Association between inflammation and cigarette smoking in cardiac remodeling after acute myocardial infarction

Abstract

Objective: In this study, we aimed to investigate the relationship between smoking and adverse cardiac remodeling after ST-elevation MI (STEMI), and the association between smoking and inflammatory markers, including cytokine levels. Methods: Forty-three patients admitted to the emergency department between June 2015 and June 2020 who were diagnosed with STEMI for the first time and underwent successful primary percutaneous coronary intervention were included in the study. Inflammatory markers (interferon (IFN)- α, - γ, - β, interleukin (IL)-6R- α, and soluble tumor necrosis factor receptor (sTNFR)-1,-2) were measured on the first day and two weeks post-MI. Left ventricular volume and functions were evaluated using cardiac magnetic resonance imaging at two weeks and six months post-STEMI. Adverse remodeling (AR) was defined as an increase in left ventricular (LV) end-diastolic volume >12%. Results: The AR ratio (65% vs. 30.4%; p= 0.024) and the levels of each inflammatory marker on the first-day post-STEMI were higher in the smokers' group than in the non-smokers' group. Smoking (OR= 4.46; p= 0.032) and IFN-β (OR= 1.07; p=0.023) levels on the first-day post-MI were independent predictors of AR. Also, smoking ( β( SE)= 8.96(2.74); p= 0.002), increased neutrophil levels (β±SE= 1.72 (0.66); p= 0.013) and inc reased LDL levels (β( SE) = 0.07(0.03); p=0.031) were independent predictors of elevated IFN-β levels. Conclusion: Baseline inflammatory marker levels and incidence of AR post-STEMI were higher in smokers. Smoking can contribute to the development of AR by increasing the severity of inflammation at the onset of acute STEMI.