Abstract
Advances in basic and clinical sciences have established the role of inflammation in the pathogenesis of atherosclerosis. Endothelial dysfunction is the initial event, which is followed by lipid oxidation, atheroma formation and rupture, as well as the formation of a thrombus, leading to a clinical event. A decreased survival due to accelerated atherosclerosis in patients with rheumatic diseases has been demonstrated; this cannot be fully explained by traditional cardiovascular risk factors, suggesting that disease-related factors are also operative. Aggressive antirheumatic therapies may impact favorably not only on the activity of these diseases but also on the cardiovascular-associated risk factors, resulting in better outcomes.
Acknowledgements
This work was supported by a MCRC-P60AR048095 grant from the National Institute of Arthritis and Musculoskeletal and Skin Diseases and the Support Training Efforts in Lupus for Latino American Rheumatologist (STELLAR) Program funded by Rheuminations, Inc. (UAB).