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Heart Failure Deemed Driving Force in Excess Mortality in RA


 

SNOWMASS, COLO. — Heart failure is a major contributor to the excess mortality in patients with rheumatoid arthritis, Dr. Sherine E. Gabriel said at a symposium sponsored by the American College of Rheumatology.

Rheumatoid arthritis (RA) patients have twice the risk of developing heart failure (HF) compared with the general population, and its lethality is markedly greater, said Dr. Gabriel, the William J. and Charles H. Mayo Professor of Medicine and Epidemiology at the Mayo Clinic, Rochester, Minn.

These are among the recent findings of the Rochester Epidemiology Project, an ongoing, primarily National Institutes of Health-funded longitudinal project drawing on the inpatient and outpatient medical records of the populace of Olmsted County, Minn. Dr. Gabriel presented highlights from published and not-yet-published studies from the project.

In 575 Rochester patients with no history of HF at the time of diagnosis with RA and 583 no-RA controls, the relative risk of new-onset HF during the subsequent 30 years was 1.9-fold greater in the RA group after adjustment in a multivariate analysis for age, gender, standard cardiovascular risk factors, and the presence of ischemic heart disease. In the subset of rheumatoid factor-positive RA patients, the relative risk climbed to 2.6 (Arthritis Rheum. 2005;52:412–20).

Another distinguishing feature of HF in RA patients is that it is far more likely to involve diastolic dysfunction with preserved left ventricular ejection fraction. Rochester patients with RA were an adjusted 2.6-fold more likely than were non-RA subjects to have a preserved ejection fraction at the time they developed HF. This is problematic because treatment options for isolated diastolic dysfunction are limited. Medications that have improved survival and quality of life in HF (ACE inhibitors, angiotensin receptor blockers, and β-blockers) have been studied almost exclusively in patients with left ventricular systolic dysfunction, and that's the HF population in which those drugs are approved.

The most likely explanation for the increased risk of HF in RA is the persistent inflammatory state that characterizes the rheumatic disease. Dr. Gabriel cited a study of 575 Rochester patients free of HF at the time of diagnosis with RA. During 15 years of follow-up, 172 patients had new-onset HF. The proportion with an elevated erythrocyte sedimentation rate of 40 mm/hour or greater was higher during the 6-month period before diagnosis of HF than in any other period during the 15 years (Ann. Rheum. Dis. 2007;66:76–80).

This suggests that regular monitoring of erythrocyte sedimentation rate and other inflammatory markers might help identify RA patients at increased near-term risk of developing HF, she noted.

Regular monitoring of erythrocyte sedimentation rate and inflammatory markers might help identify patients at risk of HF. DR. GABRIEL

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