Inflammatory joint diseases and autoimmune diseases with joint manifestations are associated with premature and accelerated atherogenesis. Patients with rheumatoid arthritis (RA) have a 5- to 10-year decrease in life expectancy compared to the general population, and those exhibiting extraarticular manifestations have the greatest excess mortality. RA is now established as an independent cardiovascular risk factor. Complex interactions linking conventional cardiovascular risk factors, systemic inflammation, and vascular function may explain the increased cardiovascular risk among RA patients. Endothelial dysfunction is now recognized as both the key step in early atherogenesis and a contributor to atheroma plaque progression at later stages. Endothelial dysfunction is defined as impaired endothelium-dependent blood-vessel dilation in response to a stimulus. The underlying mechanisms remain speculative. Over the last decade, a role for endothelial dysfunction in the cardiovascular complications of inflammatory joint disease has been hypothesized and several maintenance drugs targeting this phenomenon have been tested, with promising results.