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Remission, TNF Blockers Cut Heart Failure Risk in RA

(ACR2014) Two new studies confirm that being in remission dramatically reduces the increased risk for heart failure among rheumatoid arthritis patients. The larger one suggests that TNF-alpha inhibitors completely erase the added risk of congestive heart failure.

Schau T, Gottwald M, Butter M, Zaenker M, Disease Remission Reduces Risk of Heart Failure in Rheumatoid Arthritis Patients Independent of Treatment Strategy. ACR #945. Arthritis & Rheumatism. 2014 66(1)-Supplement.

van Sijl A, Mamas M, Mark Lunt M. 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. ACR# 1909. Arthritis & Rheumatism. 2014 66(1)-Supplement.

New studies find that the risk for heart failure (HF) in rheumatoid arthritis (RA) may be reduced by two thirds when patients achieve remission – and that risk may be cut in half with anti-tumor necrosis factor-alpha (TNF-α) drugs.

Compared with healthy individuals, German researchers report, RA patients have as much as a 4- to 6-fold greater prevalence of HF (24% versus 6%)-mostly diastolic HF, where the left ventricle can’t fill properly. Subgoup analysis showed the risk for RF distributing with disease severity. Among RA patients in disease activity in 28 joints (DAS28) remission the HF risk is just 13%, they revealed at the 2014 meeting of the American College of Rheumatology.

The prospective, cross-sectional study compared 157 consecutive patients who met ACR/EULAR criteria for RA from the center’s outpatient clinic recruited over a 3-month period, with 77 age- and gender-matched controls. Both groups had fairly equal numbers of men and women and were comparable in age (around age 60). Around one quarter of the RA patients had HF.

In addition to traditional cardiac risk factors like high blood pressure and obesity, systemic inflammation and persistent disease activity are thought to be independent contributors to HF risk in RA.

Those with HF tended to be significantly older, female, with higher rates of high blood pressure and chronic kidney disease, notes Michael Zaenker MD of the Immanuel Klinikum Bernau Rheumatology Center in Northern Brandenburg, Germany.

“We observed that younger patients also had premature heart failure and, even in remission, their risk of heart failure was increased,” observes Zaenker, one of the study authors.

Diastolic heart failure alone increases the risk of death four-fold in RA patients, he adds, and the prevalence is often underestimated due to different diagnostic criteria.

Some research has suggested that anti-TNF drugs may worsen existing congestive (CHF). However, researchers in the Netherlands say the risk for CHF appears to be reduced almost 50% among RA patients treated with TNF-α inhibitors, compared with those on non-biologic disease modifying anti-rheumatic drugs (DMARDs).

The German study found only a slight, non-significant difference between TNFs and other treatments.

The Dutch study, also reported at the ACR annual meeting, involved more than 16,000 patients enrolled in the British Society for Rheumatology Biologics Register.

Researchers found a total of 87 validated HF events: 48 among patients using DMARDs (n=3,662) and 39 among patients (n=12,397) on anti-TNF drugs. The crude incidence rate of CHF per 10,000 person-years was 25.67/10.000 patient-years for those using non-biologic DMARDs and only 6.27/10,000 patients years for the others on TNF inhibitors.

Our data suggest that there is no increased risk of congestive heart failure for tumor necrosis factor inhibitors,” lead author Alper van Sijl, PhD, told a news conference.

After adjustment for differences in baseline characteristics, the hazard ratio (95% confidence interval) of CHF in patients on anti-TNF drugs compared to non-biologic DMARDs was only 0.31, according to van Sijl.

As in the German study, Dutch RA patients with greater disease severity had a higher risk of CHF, but it’s unclear whether this was due to suppression of inflammation, drug-specific effects, or selection bias, van Sijl said.