Three Cases of Immune Myocarditis Associated with Camrelizumab Use

Introduction: Immune checkpoint inhibitors can cause immune-related adverse events in various organ systems, with myocarditis being the most serious and life-threatening. This article reports three cases of immune myocarditis induced by camrelizumab, detailing the diagnostic and treatment process. Case Report: Three cases of immune-related myocarditis caused by the use of camrelizumab are reported. Three patients (case 1, male, 44 years old; case 2, male, 69 years old; and case 3, male, 53 years old) were treated with the immune checkpoint inhibitor, camrelizumab 200 mg, intravenously for nasopharyngeal and esophageal cancers. In case 1, 18 days after the 3rd cycle of immunotherapy, the patient’s troponin levels were elevated. In case 2, 1 day after the 1st cycle of treatment, troponin levels were elevated. The electrocardiogram showed right bundle branch block with left anterior branch block and abnormal ST-T segments in the lower wall, and the echocardiogram showed segmental ventricular dyskinesia and thickening of the myocardium of the left and right ventricles. In case 3, 12 days after the 3rd cycle of treatment, the patient developed chest tightness and breathlessness, and cardiac biomarkers were elevated. The electrocardiogram showed borderline QT interval prolongation and extensive ST-T segment changes, and cardiac ultrasound showed thinning of the myocardium in the middle and lower left ventricular anterior and lower posterior walls and loss of motility. All 3 patients were diagnosed with immune-associated cardiomyositis induced by camrelizumab, and camrelizumab was discontinued. In case 1, methylprednisolone succinate was administered as an intravenous infusion of 500 mg once a day for 4 days, and the patient’s troponin levels gradually decreased. In case 2, following the administration of intravenous methylprednisolone succinate sodium (500 mg) once daily for 5 consecutive days, the patient experienced gastrointestinal bleeding. The hormone dose was then reduced, and intravenous immune globulin (IVIG) 10 g/day was added. Treatment continued for 3 days after the patient’s death due to immune myocarditis and heart failure combined with gastrointestinal bleeding. Case 3 underwent a tracheotomy and received methylprednisolone sodium succinate (240 mg) intravenous drip daily for 7 days. Camrelizumab was discontinued. Although troponin and NT-proBNP levels remained elevated with an upward trend 7 days after starting treatment, they decreased after adding IVIG 20 g/day for 3 days. Treatment continued for another 3 days after improvement in cardiac biomarkers. After gradually reducing the hormone dose over 5 days following the stabilization of the patient’s condition, he was discharged from the hospital. The patient’s follow-up status is good. Conclusion: Emphasizing the importance of baseline assessment, early detection and timely intervention, standardized use of glucocorticosteroids, and the addition of immunosuppressants where necessary, these measures can be effective in reducing mortality and ultimately improving prognosis.