Tal Friedman Korn, Omri Zveik-Lavi, Dana Ekstein, Adi Vaknin-Dembinsky, Ronen Durst, Batla Falah, Marc Gotkine
Myasthenia gravis (MG) is an autoimmune neuromuscular disorder primarily caused by autoantibodies against acetylcholine receptors (AChR), leading to muscle weakness. In 2021, efgartigimod was FDA-approved as the first neonatal Fc receptor (FcRn) blocker for generalized MG, reducing pathogenic IgG autoantibodies and improving symptoms. We present a 39-year-old woman with AChR-positive generalized MG and a history of resolved inflammatory myocarditis. Owing to persistent weakness despite intravenous immunoglobulin, she transitioned to efgartigimod. Efgartigimod induced significant neuromuscular improvement, reducing her myasthenia gravis activities of daily living (MG-ADL) score from 9 to 4. However, 3 months later, she developed fatal fulminant heart failure (LVEF 20%-25%) without concurrent skeletal muscle weakness. Despite emergency intervention with veno-arterial extracorporeal membrane oxygenation, the patient died after anoxic brain injury. Although efgartigimod effectively reduces pathogenic IgG, it may not adequately suppress cellular or cytokine-mediated inflammation driving MG-associated myocarditis. Clinicians should exercise caution and maintain cardiac monitoring when prescribing FcRn blockers to patients with a history of myocardial involvement.