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Cardiovascular morbidity and mortality in patients with rheumatoid arthritis: vascular alterations and possible clinical implications

Journal

QJM-AN INTERNATIONAL JOURNAL OF MEDICINE
Volume 104, Issue 1, Pages 13-26

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/qjmed/hcq203

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Mortality in patients with rheumatoid arthritis (RA) is higher than in the general population, which is due mainly to premature cardiovascular disease. Traditional cardiovascular risk factors cannot entirely explain the higher level of cardiovascular complications, and there is growing evidence that chronic inflammation is the main culprit. The aims of this review of the literature are to (i) summarize aspects of vascular alterations found in the cardiovascular system of RA patients and to relate them to the clinically relevant cardiovascular morbidity and mortality and (ii) evaluate what these abnormalities and complications might in the end imply for clinical management. A number of abnormalities in the cardiovascular system of RA patients have been identified, on the molecular level, in endothelial function, arterial stiffness, arterial morphology and, finally, in the clinical presentation of cardiovascular disease. Cardiovascular risk assessment should be part of the care of RA patients. While a great deal of data is published demonstrating abnormalities in the cardiovascular system of these patients, it is much less clear what specific interventions should be performed to reduce the incidence of cardiovascular complications. Cardiovascular care should be delivered in accordance with recommendations for the general population. Whether specific drugs (e.g. statins, aspirin) are of particular benefit in RA patients needs further investigation. Control of inflammation appears to be of benefit. Methotrexate and tumor necrosis factor-alpha blocking agents might reduce the number of cardiovascular events. Leflunomide, cyclosporine, non-steroidal anti-inflammatory drugs and cyclo-oxygenase-2 inhibitors may worsen cardiovascular outcome. The role of glucocorticoids in active RA remains to be determined.

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