Background/Purpose: Patients with rheumatoid arthritis (RA) may be at increased risk of developing heart failure (HF). Inflammatory activity has been linked to the pathogenesis of HF by inducing structural changes of the myocardium. Despite these indications of a potential link between RA-related factors and non-ischemic HF, the relative risk of non-ischemic HF in contemporary patients with RA has not yet been assessed. The objective of this study was therefore o assess the relative risk of incident non-ischemic heart failure in contemporary patients with prevalent RA.

Methods: Using the Swedish nationwide patient register, a cohort of patients with prevalent RA was identified between 2006 and 2012 and matched with up to 10 general population comparators based on sex, age and area of residency. An index-date, defined as the second visit listing RA (comparators received the same index-date as their corresponding case), was assigned to all study subjects and all study participants with ischemic heart disease (IHD) and/or HF prior to the index-date were excluded. Thereafter all study subjects were followed for the outcome, defined as a first-time hospitalization or outpatient visit listing a main diagnosis of HF. All subjects were followed until outcome, death, incident IHD, first emigration or 31 December 2012, whichever occurred first. Crude rates were calculated and presented as number of events per 1000 person-years. Cox regression models were used to assess the relative risk of HF in patients with RA and adjusted for potential confounders.  

Results: In total, 41982 patients with RA and 360763 general population comparators free of IHD and HF at the index-date were identified. During the follow-up period (median follow-up for RA-patients 4.6 years [iqr 2.4-6.0] and comparators 4.8 years [iqr 2.5-6.1]), 630 (1.5 %) of patients with RA and 3058 (0.8%) of the comparators were registered with incident HF. The rate of HF was 3.6 HF/1000 person-years among the RA-patients and 2.0 HF/1000 person-years among the comparators. The corresponding risk increase of incident HF among the patients with RA was approximately 70% (Crude HR 1.69 [95% CI 1.56-1.85]) and remained statistically significantly increased after adjusting for potential confounders (Adjusted HR 1.53 [95% CI 1.40-1.67]). Stratifying RA patients by RF-positivity at index-date did not reveal any major differences between these two subgroups (Crude HR RF-positive subjects 1.66 [95% CI 1.51-1.84]; Crude HR RF-negative subjects 1.78 [95% CI 1.52-2.07]).

Conclusion: Patients with prevalent RA have an increased risk of developing non-ischemic HF. Our results support the proposed involvement of RA-related factors in the pathogenesis of HF, independent of vascular disease. The role of autoantibodies and other markers of RA disease is an important subject for further research.