Implications of cigarette smoking for the management of patients with acute coronary syndromes
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
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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 JournalCitation 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.
The Effects of Active and Passive Smoking and Cardiovascular Disease
2015, Heart and ToxinsCoronary collateral circulation: The effects of smoking and alcohol
2007, AtherosclerosisCitation 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.
Changes of Brain Endothelin Levels and Peripheral Endothelin Receptors by Chronic Cigarette Smoke in Spontaneously Hypertensive Rats
2004, Journal of Pharmacological SciencesCigarette smoking and cardiovascular disease: Pathophysiology and implications for treatment
2003, Progress in Cardiovascular DiseasesMagnitude of change in cardiac health-enhancing behaviours 6 months following an acute myocardial infarction
2007, European Journal of Cardiovascular Nursing