Background Whether TNF-related apoptosis-inducing ligand (TRAIL) impacts cardiovascular risk in rheumatoid arthritis (RA) is currently unknown.
Objectives We examined the association of TRAIL concentrations with cardiovascular disease (CVD) in RA and, since osteoprotegerin (OPG) can act as a decoy receptor for TRAIL, whether TRAIL concentrations impact on the independent OPG level-atherosclerotic CVD relation that was recently documented in the present cohort (1).
Methods TRAIL concentrations were assessed by ELISA in 151 RA patients of which 75 (49.7%) had CVD comprising ischemic heart disease (n=27), cerebrovascular accident (n=26), peripheral artery disease (n=9) or/and heart failure (HF) (n=27), and 62 controls.
Results Mean RA duration was 12 years. In RA patients, C-reactive protein (CRP) levels and cholesterol-HDL cholesterol ratio related to TRAIL concentrations [partial R (p) = -0.222 (0.006) and 0.174 (p=0.04), respectively]. TRAIL concentrations were smaller in RA patients compared to controls (median (interquartile range) =80.2 (60.9-120.4) versus 130.4 (89.4-167.7) pg/ml, p<0.0001)). TRAIL levels were larger in RA patients with compared to those without HF (105.5 (66.5-143.4) versus 79.9 (57.8-110.6), p=0.02); this difference was independent of demographic characteristics and traditional cardiovascular risk factors (p=0.04) but not CRP concentrations (p=0.1). TRAIL levels were consistently unrelated to atherosclerotic CVD. Our previously reported OPG-atherosclerotic CVD relation in RA survived adjustment for TRAIL concentrations in a mixed regression model (p=0.04).
Conclusions TRAIL concentrations are markedly reduced and associated with HF in established RA, this relationship being explained by CRP levels. OPG may directly enhance CVD risk in RA (1).
Lopez-Mejias, Ubilla B, Genre F, Corrales A, Hernandez JL, Ferraz-Amaro I, Tsang L, Llorca J, Blanco R, Gonzalez-Juanatey C, Gonzalez-Gay MA, Dessein PH. Osteoprotegerin concentrations relate independently to established cardiovascular disease in rheumatoid arthritis. J Rheumatol 2015;42:39-45.
Disclosure of Interest None declared