Association between baseline smoking status and clinical outcomes following myocardial infarction

Abstract

BackgroundWhether the effect of smoking on clinical outcomes following an acute myocardial infarction (AMI) is beneficial or detrimental remains inconclusive. We invesetigated the effect of smoking on the clinical outcomes in patients following an AMI.MethodsAmong 13,104 patients between November 2011 and June 2015 from a nationwide Korean AMI registry, a total of 10,193 participants were extracted then classified into two groups according to their smoking habit: (1) smoking group (n = 6,261) and (2) non-smoking group (n = 3,932). The participants who smoked were further subclassified according to their smoking intensity quantified by pack years (PYs): (1) <20 PYs (n = 1,695); (2) 20–40 PYs (n = 3,018); and (3) ≥40 PYs (n = 2,048). Each group was compared to each other according to treatment outcomes. The primary outcome was the incidence of major adverse cardiac and cerebrovascular events (MACCEs), which is a composite of all-cause mortality, non-fatal MI (NFMI), any revascularization, cerebrovascular accident, rehospitalization, and stent thrombosis. Secondary outcomes included the individual components of MACCEs. The Cox proportional hazard regression method was used to evaluate associations between baseline smoking and clinical outcomes following an AMI. Two propensity score weighting methods were performed to adjust for confounders, including propensity score matching and inverse probability of treatment weighting.ResultsWhile the incidence of all clinical outcomes, except for stent thrombosis, was lower in the smoking group than in the non-smoking group in the unadjusted data, the covariates-adjusted data showed statistical attenuation of these differences but a higher all-cause mortality in the smoking group. For smokers, the incidence of MACCEs, all-cause mortality, cardiac and non-cardiac death, and rehospitalization was significantly different between the groups, with the highest rates of MACCE, all-cause mortality, non-cardiac death, and rehospitalization in the group with the highest smoking intensity. These differences were statistically attenuated in the covariates-adjusted data, except for MACCEs, all-cause mortality, and non-cardiac death, which had the highest incidence in the group with ≥40 PYs.ConclusionSmoking had no beneficial effect on the clinical outcomes following an AMI. Moreover, for those who smoked, clinical outcomes tended to deteriorate as smoking intensity increased.

Unfolding the reality of the smoking paradox in a South Asian cohort of patients presenting with ST-elevation acute coronary syndrome undergoing primary percutaneous coronary intervention

“…Haig et al 18 established that smoking is strongly associated with inflammation and can be considered an independent causative factor of mortality or heart failure event. Similarly, smokers had a higher all-cause mortality and risk of re-hospitalization once the covariates were adjusted in a study conducted by Oh et al 29 Smoking was to be associated with higher mortality and risk of re-infarction. 16 Similarly, our study, on the other hand, prospectively enrolled STEMI patients, especially aiming at including all the covariates to control for that results in this paradoxical effect.…”

Time to presentation and mortality outcomes among patients with diabetes and acute myocardial infarction

“…Additionally, they had more STEMI and better LVEF than did the late presenters. These findings are sufficiently predictable, given that one clinical study revealed that smokers tend to have more STEMI and better LVEF than non-smokers [ 21 ]. Patients with STEMI tend to present complete occlusion of the infarct-related artery than those with NSTEMI [ 22 , 23 ].…”

Smoking, immunity, and cardiovascular prognosis: a study of plasma IgE concentration in patients with acute myocardial infarction

“…The term “smoker's paradox” has been used to describe the controversial notion that smoking might improve cardiovascular outcomes post-AMI ( 44 , 45 ). However, conflicting evidence has emerged, refuting these paradoxical findings ( 46 – 48 ). Our data, assessed through Kaplan–Meier analysis, indicate no difference in plasma cotinine levels between patients with or without MACCE.…”