Anti-TNF therapy and other biologics — often used for the treatment of inflammatory arthritis — partially protect ankylosing spondylitis patients from heart disease, according to Australian researchers.
Their study, “Biologics and cardiovascular events in inflammatory arthritis: a prospective national cohort study,” was published the journal Arthritis Research & Therapy.
Patients with inflammatory arthritis such as rheumatoid arthritis (RA), ankylosing spondylitis (AS), and psoriatic arthritis (PsA) have a two-times higher risk of developing cardiovascular events.
Studies have suggested that this may be due to inflammatory processes driven by molecules involved in inflammatory immune responses, called cytokines, including tumor necrosis factor (TNF).
Researchers have speculated that inhibitors against TNF could help reduce the risk of heart disease by controlling inflammation. There are a variety of anti-TNF agents available, including infliximab (Remicade), adalimumab (Humira, Imraldi), golimumab (Simponi), certolizumab (Cimzia), and etanercept (Enbrel).
In fact, numerous studies have shown that treatment of inflammatory arthritis with TNF inhibitors is associated with an improvement in markers of cardiovascular health.
But there appears to be conflicting evidence regarding the effectiveness of TNF inhibitors. While some studies report a lower risk of heart disease, others report no significant differences.
Researchers now conducted a study to investigate the risk of cardiovascular events (CVEs) in patients with RA, AS, or PsA who underwent treatment with anti-TNF inhibitors and compared this risk with other biologics or non-biologic therapies.
Additionally, researchers compared the risk of CVEs between the various patients’ subgroups.
Data from 4,140 patients with RA, PsA and AS from the Australian Rheumatology Association Database was analyzed. CVEs were defined as angina (chest pain caused by reduced blood flow to the heart); myocardial infarction (heart attack); coronary artery bypass graft (surgery to improve blood flow to the heart); percutaneous coronary intervention (a stent implant to widen a blood vessel); other heart disease, stroke/transient ischaemic attack, or death from cardiovascular causes.
Researchers adjusted their analysis for confounding factors such as age, sex, diagnosis, pharmacotherapy use, smoking, alcohol consumption, high blood pressure, high blood fat levels, diabetes, and functional status (as assessed by the health assessment questionnaire disability score).
Statistical analysis revealed that anti-TNF therapy was associated with a reduction in heart disease or CVE risk by 15%.
Additionally, patients who used other biologics, including Kineret (anakinra); Rituxan (rituximab); Orencia (abatacept); and Actemra (tocilizumab); experienced a 19% reduction in CVE risk.
This benefit was not seen in patients who ceased biologic therapy, suggesting that current biologic use is necessary for protection against heart disease and other CVEs.
There were no significant differences in CVE risk between participants with RA, PsA, or ankylosing spondylitis.
“Current use of biologics, whether anti-TNF or another mechanism of action, is associated with a reduction in the CVE rate compared to the rate among people with inflammatory arthritis who are biologic-naïve,” the authors concluded.