Hs-troponin-i kinetics enable rapid diagnosis of stages of injury and hemorrhagic MI in reperfused STEMI

Background Staging of acute myocardial infarction (AMI) based on tissue injury provides a robust framework for assessing myocardial damage via Cardiovascular Magnetic Resonance (CMR). While universal CMR remains infeasible for all acute myocardial infarction patients, rapid blood-based biomarkers are needed to identify high-acuity Stage IV (hemorrhagic) injury, which carries the highest risk for adverse clinical outcomes. Intramyocardial hemorrhage (IMH) represents a critical therapeutic target in vulnerable revascularized STEMI populations. Purpose To evaluate whether serial high-sensitivity cardiac troponin I (hs-cTn-I) kinetics can reliably predict stages of myocardial injury and effectively triage reperfused STEMI patients for clinical trials and value-based imaging, with a specific focus on identifying hemorrhagic myocardial infarction. Methods We studied 267 consecutive reperfused acute MI patientsstaged according to myocardial injurycriteria using CMR for edema(T2-based) as Stage I, necrosis (Late Gadolinium Enhancement)as Stage II, microvascular obstruction (MVO) as Stage III, and IMH (T2*) as Stage IV. High-sensitivity cardiac troponin I (hs-cTn-I) was sampled seriallypre-PCI, immediately post-reperfusion, and hourly up to 12 hours, then 16, 20, 24 and 48 hours. Peak hs-cTn-I was defined as the maximum concentration withinthe first 12 hours. Diagnostic performance and optimalthresholds for differentiating stages of myocardial injurywere determined using Receiver OperatingCharacteristic (ROC) curve analysis and Youden's J statistic. Results Peak hs-cTn-I levels demonstrated a clear stepwise increase correlating with the severity of tissue injury determined by CMR. Median (IQR) peak values in ng/ml were 9.0 (2.2–18.2) for Stage I, 39.1 (14.4–82.8) for Stage II, 73.3 (31.1–127.9) for Stage III, and 210.9 (115.9–415.1) for Stage IV. A threshold of peak [hs-cTn-I] > 62.3~ng/ml separated Stage III or greater from Stage II injury with 81.7% sensitivity and 71.7% specificity (AUC 0.839). Importantly, a peak level > 156.6~ng/ml identified Stage IV hemorrhagic injury compared to Stage III with 65.8% sensitivity, 90.0% specificity, and an AUC of 0.841. Analysis at 3 hours post-PCI yielded AUC values (0.806–0.876) that closely approximated the discriminatory accuracy of 12-hour peak values. Conclusion Post-reperfusion high-sensitivity cardiac troponin I kinetics allow for accurate staging of myocardial injury in reperfused STEMI patients. These findings demonstrate that blood-based biomarkers can effectively triage patients for value-based CMR and for clinical trials aimed at therapeutic interventions targeting specific stages of tissue injury, such as intramyocardial hemorrhage.