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Immune-Mediated Myocarditis and Myositis Induced by Atezolizumab: A Case Report Highlighting Pharmacological Management

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Published online:

Correspondence: Diego Manuel de la Eranueva, diegodelaeranueva@gmail.com

Copyright:

© The Author(s). This work is open access and is licensed under CC-BY-NC 4.0. Users may copy, redistribute and make derivative works for non-commercial purposes, provided the original work is cited correctly.

Introduction: Immune checkpoint inhibitors (ICIs), such as atezolizumab, have revolutionised cancer therapy but can cause severe immune-related adverse events (irAEs). Among these, myocarditis and myositis, though rare, carry high morbidity and mortality. Optimal pharmacological management remains challenging due to their severity and unpredictable course.

Case: We report a 64-year-old male, ex-smoker, with multiple cardiovascular risk factors (hypertension, type 2 diabetes mellitus, dyslipidaemia) and chronic obstructive pulmonary disease (COPD). He was diagnosed with stage IV high-grade urothelial bladder carcinoma and started atezolizumab in October 2019. During treatment, he developed immune-mediated myocarditis and myositis, initially treated with high-dose intravenous (IV) methylprednisolone pulses (1,000 mg/day for three days), then oral corticosteroids at 1 mg/kg/day plus mycophenolate mofetil. Despite this, he developed rapid atrial fibrillation with acute heart failure due to severe left ventricular dysfunction, requiring inotropic support. Given the poor response, IV immunoglobulins were added without success. The patient progressed to refractory cardiogenic shock and died despite plasmapheresis and maximal supportive care.

Discussion: This case highlights the life-threatening potential of immune checkpoint inhibitor (ICI)-induced myocarditis and myositis and the complexity of managing them. High-dose corticosteroids are the mainstay, but many patients need further immunosuppression, including mycophenolate, IV immunoglobulins or plasmapheresis. The rapid atrial fibrillation with severe left ventricular dysfunction and decompensated heart failure further complicated care, showing the need for early cardiac monitoring and multidisciplinary management. Early detection and timely escalation of immunosuppressive therapy are critical but may still fail. Pharmacological management must balance immunosuppression with cardiac support, including antiarrhythmics, inotropes and, if needed, mechanical circulatory support.

Conclusion: ICIs have transformed oncology but can cause severe and irAEs, such as myocarditis and myositis. This case underlines the need for early detection, prompt corticosteroid treatment, escalation of immunosuppression and intensive cardiac support in cases of severe arrhythmias and left ventricular dysfunction. Increased awareness and close monitoring are vital. Further research should define optimal protocols and help identify high-risk patients.

References

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