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Soluble forms of tumor necrosis factor receptors (sTNFRs) are emerging target molecules of inflammatory disease. However, their role in vascular biology is not well known. This study was performed to investigate the association between serum concentrations of sTNFRs and arterial stiffness.
A total of 117 consecutive patients with suspected coronary artery disease (CAD) (63.6 ± 11.0 years; men, 65%) who were referred for invasive coronary angiography (ICA) were prospectively enrolled. Arterial blood sTNFR1 and sTNFR2 were measured using commercially available ELISA kits. Brachial-ankle pulse wave velocity (baPWV) measurements were made within 24 hours of blood sampling for sTNFRs measurement. Information on cardiovascular events including cardiac death, non-fatal myocardial infarction and coronary revascularization was obtained during clinical follow-up.
Most of the patients (86.3%) had significant CAD (stenosis ≥ 50%) in ICA. In simple linear regression analyses, there were significant positive correlations of baPWV with sTNFR1 (r = 0.483, P < 0.001) and sTNFR2 (r = 0.366, P < 0.001). When the sTNFRs values were stratified into tertiles, the baPWV values increased proportionally with increasing sTNFR1 (P = 0.002) and sTNFR2 (P = 0.076) tertiles. In multiple linear regression analyses, sTNFR1 (β = 0.300, P < 0.001) and sTNFR2 (β = 0.206, P = 0.013) had independent association with baPWV even after controlling for potential confounders. There were significant linear correlations of baPWV with ANC (r = 0.251, P = 0.010) and CRP (r = 0.407, P < 0.001). The serum levels of both sTNFR1 (1,263 ± 441 pg/mL versus 1,137 ± 489 pg/mL, P = 0.456) and sTFNR2 (2,813 ± 1,215 pg/mL versus 2,995 ± 1,566 pg/mL, P = 0.674) were higher in patients with events than those without, however, it were statistically insignificant.
sTNFR1 and sTNFR2 may be independently associated with baPWV in patients undergoing ICA. Our data strengthen previous findings on the role of inflammation in the pathogenesis of arterial stiffening. More important, considering the prognostic value of arterial stiffness, sTNFR1 and sTNFR2 could be potential therapeutic targets for improving outcomes of this subset of patients. Further longitudinal studies with larger sample size are needed to confirm our findings.