Elizabeth Park, Jan Griffin, Joan M. Bathon^*

Columbia University Irving Medical Center and New York Presbyterian Hospital, New York, New York

^*Address correspondence to Joan M. Bathon, MD, Division of Rheumatology, Department of Medicine, Columbia University, Vagelos College of Physicians and Surgeons, 630 West 168th Street, P&S 3-450, New York, NY 10032.

Rheumatoid arthritis (RA) patients have almost twice the risk of heart failure (HF) as individuals without RA, even with adjustment for the presence of ischemic heart disease. Moreover, RA patients remain at a 2-fold higher risk of mortality from HF compared to non–RA patients. These observations suggest that RA-specific inflammatory pathways are significant contributors to this increased risk of HF. Herein we summarize the epidemiology of HF in RA patients, the differences in myocardial structure or function between RA patients and non–RA patients without clinical signs of HF, and data on the role of systemic and local inflammation in RA HF pathophysiology. We also discuss the impact of subduing inflammation through the use of RA disease-modifying therapies on HF and myocardial structure and function, emphasizing gaps in the literature and areas needing further research.