Published: Nov 19, 2014
BOSTON -- The risk of congestive heart failure (CHF) is reduced in rheumatoid arthritis (RA) patients taking anti-tumor necrosis factor (TNF) drugs compared with those receiving nonbiologic disease-modifying anti-rheumatic drugs (nbDMARDs), according to new research.
The findings may encourage rheumatologists who may have hesitated to prescribe anti-TNF therapy, said lead author Alper van Sijl, PhD, of the ANIOS Interne Geneeskunde at Diakonessenhuis in Utrecht, the Netherlands.
"Rheumatoid arthritis patients are at increased risk of CHF, and trials in the early 2000s of anti-TNF therapy on patients with severe CHF showed no favorable effect and even a small deleterious effect of anti-TNF on the development of CHF," he said.
"Subsequently, this might have resulted in fears of clinicians for prescribing anti-TNF therapy in RA patients. However, we also know that in RA inflammation is an important factor involved in the development of CHF, and anti-TNF therapy should therefore decrease, or at least stabilize the risk of CHF in this group of patients, which we have shown in this research."
The study, which he presented at the annual meeting of the American College of Rheumatology, included all patients registered between 2001-2013 with The British Society for Rheumatology Biologics Register (BSRBR), a prospective cohort of patients treated with biologics for RA.
Rates of validated CHF were compared in 3,662 patients treated with nbDMARDs (mean age 60 years) and 12,397 patients treated with anti-TNF medication (mean age 56 years), giving 18,698 and 62,244 person years of follow-up respectively.
The study excluded all patients whose CHF was secondary to, or was preceded by an arrhythmia, valvular disease, or other causes of CHF, and CHF was defined according to the Framingham criteria.
After a median follow-up time of 5 years per patient there were 48 CHF events in the nbDMARD group and 39 CHF events in the anti-TNF group, giving an incidence rate per 10,000 person years of 25.7 versus 6.3 respectively.
"Therefore the adjusted hazard ratio of developing CHF in patients treated with TNF inhibitors was 0.25, while only looking at patients who did not have any prior ischemic heart disease, the hazard ratio was 0.30 -- both statistically significant," he said.
Adjustment was made for demographics, cardiovascular risk factors, RA-specific factors, and medication use.
"So, overall, we see that patients receiving anti-TNF therapy don't have an increased risk but seem to have a decreased risk compared to patients treated with nonbiologic DMARDS, and this finding seems to persist in patients free from ischemic heart disease," he concluded.
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