Case Report: Fulminant sintilimab-associated myocarditis complicated by complete atrioventricular block and suspected myositis-myasthenia gravis overlap syndrome
- 1School of Clinical Medicine, Shandong Second Medical University
- 2Department of Respiratory Medicine, Central Hospital Affiliated to Shandong First Medical University
- 3Department of Oncology, Central Hospital Affiliated to Shandong First Medical University
Abstract
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does not exclude life-threatening conduction disease, and myocardial injury may recur after immunosuppression is withdrawn; continued ECG and troponin surveillance is therefore warranted.
Related
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BibTeX
@article{cheng2026case,
title = {{Case Report: Fulminant sintilimab-associated myocarditis complicated by complete atrioventricular block and suspected myositis-myasthenia gravis overlap syndrome}},
author = {Pian Cheng and Xiaolin Zhao and Min Jin and Qinghua Lai and Jie Liu},
journal = {Frontiers in Cardiovascular Medicine},
year = {2026},
month = oct,
doi = {10.3389/fcvm.2026.1968961},
url = {https://www.frontiersin.org/articles/10.3389/fcvm.2026.1968961/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Case Report: Fulminant sintilimab-associated myocarditis complicated by complete atrioventricular block and suspected myositis-myasthenia gravis overlap syndrome
AU - Pian Cheng
AU - Xiaolin Zhao
AU - Min Jin
AU - Qinghua Lai
AU - Jie Liu
PY - 2026
DA - 2026/10/29
JO - Frontiers in Cardiovascular Medicine
DO - 10.3389/fcvm.2026.1968961
UR - https://www.frontiersin.org/articles/10.3389/fcvm.2026.1968961/full
AB - 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.
SN - 2297-055X
ER -