Detecting Hemorrhagic Myocardial Infarction with T2 CMR at 3T: Initial Evidence from a Large Animal Model (RF_TH_154)

Presenting Author(s)

• SD

  Sanjana Dharmakumar, N/A

  Research Department
  Krannert Cardiovascular Research Center

Primary Author(s)

• SD

  Sanjana Dharmakumar, N/A

  Research Department
  Krannert Cardiovascular Research Center

Co-Author(s)

• 

  Keyur P. Vora, MD, MS, FACC

  Cardiologist, Assistant Professor of Medicine
  Indiana University School of Medicine
• HH

  Huaibi Huo, MD

  Postdoctoral Fellow
  Indiana University School of Medicine
• GY

  Ghazal Yoosefian

  Student
  Indiana University School of Medicine
• 

  Hsin-Jung Yang, PhD

  Assistant Professor
  Cedars-Sinai Medical Center
• MK

  Mayil Singram S. Krishnam, MD

  Radiologist
  Stanford University
• AK

  Andreas Kumar, MD

  doctor
  Northern Ontario School of Medicine, Sudbury,Ontario, Canada, Canada

Background: Patients undergoing reperfusion therapy for ST-elevation myocardial infarction (MI) carry an average risk of 40% for developing intramyocardial hemorrhage (IMH) and are highly vulnerable for major adverse cardiovascular outcomes, including death. T2* CMR is the current standard for diagnosing IMH but it can be limited by imaging artifacts, which can compromise diagnosis in some patients. Given superior image quality of T2 compared to T2*, and the T2 sensitivity for IMH remnants, T2-based CMR has been investigated as an alternative to T2* for diagnosing IMH. These studies performed at 1.5T, however showed that the accuracy of T2 to detect IMH at 1.5T is weaker compared to T2*. Since the sensitivity to detect IMH is expected to be larger at 3T, we hypothesized that T2 CMR at 3T could be an alternative to T2* CMR.  

Methods: We investigated this using large animal models with reperfused hemorrhagic MI under highly controlled conditions after obtaining ethics board approval. Anaesthetized Canines (n=20) underwent occlusion of the left-anterior descending coronary artery for three hours and were then reperfused. They were imaged in a 3T clinical CMR system (Biograph mMR, Siemens Healthcare) at 1 day, 3 days, 5 days and at 7 days post MI. We acquired breath-held, ECG-gated 2D, T2 and T2* maps and LGE in short-axis orientation covering the whole LV. All images were acquired with matched spatial resolution of 1.5×1.5×8mm3. Images were analyzed using CVI42 by identifying the infarcted myocardium from LGE images and IMH territories from T2* images. Animals positive for IMH on T2* on day 3 were followed for IMH volume across study time points based on T2* and T2 CMR. Remote Mean-2SD criterion was applied to both T2* and T2 maps on a slice-by-slice basis to identify IMH regions and summed to compute IMH volume as a %LV. This was performed across all animals. IMH volumes from T2* and T2 methods were compared using paired t-test.

Results: 13 animals were positive for IMH on T2* on Day 3. Representative cases of T2 and T2* cases from a hemorrhagic animal is shown in Fig. 1. Note that IMH territories identifiable on T2* CMR were also identifiable on T2 CMR but were most clearly evident on Day 3 and after. In both cases, T2* and T2 values of IMH territories were significantly lower than the MI regions without IMH. IMH volume determined using T2 underestimated IMH volume at Day 1 (T2* 10%±15% vs T2 5%±10%, p< 0.05) and Day 3 (T2*12%±10% vs  T27%±9%, p< 0.05) but were not different on Day 5 (T2*10%±5% vs T2 9%±6% p=0.25) and Day 7 (T2*10%±5% vs T2 11%± 3%, p=0.35). 

Conclusion: T2 CMR at 3T provides excellent image quality and visually compelling images for identifying IMH. IMH volumes determined 5–7-days post MI with T2 CMR are not different from those measured with T2* CMR, while T2 underestimated hemorrhage amount on day 1 and 3 post reperfusion. These studies support the use of T2 CMR at 3T for detecting IMH. However, additional studies are needed to assess the diagnostic performance of T2 against T2* CMR for diagnosing IMH in patients.