The effect of biological DMARDs on the risk of congestive heart failure in rheumatoid arthritis: a systematic review

ABSTRACT

Introduction: A common cardiovascular manifestation in rheumatoid arthritis (RA) is congestive heart failure (CHF) in which inflammation is considered to play a pivotal role. Although anti-inflammatory therapy such as biological disease-modifying anti-rheumatic drugs (bDMARDs) have the potential of improving the cardiac function and reducing the risk of CHF, the published studies showed contrasting results. This review aims to systematically summarize and analyze literature regarding the effect of bDMARDs on the cardiac function and on the risk of CHF in RA.

Areas covered: Observational cohort, randomized controlled trials and case-controlled studies were included. The systematic literature search was conducted in PubMed, Wiley/Embase, Cochrane, Web of Science and clinicaltrials.gov (up to 2017). Two authors assessed abstracts for inclusion and methodological quality was assessed by one reviewer.

Expert opinion: RA patients have a clinically relevant increased risk of developing CHF needing further attention. However, we found a lack of high quality studies. Future studies should focus on distinguishing the effect of myocardial inflammation reduction versus antibody-specific myocardial cellular effects of bDMARDs to improve the understanding of the effects of bDMARDs in RA patients and the relation with the development of CHF.

KEYWORDS:

• Congestive heart failure
• cardiac function
• inflammation
• rheumatoid arthritis
• bDMARDs
• cardiac imaging
• incidence/prevalence
• NT-proBNP

Article highlights

• It is unlikely bDMARDs increase the risk of developing CHF in RA patients.

• bDMARDs probably have favorable effects on the cardiac function in RA patients.

• Anti-TNF agents decrease plasma NT-proBNP levels.

Future large and high quality studies, especially RCTs, are required to give a clear view of the effect of bDMARDs on cardiac function and the risk for developing CHF in RA patients.

This box summarizes key points contained in the article.

Acknowledgments

We thank Johannes C.F. Ket, MSc, Medical Information Specialist, Medical Library, VU University Amsterdam, for his contribution to the systematic literature searches.

Declaration of interest

MT Nurmohamed has received consultancy/speaking fees or research support to his institution from: Pfizer, Abbvie, Roche, BMS, MSD, Mundipharma, UCB, Janssen, Menarini, Eli Lilly, and Celgene. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

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Funding

This paper is not funded.