Key result
Multimodal immunosuppression and pacing successfully resolve sintilimab-induced fulminant myocarditis with complete AV block.
Why the study?
Immune checkpoint inhibitor-associated myocarditis can cause life-threatening conduction disturbances and may coexist with neuromuscular immune-related adverse events.
Case Report (n=1)
No
In immune checkpoint inhibitor-associated myocarditis, a preserved left ventricular ejection fraction does not exclude life-threatening conduction disease such as complete atrioventricular block, and myocardial injury may rebound after tapering immunosuppression, necessitating prolonged ECG and troponin surveillance.
Preserved LVEF does not exclude life-threatening AV block in ICI myocarditis; leaves open optimal post-treatment surveillance duration.
Immune checkpoint inhibitor (ICI)-associated myocarditis can cause life-threatening conduction disturbances and may coexist with neuromuscular immune-related adverse events. We report a 67-year-old man with stage IIIA lung squamous cell carcinoma who developed fatigue, bilateral ptosis, myalgia, weakness, and palpitations 13 days after his first dose of sintilimab following concurrent chemoradiotherapy. On admission, cardiac troponin T (cTnT) was 874.2 ng/L and creatine kinase-MB exceeded 300 μg/L. Serial electrocardiograms showed progression from bundle branch and fascicular block to complete atrioventricular block, profound bradycardia, and shock, despite a left ventricular ejection fraction of 54%. Coronary angiography revealed no obstructive coronary disease. The findings supported a clinical diagnosis of sintilimab-associated myocarditis with clinically suspected myositis–myasthenia gravis overlap syndrome; cardiac magnetic resonance imaging and confirmatory neuromuscular investigations were not performed. Treatment included intravenous methylprednisolone, immunoglobulin, mycophenolate mofetil, temporary cardiac pacing, and two limited-volume plasma exchange sessions (600 mL each). Infliximab (300 mg per infusion) was subsequently administered empirically for persistent myocardial biomarker elevation. Sinus rhythm returned, and cardiopulmonary and neuromuscular symptoms improved. Following withdrawal of immunosuppression, chest discomfort recurred alongside a cTnT rise to 299.4 ng/L, prompting resumption of corticosteroid-based therapy. At the latest follow-up on April 30, 2026, the patient remained asymptomatic with stable cardiac function, although cTnT remained mildly elevated. In ICI-associated myocarditis, a preserved ejection fraction does not exclude life-threatening conduction disease, and myocardial injury may recur after immunosuppression is withdrawn; continued ECG and troponin surveillance is therefore warranted.
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Cheng et al. (2026) conducted a case report in Fulminant sintilimab-associated myocarditis complicated by complete atrioventricular block and suspected myositis-myasthenia gravis overlap syndrome in stage IIIA lung squamous cell carcinoma (n=1). Sintilimab was evaluated on Clinical resolution of complete atrioventricular block and cardiac troponin T (cTnT) trajectory. Sintilimab induced fulminant myocarditis with complete AV block (cTnT peak 971.1 ng/L, LVEF 54%), which resolved after multimodal immunosuppression and pacing.
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