TNF-Inhibitors Decrease Risk of Myocardial Infarction in Rheumatoid Arthritis Patients

Anti-TNFs reduce severity and incidence of myocardial infarction in RA patients.

A greater decrease in the risk of myocardial infarction (MI) was found in patients with rheumatoid arthritis (RA) administered tumor necrosis factor inhibitors (TNFi), compared with those administered disease-modifying anti-rheumatic drugs (DMARDs).

In a study published in Annals of the Rheumatic Diseases, investigators identified 11,200 patients with RA treated with TNFi and 3058 RA patients treated with only DMARDs.

Although participants in the DMARD group were slightly older than those in the TNFi group (average of 59.5 years versus 55.6 years), they had a shorter disease duration of 6 years compared with 11 years.

The propensity scores of the likelihood of receiving anti-TNF therapy were adjusted for age, sex, disease activity and duration, number of prior DMARDs, and comorbidities including diabetes, hypertension, and lung disease, according to MedPage Today.

The median follow-up in the DMARDs arm was 3.5 years compared with 5.3 years in the TNFi arm.

The results of the study showed that during a median follow-up, there were 194 verified first MIs in the TNFi group and 58 MIs in the DMARDs group. The median time to MI was 2.43 years for patients receiving a TNFi and 1.56 years for patients receiving DMARDs.

Of 198 patients with MI data, 35 had never received biologics (group 1), 108 were on a TNFi at the time of MI (group 2), and 55 had used a TNFi previously, but were no longer using them.

In markers of MI severity—–including cardiac arrest, peak creatine kinase or troponin levels, or length of hospital stay­­––no significant differences were observed between the groups, according to the study.

Within 6 months of the MI, deaths were seen in 21% of patients in group 1, 13% in group 2, and 48% in group 3. The age and sex adjusted OR for death were 0.68 (95% CI 0.31-1.47) in group 2 and 3.07 (95% CI 1.42-6.62) in group 3.

A majority of patients in group 3 who stopped treatment at a median of 1.3 years before MI did so due to adverse events, suggesting higher levels of comorbidity in this patient population, according to the study.

There is a biological plausibility for the observation that MI risk is lower with TNF inhibition as TNFα plays a key role in the pathogenesis of atherosclerosis.

“Inflammation is central in all stages of atherosclerosis, including endothelial function, plaque stabilization, and postinfarct remodeling, and thus inhibition of TNFα may influence accumulation and progression of plaque leading to fewer MIs,” the authors wrote, as reported by MedPage Today.

A limitation to the study were the potential effects of unmeasured confounders, such as cumulative doses of glucocorticoids, the authors noted.

The findings showed that patients with RA who received TNFi had a decreased risk of MI compared with patients with RA who received DMARDs over the medium term. According to the authors, this may be attributed to a direct action of TNFI on the atherosclerotic process, or better overall disease control.