# Immune Checkpoint Inhibitor–Induced Myocarditis: A Late Presentation

## TL;DR

A patient developed severe heart failure 13 months after receiving an immune checkpoint inhibitor for breast cancer, highlighting the delayed and potentially fatal side effect of myocarditis.

## Contribution

This case report demonstrates the delayed onset and successful treatment of ICI-associated myocarditis, emphasizing the importance of early recognition.

## Key findings

- ICI-associated myocarditis can present as late as 13 months after treatment initiation.
- Early recognition and treatment with high-dose steroids can lead to recovery from cardiogenic shock.
- ICI myocarditis should be considered in the differential diagnosis of delayed-onset heart failure.

## Abstract

Immune checkpoint inhibitors (ICIs) have revolutionized oncology by providing a new treatment modality for a wide range of malignancies. ICIs have been shown to aid in remission of cancers with poor prognosis, including stage IV malignancies. The first ICI was approved for metastatic melanoma, but now ICI indications range from melanoma to small cell lung cancer and triple-negative breast cancer. While this drug class has revolutionized cancer treatment, ICIs can also cause a broad range of immune-related adverse events, including myocarditis. ICI myocarditis has a broad clinical presentation, from fulminant heart failure to cardiac arrhythmia, and is confirmed with a histopathology finding of myocardial infiltration by T lymphocytes and macrophages and cell death. We present a case of cardiogenic shock secondary to ICI-associated myocarditis with onset 13 months after administration of pembrolizumab for triple-negative breast cancer.

A 30-year-old female with history of triple-negative breast cancer presented to the emergency department with a 1-month history of progressive chest tightness, dyspnea on exertion, and dry cough. The patient was diagnosed with acute decompensated heart failure (stage C cardiogenic shock), started on milrinone and vasopressin, and transferred to our institution for a higher level of care. At that time, she progressed to stage D cardiogenic shock. A presumptive diagnosis of ICI-associated myocarditis was made within 12 hours, and treatment with high-dose intravenous methylprednisolone was initiated. Despite the high mortality associated with ICI-associated myocarditis, the patient improved and was discharged 9 weeks after admission.

This case highlights the importance of considering ICI myocarditis in the differential diagnosis of cardiogenic symptoms, even in delayed presentations, and supports the lifesaving potential of early recognition and treatment.