Steroids Versus Immunomodulators in Cardiac Sarcoidosis: A Systematic Review

Granulomatous inflammation of the heart causes arrhythmias, heart block, and heart failure in cardiac sarcoidosis (CS), a rare but potentially deadly condition. There is increasing interest in using immunomodulators as steroid-sparing medicines, even though corticosteroids are still the usual treatment. This study compared corticosteroids and immunomodulatory treatments through a systematic review and meta-analysis. After a thorough literature search in October 2024, 11 pertinent studies were found. These included observational studies, case series, and randomized controlled trials. Based on changes in myocardial inflammation (SUVmax) and left ventricular ejection fraction (LVEF), the effectiveness of corticosteroids, methotrexate, infliximab, rituximab, and their combinations was evaluated. The analysis revealed that all treatments significantly reduced myocardial inflammation, with methotrexate showing the highest effect size (d = 1.65, p < 0.001). Infliximab in combination with corticosteroids also demonstrated a significant reduction in SUVmax (d = 1.61, p < 0.001). LVEF improved across all treatment groups, although the effect was modest, with infliximab and corticosteroids showing the most significant increase in LVEF (d = 0.4, p = 0.05). The differences between subgroups were not statistically significant (p = 0.46 for SUVmax, p = 0.36 for LVEF). Corticosteroids remain the standard first-line treatment for CS, while methotrexate has shown the highest effect size for reducing myocardial inflammation, supporting its role as a steroid-sparing agent with fewer long-term side effects. Infliximab is effective but carries risk of infection. These findings highlight the need for customized treatment regimens in the management of CS. This study underscores the urgent need for more research to enhance combination medications, pinpoint patient subgroups that may benefit most from specific therapies, and enhance treatment regimens in the field of CS.