Overview of immune checkpoint inhibitor associated myocarditis mechanisms diagnostics and treatment.

Immune checkpoint inhibitor-associated myocarditis (ICI-M) has emerged as a rare yet fulminant immune-related adverse event, characterized by high mortality and diagnostic complexity. Recent studies implicate loss of immune tolerance through PD-1/PD-L1 or CTLA-4 blockade, expansion of autoreactive CD8+ T cells, cross-reactivity between tumor and cardiac antigens, and downstream inflammatory cascades as central drivers of myocardial injury. Oxidative stress, endothelial activation, and fibrotic remodeling further amplify damage. Clinically, ICI-M presents with heterogeneous symptoms ranging from subtle conduction abnormalities to fulminant cardiogenic shock. While cardiac troponins and electrocardiography offer early screening, advanced imaging-particularly cardiovascular magnetic resonance with updated Lake Louise Criteria and strain-based analysis-enables more sensitive detection. This review summarizes current insights into the immunopathogenesis, diagnostic approaches, and emerging therapeutic strategies for immune checkpoint inhibitor-associated myocarditis, highlighting the roles of autoreactive T cells, shared tumor-cardiac antigens, advanced imaging, and immunosuppressive interventions in mitigating its high morbidity and mortality.