Skip to main content
2025 SCMR Conference Main banner
Final Program


Schedule at a Glance
Back

Rapid Fire Abstracts

Rapid Fire 06- Tissue Characterization II

Susceptibility, Infarct Characteristics, and Reactive Oxygen Species in Myocardial Infarction Reperfusion Injury (RF_FR_353)

Friday, January 31, 2025
11:40 AM – 11:50 AM East Coast USA Time
Location: Blue Room PreFunction
Background: Patients with myocardial infarction are treated by reperfusion, but this can cause additional injury in up to 60% of patients. Prolonged ischemia followed by reperfusion could lead to hemorrhage and iron deposition, catalyzing reactive oxygen species (ROS) production and leading to increased heart failure risk. There is a need to study the spatiotemporal relationships of iron, ROS, and infarct size in MI wound healing to develop new targeted interventions. In this study using a swine model, iron content was quantified post-MI using quantitative susceptibility mapping (QSM), infarct size using LGE imaging, and ROS activity using PET and histology.

Methods: MI was induced in 6 swine by percutaneous occlusion of the left anterior descending coronary artery (Fig. 1A). Swine underwent CMR (N=6; 1.5 T Siemens Avanto) and whole-body PET (N=5; Penn PET Explorer) using a ROS-activated radiotracer [18F]ROStrace at 3 days post-MI. [18F]ROStrace myocardial perfusion was calibrated using [82]Rb fractional uptake rate (FUR). The CMR protocol included ECG-gated LGE and multi-echo gradient echo imaging to acquire T2*w images and reconstruct QSMs (Fig. 1B). LGE infarct size, hemorrhage, and remote myocardium were measured (Medis QMass 8.1). Hemorrhage and remote contours were applied to QSMs to quantify susceptibility (ppm). LGE and PET images were co-registered (Carimas). After imaging, a terminal procedure was performed. As an additional validation, an optically-activated ROS tracer dihydroethidium (DHE) was delivered percutaneously followed by 4′,6-diamidino-2-phenylindole (DAPI) staining.

Results: Perfusion-corrected ROStrace FUR in the infarcted myocardium was significantly higher compared to remote myocardium (p=0.004), which is also seen in the increased DHE staining in the infarct (Fig. 1B). The perfusion-corrected ROStrace FUR in the infarct was 0.15 ± 0.05 ml/g and remote was 0.09 ± 0.05 ml/g (Table. 1). There was increased DAPI staining in the infarct region compared to free wall due to the presence of inflammatory cells (Fig. 1B). Based on T2*w imaging, one swine did not have a hemorrhagic myocardium. Magnetic susceptibility was significantly higher in the hemorrhagic zone compared to remote myocardium (p=0.03) (Fig. 2). The susceptibility in the hemorrhage was 0.1 ± 0.06 ppm and remote was -0.03 ± 0.05 ppm (Table 1). The average infarct mass size was 17.75 ± 3.07 g (Table 1). The relationship between infarct size and the difference in susceptibility between hemorrhagic and remote myocardium was computed using Spearman’s correlation to be 0.9 and was statistically significant (p=0.04).

Conclusion: In a swine model of reperfusion injury, increased iron in the hemorrhage, increased ROS activity in the infarct, and a strong positive correlation between infarct size and the difference in susceptibility between hemorrhagic and remote myocardium were observed.