SAT0118 Association of renin-angiotensin system imbalance with subclinical atherosclerosis and disease activity in rheumatoid arthritis

Background Rheumatoid arthritis (RA) is an independent risk factor for cardiovascular disease (CVD). The renin-angiotensin system (RAS) is a hormonal cascade with important role in hydroelectrolytic homeostasis, blood pressure and regulation of cardiovascular remodeling. Angiotensin II (Ang II) acts as a proinflammatory mediator (1). Objectives To investigate the association of serum levels of RAS components with the presence of subclinical atherosclerosis using carotid ultrasonography in women with RA. Methods Women with RA according to ACR/EULAR 2010 or ACR 1987 criteria and without clinical ischemic CVD were included. Disease activity was assessed using the DAS28. The presence of atherosclerotic plaques and the thickness of the medium-intimal complex (EMI) of the arterial wall in the common carotid artery were evaluated by ultrasonography, Serum levels of angiotensin (Ang) II, Ang-(1-7), angiotensin converting enzyme (ECA) and ECA II were determined by enzyme immunoassay. Results 50 women with RA, mean age 48.2 years (±7.32), mean duration of disease of 15.35 years (±8.56), DAS28 of 4.02 (±1.41) and CDAI of 14.23 (±11.53) were included. Seven patients presented altered EMI, eight had atherosclerotic plaque. The prevalence of risk factors for CVD was: 12% of smoking, 12% of family history of premature CVD, 46% of arterial hypertension, 10% of diabetes, 62% of dyslipidemia, 94% of abdominal obesity and 46% of metabolic syndrome. The control group consisted of 30 healthy women, mean age of 46.3 years (±7.72). RA patients had a higher serum concentration of Ang II (p Conclusions Imbalance of RAS components, especially Ang II and ECA II, may be associated to CVD in RA patients. Ultrasonography of the carotid arteries can identify patients that could benefit from ECA blockade. Reference: [1] Chang Y, Wei W. Angiotensin II in inflammation, immunity and rheumatoid arthritis. Clin Exp Immunol 2015;179:137-145. doi: 10.1111/cei.12467 Acknowledgements: National Council for Scientific and Technological Development (CNPq), Foundation for Research Support of Minas Gerais (FAPEMIG) Disclosure of Interest: None declared