Chronic inflammation in rheumatoid arthritis is associated with a twofold increase in sudden cardiac death compared with the healthy population, driven by electrophysiological and structural remodeling.
The increased risk of sudden cardiac death in rheumatoid arthritis involves complex proarrhythmic electrophysiological and structural remodeling beyond just coronary artery disease.
Effect estimate: twofold increase
Chronic inflammatory disorders, including rheumatoid arthritis (RA), are associated with a twofold increase in the incidence of sudden cardiac death (SCD) compared with the healthy population. Although this is partly explained by an increased prevalence of coronary artery disease, growing evidence suggests that ischemia alone cannot completely account for the increased risk. The present review explores the mechanisms of cardiac electrophysiological remodeling in response to chronic inflammation in RA. In particular, it focuses on the roles of nonischemic structural remodeling, altered cardiac ionic currents, and autonomic nervous system dysfunction in ventricular arrhythmogenesis and SCD. It also explores whether common genetic elements predispose to both RA and SCD. Finally, it evaluates the potential dual effects of disease-modifying therapy in both diminishing and promoting the risk of ventricular arrhythmias and SCD.
Patel et al. (Fri,) conducted a review in Rheumatoid arthritis. Rheumatoid arthritis (chronic inflammation) vs. Healthy population was evaluated on Sudden cardiac death (twofold increase). Chronic inflammation in rheumatoid arthritis is associated with a twofold increase in sudden cardiac death compared with the healthy population, driven by electrophysiological and structural remodeling.