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Biologics Could Reduce Risk of Heart Attack in Arthritis Patients by 40%

RHEUMATOID arthritis patients receiving biological treatments can have a reduced heart attack risk of 39% when compared to patients receiving only synthetic drugs, according to the results of a new study.

The findings that tumour necrosis factor inhibitor (TNFi) biologic drugs may lead to fewer heart attacks in arthritis patients could inform a review of existing treatment guidelines, according to researchers. “Further research is needed to investigate the mechanisms behinds this, but we think that TNFis reduce the inflammation in the arteries, helping to keep blood flowing freely to the heart,” explained Prof Chris Gale, University of Leeds, Leeds, UK, who was involved in the research. “We are now keen to find out whether immunosuppressive agents can reduce the risk of heart attack in other high-risk populations.”

Prof Gale and colleagues examined the British Society for Rheumatology Biologics Register and the Myocardial Ischaemia National Audit Project to analyse the risk of heart attacks in patients. They looked at 11,200 rheumatoid arthritis patients receiving a TNFi and 3,058 patients who were receiving a synthetic disease-modifying anti-rheumatic drug (sDMARD). Rheumatoid arthritis causes a much higher risk of heart attack, thought to be due to it causing inflammation in the body.

In their recently publishing findings, the team found that over 3–5 years follow-up, those taking a TNFi had a 39% risk reduction in having a heart attack compared to those receiving only a sDMARD. Guidelines in the UK currently restrict the prescription of TNFi drug to rheumatoid arthritis patients with a highly active and sustained form of the disease and only after failure to respond to sDMARDs. Around 15% of patients receive biologic therapies while those with more moderate forms of the disease are not eligible.

“Rheumatoid arthritis patients already have to endure a debilitating condition, but to have an elevated risk of heart attacks because of their disease is a very worrying complication,” Research Leader Prof Kimme Hyrich, University of Manchester, Manchester, UK, explained. “The prescribing guidelines for TNFi therapies are very specific, and for good reason. However, the biologically plausible explanation for our findings – not only that TNFi reduces the inflammation associated with atherosclerosis (where plaque builds in the arteries) but that it also may inhibit the accumulation and progression of plaque leading to fewer heart attacks – could be used to review existing guidelines and in particular, extend the use to patients with moderate levels of disease activity.”

Jack Redden, Reporter

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