An Interferon-γ-Driven Myeloid Inflammatory Signature defines Glucocorticoid-Resistance of Immune Checkpoint Inhibitor-Associated Myocarditis

Although high-dose glucocorticoids represent first-line therapy, a subset of patients exhibits persistent myocardial injury despite treatment. In this study, we analyzed a cohort of 74 patients with ICI-myocarditis and classified patients based on longitudinal high-sensitivity cardiac troponin T (hs-cTnT) trajectories following glucocorticoid initiation into glucocorticoid-sensitive (GC-S) and glucocorticoid-refractory (GC-R) groups.

Clinical outcomes, including major adverse cardiac events (MACE), were assessed. To investigate underlying biological differences, single-nucleus RNA sequencing (snRNA-seq) was performed on endomyocardial biopsy samples from GC-S (n=2) and GC-R (n=4) patients. The dataset provides high-resolution transcriptional profiles of myocardial cell populations, enabling analysis of cellular composition and inflammatory signaling pathways associated with differential treatment response.