Raised erythrocyte sedimentation rate signals heart failure in patients with rheumatoid arthritis
- Correspondence to:
Dr Sherine E Gabriel
Department of Health Sciences Research, Mayo Clinic, 200 1st St SW, Rochester, MN 55905, USA;
- Accepted 9 June 2006
- Published Online First 3 July 2006
Background: Inflammatory markers are associated with heart failure. Patients with rheumatoid arthritis have twice the risk of heart failure compared with people without rheumatoid arthritis.
Objective: To assess whether heart failure in patients with rheumatoid arthritis is preceded by an inflammatory activation as shown by erythrocyte sedimentation rate (ESR), a systemic marker of inflammation.
Methods: A population-based inception cohort of 575 patients with rheumatoid arthritis, free of heart failure at their rheumatoid arthritis incidence date, was followed up longitudinally until death or 2001. During 15 years of follow-up, they had a median of 15 ESR tests, and 172 patients had new-onset heart failure (Framingham Heart Study criteria). The follow-up period, beginning with the rheumatoid arthritis incidence date and ending with date of the last follow-up, was divided into 6-month intervals. The proportions of patients with at least one ESR value ⩾40 mm/h and with anaemia (haemoglobin <11 g/dl) within each 6-month interval were plotted against time from fulfilment of heart failure criteria. A binomial test was used to compare proportions.
Results: In patients with rheumatoid arthritis who developed heart failure, the proportion with ESR ⩾40 mm/h was highest (23%) during the 6-month period immediately preceding the new-onset heart failure, as compared with the average ESR during the entire remaining follow-up period, both before and after heart failure (10.6%; p<0.01). The proportion of patients with anaemia peaked (54%) during the 6-month period after heart failure.
Conclusions: Inflammatory stimuli may be involved in the initiation of heart failure among patients with rheumatoid arthritis.
Published Online First 3 July 2006
Funding: This study was supported in part by grants from the National Institutes of Health, NIAMS (R01 R46849) and the National Institutes of Health (AR-30582) US Public Health Service.
Competing interests: None declared.