Heart failure risk among patients with rheumatoid arthritis starting a TNF antagonist
- Daniel H Solomon1,
- Jeremy A Rassen1,
- Bindee Kuriya2,
- Lang Chen3,
- Leslie R Harrold4,
- David J Graham5,
- James D Lewis6,
- Joyce Lii1,
- Liyan Liu7,
- Marie R Griffin8,
- J R Curtis3
- 1Division of Pharmacoepidemiology, Brigham and Women's Hospital, Boston, Massachusetts, USA
- 2Department of Medicine, University of Toronto, Toronto, Ontario, Canada
- 3Department of Biostatistics, University of Alabama at Birmingham, Birmingham, Alabama, USA
- 4Department of Medicine, University of Massachusetts, Worcester, Massachusetts, USA
- 5Office of Drug Safety, Food and Drug Administration, Baltimore, Maryland, USA
- 6Department of Medicine, University of Pennsylvania, Philadelphia, Philadelphia, USA
- 7Division of Research, Kaiser Permanente, Oakland, California, USA
- 8Department of Preventive Medicine, Vanderbilt University and Veterans Affairs Tennessee Valley Health Care System, Memphis, Tennessee, USA
- Correspondence to Dr Daniel H Solomon, Division of Rheumatology, Division of Pharamacoepidemiology, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115; USA;
- Accepted 21 October 2012
- Published Online First 15 November 2012
Background While heart failure (HF) is associated with elevations in tumor necrosis factor (TNF)α, several trials of TNF antagonists showed no benefit and possibly worsening of disease in those with known severe HF. We studied the risk of new or recurrent HF among a group of patients receiving these agents to treat rheumatoid arthritis (RA).
Methods We used data from four different US healthcare programmes. Subjects with RA receiving methotrexate were eligible to enter the study cohort if they added or switched to a TNF antagonist or another non-biological disease modifying antirheumatic drug (nbDMARD). These groups were compared in Cox regression models stratified by propensity score decile and adjusted for oral glucocorticoid dosage, prior HF hospitalisations, and the use of loop diuretics.
Results We compared 8656 new users of a nbDMARD with 11 587 new users of a TNF antagonist with similar baseline covariates. The HR for the TNF antagonists compared with nbDMARD was 0.85 (95% CI 0.63 to 1.14). The HR was also not elevated in subjects with a history of HF. But, it was elevated prior to 2002 (HR 2.17, 95% CI 0.45 to 10.50, test for interaction p=0.036). Oral glucocorticoids were associated with a dose-related gradient of HF risk: compared with no use, 1≤5 mg HR 1.30 (95% CI 0.91 to 1.85), ≥5 mg HR 1.54 (95% CI 1.09 to 2.19).
Conclusions TNF antagonists were not associated with a risk of HF hospital admissions compared with nbDMARDs in this RA population.