Highly suspected fulminant myocarditis induced by the immune checkpoint inhibitor tislelizumab: a case report with third-degree atrioventricular block and recurrent ventricular tachycardia.

INTRODUCTION: Immune checkpoint inhibitors (ICIs) have significantly advanced the treatment of malignant tumors. Tislelizumab, a recombinant humanized anti-programmed death 1 (PD-1) monoclonal antibody, is widely used in the management of advanced cancers. However, like other ICIs, tislelizumab can trigger immune-related adverse events (irAEs). Among irAEs, immune checkpoint inhibitor-associated myocarditis (ICI-associated myocarditis) is rare but life-threatening, underscoring the need for early recognition and intervention. This case report describes a case of highly suspected fulminant myocarditis induced by ICI in a patient with gallbladder adenocarcinoma and intrahepatic cholangiocarcinoma (iCCA) following treatment with tislelizumab.

CASE PRESENTATION: A 72-year-old female presented with a 4-h history of palpitations and dyspnea on June 16, 2025. Initial electrocardiography (ECG) revealed ventricular tachycardia (VT), which was successfully terminated with 200 J cardioversion. Subsequent monitoring showed third-degree atrioventricular block (AVB). She had been diagnosed with iCCA and gallbladder adenocarcinoma on May 7, 2025, and had undergone partial hepatectomy and cholecystectomy. She later received intravenous tislelizumab (200 mg) on May 22, 2025, followed by a second 200 mg dose on June 10, with no adverse effects observed during either infusion. Upon admission, investigations revealed no coronary abnormalities on coronary computed tomography, a left ventricular ejection fraction (LVEF) of 42%, markedly elevated cardiac biomarkers [e.g., cardiac troponin I (cTnI) 3.80 μg/L], hypoxemia, and 24-h Holter monitoring that documented short episodes of VT and third-degree AVB. Based on the temporal relationship to ICI therapy, the clinical presentation, laboratory and imaging findings, and the exclusion of alternative etiologies, fulminant ICI-associated myocarditis was highly suspected. Treatment included noninvasive mechanical ventilation, temporary pacing, high-dose methylprednisolone, intravenous immunoglobulin, antiarrhythmic agents, and heart failure (HF) management. On hospital day 4, the patient's symptoms had improved, although third-degree AVB persisted. On hospital day 15, her atrioventricular conduction had improved from third-degree to first-degree block, with cardiac biomarkers decreasing to much lower levels. On hospital day 18, repeat transthoracic echocardiography (TTE) showed an LVEF of 49% with generalized hypokinesis of the left ventricular wall, and a repeat ECG revealed first-degree AVB, complete right bundle branch block, and left anterior fascicular block. She was discharged on the same day. During the subsequent 2-month follow-up after discharge, the patient remained clinically stable but developed symptoms of muscle weakness, for which she did not seek further medical evaluation.

CONCLUSION: ICI-associated myocarditis is characterized by a low incidence but carries a high risk of fatal outcomes. Early recognition of severe cases and timely intervention can substantially improve prognosis. In this case, fulminant myocarditis related to the ICI tislelizumab was highly suspected but not pathologically confirmed, as cardiac magnetic resonance imaging and endomyocardial biopsy were not performed. Despite this limitation, the case may still provide a useful clinical reference for the diagnosis and management of severe ICI-associated myocarditis.