Association between smoking and subclinical cardiac biomarkers: a cross-sectional pilot study

Abstract

The cardiovascular effects of smoking are generally evaluated in the context of acute ischemic injury. The possible association of smoking with subclinical cardiac autoimmunity and oxidative/inflammatory processes has been examined in relatively few studies. In this cross-sectional pilot study, we compared levels of cardiac troponin I autoantibody (cTnI-Ab), tumor necrosis factor-alpha (TNF-α), high-sensitivity C-reactive protein (hsCRP), Na⁺/K⁺-ATPase, and 8-isoprostane between asymptomatic smokers and non-smokers, and assessed whether these biomarkers showed a cross-sectional association with smoking burden (pack-years). This cross-sectional pilot study was conducted at Ağrı Training and Research Hospital, with volunteers prospectively enrolled. No formal sample size calculation was performed given the pilot nature of the study. Participants were recruited via convenience sampling by two researchers; among eligible volunteers enrolled in order of presentation, a total of 91 volunteers were reached, comprising 48 smokers (pack-years > 0) and 43 non-smokers (pack-years = 0). Serum biomarker levels were measured by ELISA. Sex distribution differed between groups. Between-group comparisons used the Mann-Whitney U test for non-normally distributed variables and the independent-samples t-test for normally distributed variables. Categorical variables were compared with Fisher’s exact test. The relationship between smoking burden and biomarkers was examined using Spearman correlation analysis. To control for this sex imbalance, sex-adjusted multivariable linear regression was performed for all biomarkers. Sex was selected as the covariate for these models because it was the only demographic variable showing a significant imbalance between groups (Table 1); sex is also a recognized potential effect modifier in smoking-related cardiovascular research. Age, weight, BMI, and blood pressure did not differ significantly between groups and were therefore not included as additional covariates. Levels of cTnI-Ab (smokers: 27.80 ng/mL, non-smokers: 17.80 ng/mL; p = 0.001) and 8-isoprostane (smokers: 67.93 ng/L, non-smokers: 51.30 ng/L; p = 0.002) were significantly higher in smokers. Both findings remained significant after Bonferroni correction, whereas no significant between-group differences were found for TNF-α, hsCRP, or Na⁺/K⁺-ATPase. The association between cTnI-Ab and smoking remained significant independent of sex ( p = 0.015), with smokers showing on average 1.25-fold higher levels (95% CI: 1.05–1.50). The association between 8-isoprostane and smoking also remained significant independent of sex ( p < 0.001), with smokers showing on average 1.41-fold higher levels (95% CI: 1.20–1.66). cTnI-Ab also showed a positive correlation with pack-years among smokers (rho = 0.441, p = 0.002), indicating a positive cross-sectional association between pack-years and cTnI-Ab. Smoking is associated with elevated cTnI-Ab and 8-isoprostane levels in the absence of overt myocardial injury; cTnI-Ab additionally showed a positive cross-sectional association with smoking burden (pack-years). These findings suggest that smoking may be associated with subclinical cardiac and oxidative stress at an early stage. Our study is hypothesis-generating and requires validation in larger, multicenter cohorts.