Arthritis drug cuts heart attack risk

A drug used to treat rheumatoid arthritis can reduce the risk of heart attacks in such patients by nearly 40%, a new study has found.

Those with rheumatoid arthritis have a much higher risk of heart attacks, which is thought to be due to inflammation in the body caused by the disease.

Now doctors have discovered that a biologic drug used to treat inflammation in joints – called a tumour necrosis factor inhibitor (TNFi) – appears to have a protective effect on the heart.

Biologic drugs are genetically-engineered proteins which suppress parts of the immune system.

University of Leeds Associate Professor of Cardiovascular Health Sciences and Honorary Consultant Cardiologist, Dr Chris Gale, was involved in the multi-institutional research.

He said: “This study, which linked the national registry of patients with rheumatoid arthritis (RA) with the national health attack registry, shows a striking relationship between the use of biological treatments for rheumatoid arthritis and reduced risk of heart attack. 

“Further research is needed to investigate the mechanisms behind this, but we think that TNFis reduce the inflammation in the arteries, helping to keep blood flowing freely to the heart.

High-risk populations 

“We’re now keen to find out whether immunosuppressive agents can reduce the risk of heart attack in other high-risk populations.”

The researchers used the British Society for Rheumatology Biologics Register and the Myocardial Ischaemia National Audit Project to analyse the heart attack risk of two groups of RA patients who were taking different types of drugs.

The first group of 11,200 patients were taking a TNFi; the second group of 3,058 patients were taking a synthetic Disease-Modifying Anti-Rheumatic Drug (sDMARD).

Over three to five years of follow-up, the researchers noted that the risk of heart attacks was reduced by 39% in patients who received a TNFi compared to those who had received a sDMARD only.

Current guidelines in the UK restrict the prescribing of TFNi in RA patients to those with a sustained and highly active disease which has failed to respond to therapeutic doses of sDMARDS.

Other patients with persistent inflammation at a more moderate level are not eligible. It is estimated that around 15% of patients with RA are receiving biologic therapies.

Research leader Professor Kimme Hyrich, from the University of Manchester’s Division of Musculoskeletal and Dermatological Sciences said: “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.

“In addition to managing risk factors such as high blood pressure and high cholesterol, achieving excellent control of inflammation can also reduce this risk.

“Our team has been able to show that this elevated risk can be reduced significantly by using biological drug therapies such as TNFi.

“The prescribing guidelines for TFNi therapies are very specific, and for good reason.

“However, the biologically plausible explanation for our findings – not only that TFNi 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.”

The study is published in the Annals of the Rheumatic Diseases.