Epicardial Fat Thickness as Cardiovascular Risk Factor and Therapeutic Target in Patients with Rheumatoid Arthritis Treated with Biological and Nonbiological Therapies
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. 1. Introduction Rheumatoid arthritis (RA) is a chronic inflammatory disease associated with high cardiovascular morbidity and mortality [1]. Traditional risk factors along with inflammation and autoimmunity contribute to the development of coronary artery disease in RA patients [1]. Furthermore, a growing body of evidence has proved that these subjects present early alterations in some subclinical atherosclerosis markers [2, 3]. Tumor necrosis factor-alpha (TNF-α) is the key cytokine in RA inflammatory processes. Several clinical studies have proved that TNF-α inhibitors are effective in reducing the clinical signs of inflammation in RA patients whose treatment with nonbiological disease-modifying antirheumatic drugs (DMARDs) has been unsatisfactory [4, 5]. An additional benefit of the treatment with TNF-α inhibitors is the reduction in the risk of cardiovascular events [6]. Epicardial adipose tissue (EAT) thickness has recently emerged as new marker of cardiometabolic risk [7]. Clinically, the thickness of epicardial fat can be easily and accurately measured [8]. Epicardial fat thickness can serve as marker of visceral adiposity and visceral fat changes during treatments with drugs targeting the fat [9, 10]. A meta-analysis conducted
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