Biologic disease modifying antirheumatic drugs (bDMARDs) may confer protection against major cardiovascular events (MACE) by acting directly on atherosclerotic plaque as well as reducing systemic inflammation, George Karpouzas, MD, stated in his abstract presentation at the American College of Rheumatology (ACR) Convergence on November 12.

Dr Karpouzas is professor of medicine at the David Geffen School of Medicine at UCLA and chief of the Division of Rheumatology at the Harbor-UCLA Medical Center.

Noting that chronic inflammation increases the risk of cardiovascular events among patients with rheumatoid arthritis (RA), Dr Karpouzas said that bDMARDS have been shown to improve outcomes and control inflammation for many patients who did not respond to conventional synthetic DMARD.

He and colleagues “explored whether baseline bDMARD use may influence the impact of disease activity and systemic inflammation on long-term cardiovascular risk in RA,” he explained. The team prospectively followed 4370 patients who did not have cardiovascular disease upon registration to An International Cardiovascular Consortium for people with RA (ATACC-RA). The outcomes included major adverse cardiovascular events (MACE)— defined as nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death— and any ischemic cardiovascular events (CVE) comprising MACE, coronary revascularization, stable angina pectoris, transient ischemic attack, and peripheral arterial disease with or without revascularization.

Using multivariable Cox models stratified by center, the researchers evaluated the impact of disease activity (DAS28-CRP), inflammation (CRP), bDMARD use, and their respective interactions on the risk of CVEs, after adjusting for age, gender, hypertension, diabetes, family history, smoking, and the ratio of total cholesterol to high-density lipoprotein.

Over a total of 26,534 patient years, 239 first MACE and 362 total ischemic CVE occurred. Among patients who did not use bDMARDs, the incidence of MACE and any ischemic CVE was 9.3 (95% CI 8.2-10.6) and 14.2 (12.8-15.8) events/1000PY respectively. Among users of bDMARDs those rates were 5.4 (95% CI 2.9-10.1) and 8.2 (5.0-13.6) events/1000PY.

“In the entire cohort, DAS-28 CRP and CRP(ln) associated with greater risk of MACE [(adjusted hazards ratio [aHR] 1.19 (95%CI 1.06-1.34), p=0.004 and HR 1.15 (1.02-1.28), p=0.017], while for all ischemic CVE the association was significant for DAS28-CRP [aHR 1.1 (95%CI 1.07-1.30)], but not CRP(ln) [aHR 1.06 (0.97-1.16)],” Dr Karpouzas explained.

In bDMARD nonusers, higher DAS28-CRP and CRP(ln) were associated with greater risk of MACE but not among bDMARD users. However, the researchers found no significant interaction between DAS28-CRP or CRP and bDMARD use on any ischemic CVE risk.

“Higher disease activity and systemic inflammation at baseline associated with greater risk of MACE in bDMARD nonusers but not in users,” he concluded. “This may suggest the presence of additional bDMARD-specific benefits directly on atherosclerotic plaque —such as plaque stabilization— above and beyond effects on systemic inflammation.”

Reference:

Karpouzas G. 0391: Biologic use regulates the impact of inflammation on ischemic cardiovascular risk in rheumatoid arthritis. Presented at: American College of Rheumatology Convergence. November 12, 2023. San Diego.