Abstract

Arthritides have been associated with accelerated atherosclerosis to increased vascular disease risk. Traditional risk factors, as well as the role of systemic inflammation including cytokines, chamokines, proteases, autoantibodies, adhesion receptors and others have been implicated in the development of these vascular diseases. Accelerated atherosclerosis and increased cardio- and cerebrovascular morbidity and mortality have been observed in rheumatoid arthritis (RA) and spondyloarthropathies (SpA).

Endothelial dysfunction, overt atherosclerosis and vascular stiffness may be indicated by brachial artery flow-mediated vasodilation (FMD), common carotid intima-media thickness (ccIMT) and aortic pulse-wave velocity (PWV), respectively. These abnormalities have been described in most inflammatory rheumatic diseases. While ccIMT and stiffness are relatively stable, FMD may be influenced by many confounding factors.

In addition to traditional vasculoprotection, immunosuppressive agents including corticosteroids, traditional and biologic DMARDs may have significant vascular and metabolic effects. The official EULAR recommendations on the assessment and management of cardiovascular disease in arthritides have been published.