Detecting Hemorrhagic Myocardial Infarction With 3.0-T CMR: Insights Into Spatial Manifestation, Time-Dependence, and Optimal Acquisitions.

Background: Hemorrhagic myocardial infarction (hMI) can rapidly diminish the benefits of reperfusion therapy and direct the heart toward chronic heart failure. T2∗ cardiac magnetic resonance (CMR) is the reference standard for detecting hMI. However, the lack of clarity around the earliest time point for detection, time-dependent changes in hemorrhage volume, and the optimal methods for detection can limit the development of strategies to manage hMI.
Objectives: The authors investigated CMR signal characteristics of hMI through time-lapse multiparametric mapping using a clinically relevant animal model and evaluated the translatability in ST-segment elevation MI patients when possible.
Methods: Canines (N = 20) underwent 3.0-T CMR at baseline and various time points over the first week of reperfused MI. Time-dependent relationships between T1, T2, and T2∗ mapping of hMI, non-hMI, and remote territories were determined. Reperfused ST-segment elevation MI patients (N = 50) were studied to establish clinically feasibility.
Results: Although hMI was evident <1 hour after reperfusion on histopathology, it was not reliably detected with T1, T2, or T2∗ CMR. However, 24 hours to 7 days postreperfusion, hMI was detectable on T2∗ (27.0 ± 2.4 ms [baseline] vs 11.7 ± 2.8 ms [hMI]; P < 0.001), with stable volume and transmurality. In T2 maps, hMI was most visible 5 to 7 days postreperfusion with an area under the curve of 0.98 (sensitivity and specificity ≥0.95) relative to T2∗. However, this was not the case with T1 (sensitivity <0.8, across all time points).
Conclusions: HMI cannot be reliably detected with T1, T2, or T2∗ on 3.0-T CMR immediately after reperfusion. However, T2∗ CMR can be used to diagnose hMI between 24 hours and 7 days postreperfusion. T2 maps at 3.0-T are a strong alternative to T2∗ maps for diagnosing hMI, provided CMR is performed 5 to 7 days postreperfusion. However, diagnosing hMI with T1 is significantly more challenging at 3.0-T compared with both T2∗ and T2.
Competing Interests: Funding Support and Author Disclosures This work was supported in part by National Institutes of Health/National Heart, Lung, Blood Institute grants HL133407, HL136578, and HL147133 (Dr Dharmakumar) and HL169877 (Dr Z. Chen). Dr Z. Chen has received support from American Heart Association (23TPA1069000) and from the National Natural Science Foundation of China (grant number 81701643) and Shanghai Pujiang Program (grant number 21PJD012). Dr Zeng has received support from the Joint Research Development Project between Shenkang and United Imaging on Clinical Research and Translation (grant number SKLY2022CRT201). Dr Dharmakumar has ownership interest in Cardio-Theranostics, LLC. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
(Copyright © 2025 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)