Troponin T versus troponin I in immune checkpoint inhibitor-associated myocarditis: Complementary roles in screening and confirmation

Immune checkpoint inhibitor-associated myocarditis is a rare but highly fatal complication. Cardiac troponin T (cTnT) and cardiac troponin I (cTnI) are central to diagnosis and prognostic assessment, yet their clinical differences remain poorly defined. This review compares the biological characteristics, analytical factors, and clinical interpretation of cTnT and cTnI in ICI-associated myocarditis. Available evidence suggests that cTnT is more frequently elevated and has a stronger evidence base for surveillance, whereas cTnI provides complementary information for myocardial source attribution, particularly when skeletal muscle involvement or other confounding factors are present. However, neither biomarker alone can confirm or exclude ICI-associated myocarditis. Appropriate interpretation requires integration of troponin trajectories, clinical presentation, electrocardiography, imaging findings, and evaluation of potential non-cardiac causes. • cTnT and cTnI provide complementary information in ICI-associated myocarditis. • cTnT offers higher sensitivity for screening and surveillance. • cTnI improves myocardial specificity when skeletal muscle interference exists. • Troponin interpretation requires integration with clinical and imaging findings. • A sequential cTnT/cTnI strategy may improve diagnostic accuracy.