Poster 015: When MRI Is Not Enough: Empiric Treatment and Biopsy-Guided T-Cell–Targeted Therapy in Immune Checkpoint Inhibitor Myocarditis Presenting as Cardiogenic Shock

Background: Immune checkpoint inhibitor (ICI)–associated myocarditis carries high early mortality and may evade detection by cardiac MRI. Clinical deterioration despite nondiagnostic imaging presents a critical management dilemma in patients with cardiogenic shock, where delayed treatment may be fatal.

Methods: A 68-year-old man with metastatic renal cell carcinoma treated with ipilimumab/nivolumab presented with acute decompensated heart failure, marked troponin elevation (>10,000 ng/L), and a rapid decline in left ventricular ejection fraction from 50% to 25–30%. Coronary angiography demonstrated nonobstructive disease. Cardiac MRI was negative for myocarditis; however, given the severity of shock and strong clinical suspicion, the patient was empirically treated for ICI myocarditis.

He developed mixed shock with a dominant cardiogenic component requiring vasopressors and inotropic support, along with hypoxic respiratory failure and acute kidney injury requiring continuous renal replacement therapy. Right heart catheterization revealed low cardiac output with preserved filling pressures, supporting cardiogenic shock physiology.

Outcome: High-dose intravenous corticosteroids were initiated empirically despite negative MRI findings. Due to persistent hemodynamic instability and inadequate response to steroids, endomyocardial biopsy was pursued and confirmed lymphocytic myocarditis with CD4/CD8-positive T-cell infiltration.

Based on biopsy results, immunosuppression was escalated to targeted T-cell–directed therapy with mycophenolate mofetil, along with infliximab. Hemodynamics improved, allowing discontinuation of vasopressors and inotropes, and cardiac biomarkers trended downward with partial recovery of ventricular function.

The patient survived the acute myocarditis and cardiogenic shock phase, remaining hemodynamically stable for approximately three months. His subsequent course was complicated by immune-mediated myasthenia gravis, profound neuromuscular weakness, and prolonged ventilator dependence despite plasmapheresis and intravenous immunoglobulin. He ultimately died from non-cardiac complications related to neuromuscular respiratory failure rather than recurrent shock.

Conclusion: This case highlights that ICI myocarditis may require empiric treatment despite a negative cardiac MRI, and that early myocardial biopsy can be decisive when steroid response is inadequate. Biopsy-guided, T-cell–targeted immunosuppression can stabilize cardiogenic shock and permit meaningful short-term survival, even when ultimate outcomes are determined by other immune-related toxicities.