The Dyspnea Dilemma: Immune Checkpoint Inhibitor-Associated Myocarditis Mimicking Overlapping Cardiac Pathologies-A Case Report.

BACKGROUND

Immune checkpoint inhibitors (ICIs) such as durvalumab improve survival in solid tumors but can rarely cause fulminant myocarditis (reported in 1% of cases, with 25%-40% mortality). Clinical overlap with coronary artery disease (CAD), chemotherapy-related cardiomyopathy, or malignancy-associated complications makes diagnosis challenging.

CASE PRESENTATION: A 62-year-old woman with gallbladder adenocarcinoma on gemcitabine, cisplatin, and durvalumab presented with 1 week of progressive dyspnea, leg edema, and chest pain. She had a history of portal vein thrombosis on apixaban. On exam, she was tachycardic and hypoxic with signs of volume overload. Labs showed elevated BNP and troponin. EKG revealed lateral T-wave inversions and chest x-ray demonstrated pulmonary edema. Echocardiography showed a large fibrinous pericardial effusion without tamponade and reduced LVEF (41%) with apical wall motion abnormalities. Differentials included ischemia, chemotherapy toxicity, ICI myocarditis, or malignant/hemorrhagic effusion. After a multidisciplinary discussion, anticoagulation was held, and the patient was transfused. Serial echocardiography showed a stable effusion but persistent ST-T changes. Coronary angiography excluded obstructive CAD. Cardiac MRI demonstrated diffuse myocardial edema, most pronounced in apical segments, consistent with myocarditis. Given the temporal relationship to ICI therapy, durvalumab-associated myocarditis was diagnosed. High-dose corticosteroids were initiated with symptomatic improvement. She was discharged on gemcitabine-cisplatin, with durvalumab omitted. Anticoagulation was resumed. Discharge echocardiography showed persistent apical wall motion abnormalities with a small effusion.

CONCLUSION

This case highlights the diagnostic complexity of dyspnea in oncology patients, where multiple cardiac pathologies may coexist. A systematic, multidisciplinary approach-progressing from pericardial evaluation to ischemic work-up to advanced imaging-was crucial for diagnosis. Clinicians should maintain suspicion for ICI myocarditis when new heart failure or wall motion abnormalities occur without obstructive CAD, as early immunosuppressive therapy is critical.