Association between baseline smoking status and clinical outcomes following myocardial infarction

Abstract

Background: Whether 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.

Methods: Among 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.

Results: While 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.

Conclusion: Smoking 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.

Keywords: coronary artery disease; ischemic heart disease; myocardial infarction; smoking; treatment outcome.

FIGURE 1

Flow chart of the study participants. AMI, acute myocardial infarction; KAMIR-NIH, Korea acute myocardial infarction Registry-National Institutes of Health; PCI, percutaneous coronary intervention; PY, pack year.

FIGURE 2

Rates of primary and secondary outcomes for the smoking population after a 3-year follow-up (before IPTW adjustment). The Kaplan–Meier survival curves for cumulative event rates are illustrated according to the baseline smoking status. Blue line indicates the group with <20 PYs. Red line indicates the group with 20–40 PYs. Green line indicates the group with ≥40 PYs. CVA, cerebrovascular accident; IPTW, inverse probability of treatment weighting; MACCE, major adverse cardiac and cerebrovascular event; NFMI, non-fatal myocardial infarction; PY, pack year.

FIGURE 3

Rates of primary and secondary outcomes for the smoking population after a 3-year follow-up (after IPTW adjustment). The Kaplan–Meier survival curves for cumulative event rates are illustrated according to the baseline smoking status. Blue line indicates the group with <20 PYs. Red line indicates the group with 20–40 PYs. Green line indicates the group with ≥40 PYs. CVA, cerebrovascular accident; IPTW, inverse probability of treatment weighting; MACCE, major adverse cardiac and cerebrovascular event; NFMI, non-fatal myocardial infarction; PY, pack year.