P.65 Increased Biomarkers of Endothelial Dysfunction and Thrombotic Microenvironment in Patients with Autoimmune Rheumatic Disorders Free from Cardiovascular Comorbidities

Abstract

Purpose/Background/Objectives

Cardiovascular risk is increased in patients with autoimmune rheumatic disorders [1]. Endothelial and platelet MVs (EMVs, PMVs) are small vesicles (0.1–1 μm) released from plasma membrane and represent novel markers of endothelial dysfunction and thrombosis. Their levels increase substantially in patients with cardiovascular diseases [2,3]. We tested whether EMVs and PMVs are increased in patients with autoimmune rheumatic disorders in the absence of cardiovascular comorbidities.

Methods

Consecutive patients with rheumatoid arthritis or systemic lupus erythematosus were studied, provided they were free from cardiovascular comorbidities (hypertension, diabetes, heart disease, history of cardiovascular or cerebrovascular events). We additionally used (a) a control group consisting of healthy volunteers and (b) a reference group including patients with stable coronary artery disease (CAD). MVs were measured by a standardized flow cytometry protocol [2,3].

Results

We studied 74 participants: 17 patients with autoimmune rheumatic diseases; 34 healthy volunteers, and 23 stable CAD patients. Patients with rheumatic diseases presented increased levels of both EMVs (283.3 ± 195.0/μL vs 168.5 ± 54.8/μL, p = 0.029) and PMVs (374.0 ± 275.3/μL vs 225.7 ± 101.1/μL, p = 0.046) compared to controls. In addition, they presented similar levels of EMVs compared to CAD patients (283.3 ± 195.0/μL vs 297.0 ± 211.8/μL, p = 0.846), whereas PMVs were substantially elevated in the latter (374.0 ± 275.3/μL vs 1034.8 ± 374.0/μL, p = 0.029).

Conclusions

Endothelial dysfunction and thrombotic predisposition, shown by increased levels of EMVs and PMVs, respectively, may be evidenced in patients with autoimmune rheumatic diseases, even in the absence of cardiovascular comorbidities and before the establishment of clinically evident cardiovascular complications. In these patients, levels of EMVs appear to be comparable with those of stable CAD patients.

Acknowledgements

This research is co-financed by Greece and the European Union (European Social Fund-ESF) through the Operational Programme “Human Resources Development, Education and Lifelong Learning 2014–2020” in the context of the project “Evaluation of novel markers of endothelial dysfunction and thrombotic microenvironment in patients with rheumatoid arthritis: association with markers of subclinical inflammation and cardiovascular damage (MIS 5047870)”.