Impact of Smoking on Circulating Cardiac Troponin i Concentrations and Cardiovascular Events in the General Population: The HUNT Study (Nord-Trøndelag Health Study)

Background: Both tobacco smoking and circulating cardiac troponin I (cTnI) levels are associated with the risk of acute myocardial infarction, heart failure, and cardiovascular death. However, whether cTnI levels differ according to smoking status and whether smoking modifies the prognostic relationship between cTnI and outcomes remain unclear. Methods: Using data from a large, population-based cohort, we assessed the association between smoking and cTnI and the impact of smoking on the associations between cTnI levels and the incidence of acute myocardial infarction, heart failure, and cardiovascular death. cTnI was measured with a high-sensitivity assay in 3824 never smokers, 2341 former smokers, and 2550 current smokers participating in the prospective observational HUNT Study (Nord-Trøndelag Health Study). All subjects were free from known prior cardiovascular disease and diabetes mellitus at baseline. Results: The age of the participants ranged from 19 to 94 years; 55.5% were women. Current smokers exhibited significantly lower levels of cTnI (median, 2.9 ng/L; interquartile range, 2.0-4.1 ng/L) than never smokers (3.2 ng/L; interquartile range, 2.2-4.7 ng/L; P<0.001) and former smokers (3.4 ng/L; interquartile range, 2.3-5.0 ng/L; P<0.001). This association remained significant after adjustment for potential confounders (B=-0.098; 95% confidence interval, -0.129 to -0.068). We observed an association between increasing concentrations of cTnI and clinical end points in the total study cohort (adjusted hazard ratio per log unit increase in cTnI, 1.41; 95% confidence interval, 1.29-1.54). This association was attenuated for current smokers (hazard ratio, 1.17; 95% confidence interval, 0.98-1.40) and was significantly weaker than in never/former smokers (P for interaction=0.003). Prognostic accuracy, as assessed by C statistics, was significantly lower in current smokers than in never smokers (P<0.001). In addition, cTnI provided no incremental prognostic information to the Framingham Cardiovascular Disease risk score in current smokers (P=0.08). Conclusions: Current smoking is associated with lower concentrations of cTnI, suggesting that substances in tobacco smoke may affect cardiomyocyte injury. The association between cTnI levels and cardiovascular end points is stronger in never/former smokers than in current smokers, compatible with the theory that the detrimental cardiovascular impact of current smoking is mediated via mechanisms other than subclinical myocardial injury.