Newswise — BOSTON — Not only does treatment with tumor necrosis factor (TNF) inhibitor biologic drugs not increase the risk of congestive heart failure in people with rheumatoid arthritis, but it may decrease the incidence of this serious cardiovascular disease in these patients, according to new research findings presented this week at the American College of Rheumatology Annual Meeting in Boston.
Rheumatoid arthritis is a chronic disease that causes pain, stiffness, swelling and limitation in the motion and function of multiple joints. Though joints are the principal body parts affected by RA, inflammation can develop in other organs as well. An estimated 1.3 million Americans have RA, and the disease typically affects women twice as often as men.
RA often is associated with a higher risk of cardiovascular disease, including an increased incidence of congestive heart failure (CHF) in this patient population. RA inflammation may be a factor in this increased CHF risk. TNF-inhibitor drugs may control RA inflammation and thereby offer protection against the onset of CHF, but past research suggested that these biologic drugs may worsen existing CHF.
Researchers in Manchester, United Kingdom, compared CHF incidence in RA patients on TNF-inhibitor therapy versus therapy with non-biologic disease-modifying antirheumatic drugs (DMARDs). Using data from patients diagnosed with RA who were enrolled in the British Society for Rheumatology Biologics Register, the researchers identified and validated 87 cases of CHF events, including 48 in 3,662 patients using DMARDs and 39 in 12,397 patients using TNF-inhibitor therapy.
“The primary aim of this study was to examine the incidence of CHF in subjects with RA treated with TNF inhibitors and to compare this to the incidence in subjects with RA treated with non-biologic DMARDs,” said Alper van Sijl, PhD, of the ANIOS Interne Geneeskunde at Diakonessenhuis in Utrecht, The Netherlands, and a lead author of the study.
Potential CHF events were verified according to Framingham criteria by a cardiologist from the patients’ death certificates and from clinical follow-up forms. New CHF events which occurred within six months after another cardiac event (such as a myocardial infarction) were excluded. Risk of CHF was compared between the two cohorts using a Cox regression model, propensity scores adjusted.
The researchers found a much lower incidence of CHF among patients using TNF-inhibitors. After adjustment for differences in baseline characteristics, the hazard ratio (95-percent confidence interval) of CHF in patients on TNF-inhibitors compared to non-biologic DMARDs was 0.31. The crude incidence rate of verified CHF per 10,000 person-years was 25.67 for patients using non-biologic DMARDs and only 6.27 for patients using TNF-inhibitors. Similar results were found for analysis limited to first TNF-inhibitors only and in patients without prior history of ischemic heart disease.The study’s authors concluded that TNF-inhibitor therapy causes no increased risk of CHF in RA patients compared to using non-biologic DMARDs, and patients on the biologic therapy actually had a decreased risk of CHF.
“These data add to the currently available body of evidence suggesting no increased risk of CHF in subjects exposed to TNF inhibitors,” says Dr. van Sijl. “A reduced risk of CHF was even noted in subjects treated with TNF inhibitors. Subjects with markers of disease severity were at the highest risk of developing CHF. Whether this result is attributable to suppression of inflammation, drug-specific effects or channeling bias remains unknown.”
Funding sources for this study included restricted income financial support from Abbvie, Amgen, Swedish Orphan Biovitrum (SOBI), Merck, Pfizer Ltd., Roche products Ltd., UCB Pharma Ltd. This income finances a separate contract between the BSR and the University of Manchester who provide and run the BSRBR.
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The American College of Rheumatology is an international professional medical society that represents more than 9,500 rheumatologists and rheumatology health professionals around the world. Its mission is to Advance Rheumatology! The ACR/ARHP Annual Meeting is the premier meeting in rheumatology. For more information about the meeting, visit http://www.acrannualmeeting.org/ or join the conversation on Twitter by using the official #ACR14 hashtag. Paper Number: 1909
Incidence of Congestive Heart Failure in Subjects with Rheumatoid Arthritis Receiving Anti-Tumour Necrosis Factor Drugs: Results from the British Society for Rheumatology Biologics Register for Rheumatoid Arthritis
Alper van Sijl1, Mamas Mamas2, Mark Lunt3, . BSRBR Control Centre Consortium4, Kath Watson5, Deborah P. Symmons4 and Kimme L. Hyrich6, 1Arthritis Research UK Centre for Epidemiology, Centre for Musculoskeletal Research, Manchester Academic Health Science Centre, University of Manchester, Manchester, United Kingdom, 2Manchester Heart Centre, Manchester Royal Infirmary, Oxford Road, Manchester, UK; Institute of Cardiovascular Sciences, University of Manchester, Manchester, United Kingdom, 3University of Manchester, Manchester, United Kingdom, 4Arthritis Research UK Centre for Epidemiology, University of Manchester, Manchester, United Kingdom, 5Arthritis Research UK Epidemiology Unit, The University of Manchester, Manchester, United Kingdom, 6Centre for Musculoskeletal Research, University of Manchester, Manchester, United Kingdom
Background/Purpose Subjects with rheumatoid arthritis (RA) are at a higher risk of developing cardiovascular (CV) disease compared to the general population, with an increased incidence of congestive heart failure (CHF) possibly mediated by chronic inflammation. Anti-tumour necrosis factor (TNFi) drugs might reduce the incidence of new CHF by supressing inflammation. However, TNFi are associated with a worsening of existing CHF. The aim of this analysis was to compare the incidence of CHF in subjects with RA treated with TNFi to that in those receiving non-biologic drugs (nbDMARDs).
Methods Patients with a physician diagnosis of RA enrolled in the British Society for Rheumatology Biologics Register, a national prospective cohort study established in 2001 to monitor the long-term safety of TNFi. Potential CHF events were verified according to Framingham criteria by a cardiologist from death certificates and from clinical follow-up forms of consultants. New CHF which occurred within 6 months after another cardiac event (eg. myocardial infarction) was excluded. Risk of CHF was compared between the two cohorts using a Cox regression model, propensity scores adjusted. Subjects were censored at first episode of CHF, death, first missed dose of TNFi + 180 days, last returned clinician follow-up or 31/01/2014, whichever came first.
Results A total of 87 validated first CHFs were analysed: 48 in 3,662 nbDMARD subjects and 39 in 12,397 TNFi-exposed subjects. After adjustment for differences in baseline characteristics, the hazard ratio (95%-confidence interval) of CHF in patients on TNFi compared to nbDMARD was: 0.31 (0.18-0.52). Similar results were found for analysis limited to first TNFi only and in patients without prior history of ischaemic heart disease. Conclusion No increased risk of CHF was observed in those patients selected for TNFi therapy compared to those receiving nbDMARD therapy. A reduced risk of CHF was noted in patients treated with TNFi.
Fully adjusted model by propensity score (PD) consisting of age, gender, DAS28, disease duration, HAQ, steroid use, NSAIDs, COXIBs, hypertension, diabetes mellitus, angina pectoris, myocardial infarction, smoking history and use of statins, antiplatelets, ACE-inhibitors, warfarin and digoxin.
Disclosures: A. van Sijl, NoneM. Mamas, NoneM. Lunt, NoneBSRBR Control Centre Consortium, NoneK. Watson, NoneD. P. Symmons, NoneK. L. Hyrich, Pfizer Inc, 9, Abbott Immunology Pharmaceuticals, 9
Meeting Link: American College of Rheumatology Annual Meeting
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