Why the study?
Reports of decreased hs-cTnI levels and altered prognostic value for cardiovascular events among smokers prompted evaluation of hs-cTnI's predictive ability across smoking statuses in a Russian cohort.
Does smoking status influence the predictive ability of hs-cTnI for adverse cardiovascular events in adults without a history of cardiovascular disease?
Does smoking status influence the predictive ability of hs-cTnI for adverse cardiovascular events in adults without a history of cardiovascular disease?
Smoking status does not significantly alter the baseline levels of hs-cTnI or its prognostic utility for predicting cardiovascular death and nonfatal myocardial infarction in a general population without prior cardiovascular disease.
hs-cTnI predictive ability is unaffected by smoking status; supports use in mixed populations but leaves open adjustment needs in risk models.
Data on the level of cardiac troponin I determined by a high-sensitivity method (hs-cTnI) may improve the accuracy of predicting adverse cardiovascular events in the general population. Some foreign publications describe a decrease in the hs-cTnI level and its prognostic value for adverse outcomes of cardiovascular diseases (CVD) in smokers and ex-smokers. This urges the study of the hs-cTnI predictive ability in the Russian population depending on smoking status. Objective. To analyze the hs-cTnI level association with the smoking status in a population sample from 9 regions of the Russian Federation and test the hypothesis that smoking influences the hs-cTnI predictive ability for adverse CVD outcomes. Material and methods. We analyzed the data of 10.277 people aged 35 to 64 years (60% women) without a history of CVD, previously included in the ESSE-RF and ESSE-RF2 observational multicenter studies (Epidemiology of cardiovascular diseases and their risk factors in the regions of the Russian Federation). For all participants, we knew their smoking status and hs-cTnI levels in blood plasma determined by a highly sensitive microparticle immune chemiluminescence assay. The median follow-up period was 7.5 years. A combined end-point was the death from cardiovascular disease or nonfatal myocardial infarction. Results. Smoking status in men and women did not influence the median hs-cTnI level (p>0.1). During the follow-up, the end-point was achieved in 267 cases, including 114 (1.8%) non-smokers, 66 (3.6%) ex-smokers, and 87 (4.3%) smokers. The hazard ratio analysis for the hs-cTnI gender-specific cut-off levels showed that the probability of reaching an end-point at the hs-cTnI values above the cut-off levels was the highest among ex-smokers and the lowest among smokers; however, the differences did not reach statistical significance. In the ROC analysis to evaluate the predictive ability of hs-cTnI depending on smoking status, the area under the curve (AUC) adjusted for gender, age, and region amounted to 0.799 among non-smokers, 0.819 among ex-smokers, and 0.789 among smokers; the differences did not reach statistical significance. Conclusion. This study evidences that smoking status does not influence the hs-cTnI blood plasma level or the hs-cTnI predictive ability for cardiovascular diseases.
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Иванова et al. (2024) studied this question.
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