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Arthritis
Volume 2014, Article ID 782850, 7 pages
http://dx.doi.org/10.1155/2014/782850
Research Article

Epicardial Fat Thickness as Cardiovascular Risk Factor and Therapeutic Target in Patients with Rheumatoid Arthritis Treated with Biological and Nonbiological Therapies

1Division of Medical Physiology, Department of Physiological Sciences, University of Oriente, Ciudad Bolívar 8001, Venezuela
2Endocrinology, Diabetes, Metabolism and Nutrition Unit, Orinoco Medical Center, Annex A. Siegert Avenue, Ciudad Bolívar 8001, Venezuela
3Endocrinology Unit, University Hospital of Los Andes, Mérida 5101, Venezuela
4Rheumatology Service, Ruiz y Paez University Hospital, Ciudad Bolívar 8001, Venezuela
5Cardiology Service, Ruiz y Paez University Hospital, Ciudad Bolívar 8001, Venezuela
6El Valle Medical Center, Nueva Esparta 6301, Venezuela
7Intensive Coronary Care Unit, Hospital Manuel Fajardo, 10400 Havana, Cuba
8Division of Endocrinology, Department of Medicine, University of Miami Miller School of Medicine, Miami, FL 33136, USA

Received 17 August 2014; Revised 23 November 2014; Accepted 24 November 2014; Published 10 December 2014

Academic Editor: George D. Kitas

Copyright © 2014 Marcos M. Lima-Martínez et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Rheumatoid arthritis (RA) is a chronic inflammatory disease associated with high cardiovascular morbidity and mortality. Epicardial adipose tissue (EAT) thickness may act as a therapeutic target during treatments with drugs modulating the adipose tissue. We evaluate EAT thickness in RA patients treated with biological and nonbiological disease-modifying antirheumatic drugs (DMARDs). A cross-sectional study was conducted with a cohort of 34 female RA patients and 16 controls matched for age and body mass index (BMI). Plasma glucose, basal insulin, plasma lipids, and high-sensitivity C-reactive protein (hs-CRP) were assessed. EAT thickness and left ventricular mass (LVM) were measured by echocardiography. No significant differences in waist circumference (WC), blood pressure, fasting blood glucose, basal insulin, and lipid parameters were found between the groups. The control group showed lower concentrations () of hs-CRP and LVM () than those of the two RA groups. Patients treated with TNF-α inhibitors showed significantly lower EAT thickness than those treated with nonbiological DMARDs (8.56 ± 1.90 mm versus 9.71 ± 1.45 mm; ). Women with no RA revealed reduced EAT thickness (5.39 ± 1.52 mm) as compared to all RA patients (). Results suggest that RA patients have greater EAT thickness than controls regardless of BMI and WC.