Retinal vascular calibers in contemporary patients with chronic systemic inflammatory diseases: The Greek REtinal Microcirculation (GREM) study

摘要

Abstract Background Chronic systemic inflammatory diseases (CSID) are associated with increased cardiovascular morbidity and mortality. Widening of retinal venular calibers has been independently associated with systemic inflammation and cardiovascular risk in the general population. We aimed to test the hypothesis that retinal vessel calibers are altered in a population with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and spondyloarthropathies (SpA) compared to a reference group (RG). Methods Between 2012 and 2014 digital retinal images were obtained from consecutive individuals and retinal vessel calibers were measured with validated software to determine central retinal arteriolar and venular equivalents. Results One hundred eighty-eight patients with CSID [(74 RA, 75 SLE, 39 SpA), (70.2% females, mean age 50.4?±?12.5 years)] and 512 non-CSID individuals [(187 normotensives and 325 hypertensives, 90 of whom untreated; RG), (43.7% females, mean age 52.3?±?11.7)] were recruited. Logistic regression analysis after adjustment for all factors associated with retinal vessel calibers in univariate analysis (age, sex, body mass index, blood pressure, anti-hypertensive/lipid modifying drugs and disease duration), showed that both arteriolar and venular retinal vessel calibers were comparable between CSID patients and the RG. No significant differences were found regarding retinal vessel calibers between each patient subgroup and the RG. Conclusions Retinal vessel calibers were not significantly altered in patients with CSID. Well-controlled disease, as indicated by inflammatory indices, may be an explanation of our results suggesting that sufficient control of inflammation could improve microvascular abnormalities in these populations. Highlights ? No differences regarding retinal vessel diameters were found between patients with CSID and RG. ? Suppression of inflammation could be an explanation of our results. ? Therapies targeting in suppression of inflammation might improve microcirculation in these populations.