scholarly journals Tobacco Consumption and High‐Sensitivity Cardiac Troponin I in the General Population: The HUNT Study

Author(s):  
Julia Brox Skranes ◽  
Magnus Nakrem Lyngbakken ◽  
Kristian Hveem ◽  
Helge Røsjø ◽  
Torbjørn Omland

Background Cardiac 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 Results hs‐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. Conclusions In 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.

2019 ◽  
Vol 42 (11) ◽  
pp. 1768-1775 ◽  
Author(s):  
Tomonori Sugiura ◽  
Yasuaki Dohi ◽  
Hiroyuki Takase ◽  
Sumiyo Yamashita ◽  
Tatsuya Mizoguchi ◽  
...  

2015 ◽  
Vol 61 (4) ◽  
pp. 646-656 ◽  
Author(s):  
Torbjørn Omland ◽  
James A de Lemos ◽  
Oddgeir L Holmen ◽  
Håvard Dalen ◽  
Jūratė Šaltytė Benth ◽  
...  

Abstract BACKGROUND A new, high-sensitivity assay for cardiac troponin I (hs-cTnI) permits evaluation of the prognostic value of cardiac troponins within the reference interval. Men have higher hs-cTnI concentrations than women, but the underlying pathophysiological mechanisms and prognostic implications are unclear. The aim of this study was to assess the potential impact of sex on the association between hs-cTnI and cardiovascular death. METHODS By use of the Architect STAT High-Sensitive Troponin assay, we measured hs-cTnI in 4431 men and 5281 women aged ≥20 years participating in the prospective observational Nord-Trøndelag Health Study (HUNT). RESULTS hs-cTnI was detectable in 98.5% of men and 94.7% of women. During a mean follow-up period of 13.9 years, 708 cardiovascular deaths were registered. hs-cTnI was associated with the incidence of cardiovascular death [adjusted hazard ratio (HR) per 1 SD in log hs-cTnI 1.23 (95% CI 1.15–1.31)], with higher relative risk in women than men [HR 1.44 (1.31–1.58) vs 1.10 (1.00–1.20); Pinteraction &lt; 0.001]. This finding was mediated by both lower risk associated with low hs-cTnI concentrations in women than in men and higher risk associated with high concentrations of hs-cTnI in women than in men. Male sex was associated with a higher risk of cardiovascular death [HR 1.28 (1.11–1.49)], but after adjustment for hs-cTnI, this association disappeared [HR 0.87 (0.75–1.02)]. CONCLUSIONS The prognostic value of hs-cTnI concentrations in the general population is stronger in women than in men. Subtle impairment of cardiovascular status may contribute to higher hs-cTnI concentrations in men, reflecting sex-dependent differences in cardiovascular risk.


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