on outcome after thrombolytic therapy for myocardial infarction

    Circulation

    (1995)
  • H.E. Roald et al.

    Modulation of thrombotic responses in moderately stenosed arteries by cigarette smoking and aspirin ingestion

    Arterioscler Thromb

    (1994)
  • J. Hung et al.

    Cigarette smoking acutely increases platelet thrombus formation in patients with coronary artery disease taking aspirin

    Circulation

    (1995)
  • S. Matetzky et al.

    Smoking increases tissue factor expression in atherosclerotic plaques

    Circulation

    (2000)
  • K. Ichiki et al.

    Long-term smoking impairs platelet-derived nitric oxide release

    Circulation

    (1996)
  • Cited by (19)

    • Change in left ventricular systolic function in patients with ST elevation myocardial infarction: Evidence for smoker's paradox or pseudo-paradox?

      2016, Indian Heart Journal
      Citation Excerpt :

      This vexing problem is currently being addressed by the Joint Commission for Smoking Cessation.39 Whereas persistent smokers in the presence of established coronary artery disease have an increased risk of re-infarction and sudden cardiac death, even after coronary revascularization with PCI or bypass grafting,40 many CS-mediated prothrombotic changes are quickly reversible upon CS cessation.41 This message needs to be disseminated to patients, primary and secondary care physicians, and the general population.

    • Coronary collateral circulation: The effects of smoking and alcohol

      2007, Atherosclerosis
      Citation Excerpt :

      However, data are very scarce, and the mechanism whereby these life-style factors may affect collateral formation is at present still unknown [6–10]. While smoking is a well-established risk factor for cardiovascular disease and acute myocardial infarction [11–14], moderate alcohol intake has been associated with a reduced incidence of, and mortality from, coronary heart disease [15,16]. In the present study, we examined the extent to which smoking and alcohol use affect the presence of coronary collaterals in patients with documented coronary artery disease.

    View all citing articles on Scopus
    View full text