Abstract
Background
Immune-mediated myocarditis is a rare and potentially fatal complication of oncologic immunotherapy. While most reported cases have been associated with the use of immune checkpoint inhibitors (ICIs), novel immunotherapy agents may also pose cardiac risks that warrant further attention. We report a case of fulminant, steroid-refractory myocarditis following initiation of talquetamab, a bispecific T-cell engager (BiTE) targeting CD3 and GPRC5D used for relapsed or refractory multiple myeloma (MM).Case presentation
A 69-year-old man with MM refractory to multiple lines of treatment presented to his outpatient cardio-oncologist with syncope and intermittent chest pain 4 weeks after starting talquetamab. He was found to have elevated high-sensitivity troponin and new inferior Q waves on EKG. He presented to the hospital, where he was admitted to the cardiac intensive care unit. New ST-segment elevations in the inferior leads were subsequently observed on serial EKGs. Transthoracic echocardiography showed a decreased left ventricular (LV) ejection fraction with new regional wall motion abnormalities. Left and right heart catheterization and endomyocardial biopsy were unremarkable. Cardiac magnetic resonance imaging (MRI) revealed segmental late gadolinium enhancement, myocardial edema, increased T1 time, and increased extracellular volume. Acute myocarditis due to talquetamab was presumed, and intravenous steroid therapy was initiated. His symptoms and biomarkers initially improved but later worsened despite steroid therapy. He received additional immunosuppressive therapies including tocilizumab, mycophenolate mofetil, intravenous immunoglobulin, and ruxolitinib. However, his biomarkers and LV systolic function continued to worsen, ultimately resulting in death.Conclusions
This case underscores the potential for immune-mediated myocarditis associated with talquetamab to follow a fulminant and treatment-refractory course despite guideline-directed escalation of immunosuppression, with important implications for clinical recognition and management. It also illustrates the diagnostic challenge of immune-mediated myocarditis presenting as an ST-segment elevation myocardial infarction (STEMI) mimic with non-obstructive coronary arteries. Finally, it emphasizes the complementary role of cardiac MRI in establishing the diagnosis when endomyocardial biopsy is non-diagnostic.