What is the clinical evidence from this study?

Study design: Case Report. Population: Fulminant myocarditis (n=1). Intervention: Talquetamab.

What question did this study set out to answer?

To report a rare case of fulminant myocarditis induced by talquetamab, an immunotherapy agent, associated with significant cardiac complications.

June 19, 2026Cardio-Oncology0 citationsOpen Access

A rare case of fulminant talquetamab-induced myocarditis presenting as a STEMI mimicker

EKEric J. KimIcahn School of Medicine at Mount Sinai SSSara Diaz SaraviaIcahn School of Medicine at Mount Sinai GSGagan SahniMount Sinai Hospital

Key Result

Talquetamab therapy for multiple myeloma can cause fulminant, treatment-refractory myocarditis that mimics an acute ST-segment elevation myocardial infarction and can lead to death.

Key Points

To report a rare case of fulminant myocarditis induced by talquetamab, an immunotherapy agent, associated with significant cardiac complications.
Patient presented with syncope and chest pain after starting talquetamab.
Diagnosis was supported by elevated troponin levels and echocardiography findings.
Cardiac MRI helped reveal myocardial edema and late gadolinium enhancement.
Patient exhibited worsening cardiac function despite escalating immunosuppressive therapy.
Cardiac MRI findings indicated acute myocarditis and guided diagnosis.
Ultimately, the patient succumbed to heart failure associated with myocarditis.

Study Design

Type

Case Report (n=1)

Multicenter

Structured PICO

Population

A 69-year-old man with refractory multiple myeloma who developed fulminant, steroid-refractory myocarditis 4 weeks after initiating talquetamab.

Intervention

Talquetamab (a bispecific T-cell engager targeting CD3 and GPRC5D), followed by immunosuppressive therapies (intravenous steroids, tocilizumab, mycophenolate mofetil, intravenous immunoglobulin, and ruxolitinib) for presumed acute myocarditis.

Talquetamab can cause fulminant, treatment-refractory immune-mediated myocarditis that may present as a STEMI mimic and require cardiac MRI for diagnosis when biopsy is non-diagnostic.

Limitations

Single case report
Patient had pre-existing borderline cardiomyopathy with fibrotic or infiltrative changes
Recent rhinovirus infection could theoretically be an alternative etiology

Abstract

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). 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. 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.

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