Abstract

BackgroundCardiac troponins represent a sensitive index of subclinical myocardial injury and are associated with increased risk of cardiovascular events in the general population. Despite positive associations with cardiovascular risk of both cardiac troponins and cigarette smoking, concentrations of cardiac troponin I measured by high‐sensitivity assays (hs‐cTnI) are paradoxically lower in current smokers than in never‐smokers. The impact of smoking intensity and time from smoking cessation on hs‐cTnI remains unknown.Methods and Resultshs‐cTnI concentrations were measured in 32028 subjects free from cardiovascular disease enrolled in the prospective, population‐based HUNT (Trøndelag Health Study). Tobacco habits were self‐reported and classified as never (n=14 559), former (n=14 248), and current (n=3221) smokers. Current smokers exhibited significantly lower concentrations of hs‐cTnI than never‐smokers (P<0.001). In adjusted models, both current smoking (−17.3%; 95% CI, −20.6 to −13.9%) and former smoking (−6.6%; 95% CI, −8.7 to −4.5%) were associated with significantly lower hs‐cTnI concentrations. Among former smokers, higher smoking burden (>10 pack‐years) were associated with lower concentrations of hs‐cTnI. Time since smoking cessation was associated with increasing concentrations of hs‐cTnI in a dose‐dependent manner (P for trend<0.001), and subjects who quit smoking >30 years ago had concentrations of hs‐cTnI comparable with those of never‐smokers.ConclusionsIn the general population, both current and former cigarette smoking is associated with lower concentrations of hs‐cTnI. In former smokers, there was a dose‐response relationship between pack‐years of smoking, and hs‐cTnI. Time since smoking cessation was associated with increasing concentrations of hs‐cTnI, indicating a continuum of hs‐cTnI from current smoker to never‐smokers.

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