Background Patients with rheumatoid arthritis (RA) experience premature mortality that is largely due to cardiovascular disease (CVD). Selective biomarkers have been proposed for CVD prediction. Indeed, ultrasensitive troponin (hs-cTn), a biomarker of myocardial injury, and NT-proBNP, a marker of myocardial dysfunction, have been recently identified as predictors of increased cardiovascular (CV) mortality, both in patients with diagnosed ischemic heart disease and in the general population.
Objectives Our aim was to measure hs-cTn and NT-proBNP in RA patients and to examine associated factors with increased concentrations of these biomarkers.
Methods The plasma hs-cTn concentrations were measured using an electrochemiluminescence immunoassay (Roche Diagnostic, Meylan, France). The 99th percentile, with a CV ≤10% was achieved for 14 ng/L. Plasma NT-proBNP levels were assessed by an immunoenzymatic assay (Roche Diagnostic). Concentrations of these biomarkers were measured in consecutive RA patients and age- and gender-matched healthy controls.
Results 236 consecutive RA patients were included (192 females, 81%) with a mean ± standard deviation, SD, age of 57±13 years and a mean ±SD disease duration of 15±10 years; 79% had radiographic erosions, 79% positive rheumatoid factors and 84% positive anti-CCP antibodies. The mean±SD DAS28 was 3.7±1.4 (116 patients, 49%, with DAS28 >3.2 and 33, 14%, with DAS28 >5.1). At the time of the dosage, 189 (80%) patients received corticosteroids (mean±SD dose 7.1±3.2 mg/day), 200 (85%) a conventional DMARD, and 146 (62%) a biologic agent. We also included 213 controls (165 females, 77%), with a mean±SD age of 54±15 years.
RA patients had increased hs-cTn concentrations (5.8±10.1 ng/l vs. 4.1±3.2 ng/l, p=0.02) and NT-proBNP levels (187±441 ng/l vs. 76±259 ng/l, p=0.001) compared to controls. These results remained consistent after stratification for CV risk factors by multivariate linear regression. Hs-cTn and NT-proBNP levels were correlated in RA patients (r=0.34, p<0.0001). RA patients with C-reactive protein (CRP) >10 mg/l and a DAS28 >5.1 were more likely to have higher hs-cTn concentrations (respectively 5.9±7.1 ng/l vs. 4.3±3.6 ng/l, p=0.03, and 10.7±23.1 ng/l vs. 5,3±8,4 ng/l, p= 0,02). In addition, patients with increased hs-cTn levels (>14 ng/l) were more likely to have a DAS28 >5.1 (p=0.03). hs-cTn levels were not associated with CV risk factors, the presence of radiographic erosions, treatment received or autoantibody status. No association was identified between NT-proBNP levels and CV risk factors or RA disease characteristics.
Conclusions hs-cTn concentrations are increased in patients with RA, independent of CV risk factors. Our results showed for the first time an association between increased hs-cTn concentrations, CRP levels and high RA disease activity, which support the link between myocardial injury and inflammation. Increased hs-cTn in RA may indicate subclinical, indolent myocardial injury, which may be related to myocardial dysfunction, supported by increased NT-proBNP levels. Further studies are now necessary to study the merit of hs-cTn to predict CVD in RA.
Disclosure of Interest None Declared
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