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TNF-related apoptosis-inducing ligand and cardiovascular disease in rheumatoid arthritis

1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13

 

  1. Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa.
  2. Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Rheumatology Division, Hospital Universitario Marques de Valdecilla, IDIVAL, Santander, Spain.
  3. Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Rheumatology Division, Hospital Universitario Marques de Valdecilla, IDIVAL, Santander, Spain.
  4. Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Rheumatology Division, Hospital Universitario Marques de Valdecilla, IDIVAL, Santander, Spain.
  5. Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Rheumatology Division, Hospital Universitario Marques de Valdecilla, IDIVAL, Santander, Spain.
  6. Department of Internal Medicine, Hospital Universitario Marques de Valdecilla, University of Cantabria, RETICEF, IDIVAL, Santander, Spain.
  7. Rheumatology Division, Hospital Universitario de Canarias, Tenerife, Spain.
  8. Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa.
  9. Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Rheumatology Division, Hospital Universitario Marques de Valdecilla, IDIVAL, Santander, Spain.
  10. Department of Epidemiology and Computational Biology, School of Medicine, University of Cantabria, and CIBER Epidemiología y Salud Pública (CIBERESP), IDIVAL, Santander, Spain.
  11. Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Rheumatology Division, Hospital Universitario Marques de Valdecilla, IDIVAL, Santander, Spain.
  12. Cardiology Division, Hospital Lucus Augusti, Lugo, Spain.
  13. Cardiovascular Pathophysiology and Genomics Research Unit, University of the Witwatersrand, Johannesburg, South Africa; and Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Rheumatology, IDIVAL, Santander, Spain

CER8226
2015 Vol.33, N°4
PI 0491, PF 0497
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PMID: 25962765 [PubMed]

Received: 22/12/2014
Accepted : 19/02/2015
In Press: 11/05/2015
Published: 20/07/2015

Abstract

OBJECTIVES:
We examined the association of TNF-related apoptosis-inducing ligand (TRAIL) concentrations with cardiovascular disease (CVD) in rheumatoid arthritis (RA) and, since osteoprotegerin (OPG) can act as a decoy receptor for TRAIL, whether TRAIL concentrations impact on the OPG level-atherosclerotic CVD relation that was recently documented in the present cohort.
METHODS:
TRAIL concentrations were assessed by ELISA in 151 RA patients of which 75 (49.7%) had CVD comprising ischaemic 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=-0.222 (p=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.

Rheumatology Article