Estimating Infarct Size in the Troponin Era: Why No Biomarker Has Replaced Creatine Kinase-Myocardial Band Area Under the Curve (CK-MB AUC) and Where the Field Must Go Next

Infarct size remains a clinically meaningful determinant of prognosis after myocardial infarction (MI) and an important surrogate endpoint in cardiovascular research. Although cardiac troponins have appropriately replaced creatine kinase-myocardial band (CK-MB) for diagnosis because of superior sensitivity and specificity, they have not replaced the quantitative role historically served by serial CK-MB area-under-the-curve (AUC) analysis. Troponin release is prolonged, assay-dependent, and frequently influenced by baseline myocardial injury, making cumulative troponin exposure difficult to interpret as a direct measure of infarct mass. Imaging modalities, especially late gadolinium enhancement cardiac magnetic resonance (CMR), provide accurate infarct characterization but are limited by cost, access, timing, workflow, and scalability. This narrative review revisits the historical utility of CK-MB AUC, explains why troponin has not provided an equivalent biomarker-based infarct-size estimate, and argues for renewed development of practical biomarker strategies, including kinetic modeling, multi-marker panels, and novel biomarkers designed specifically for infarct-size quantification.