Investigative radiology · 2026
Ferumoxytol-Enhanced Cardiac Magnetic Resonance for Delineation of Hyperacute Intramyocardial Hemorrhage With Ex Vivo Validation.
СтатьяВалидационное исследованиеНазвание и аннотация: Перевод пока не подготовлен
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Pogosyan Arutyun, Colbert Caroline M, Mahmoudi Mostafa, Keushkerian Mary J, Llanes Aaron C, Sim Myung S, Fishbein Gregory A, Zhu Chunni, Finn J Paul, Currier Jesse W, Nguyen Kim-Lien
Аннотация
OBJECTIVES: Intramyocardial hemorrhage (IMH) is the most severe form of injury associated with reperfusion therapy during acute myocardial infarction (AMI). Although T 2 *-weighted cardiac MRI is regarded as the reference standard for IMH detection, its application is limited in the hyperacute phase. Ferumoxytol, an iron-based contrast agent characterized by potent T 1 -shortening and a long intravascular half-life, may enable earlier detection. This study assessed a T 1 -weighted approach using ferumoxytol-enhanced MRI (FE-MRI) for early detection of IMH after ischemia-reperfusion injury in a swine model.
MATERIALS AND METHODS: IMH was induced in 22 Yorkshire swine using a closed-chest ischemia-reperfusion model with intracoronary collagenase administration. FE-MRI was performed immediately after reperfusion using T 1 -weighted cine imaging and serial T 1 mapping with a modified Look-Locker inversion recovery (MOLLI) pulse sequence. Imaging findings were compared among IMH-positive (IMH+), IMH-negative (IMH-), and control animals. Results were validated through gross pathology, histology, and electron microscopy.
RESULTS: Nine animals completed imaging, of which 5 were IMH+ and 4 IMH- based on histopathology and FE-MRI. In IMH+ animals, the T 1 within hemorrhagic reperfused myocardium was significantly lower than remote myocardium [420.8 ms (380.5, 656.3) vs. 806.0 ms (781.0, 818.8); P <0.001], and lower than healthy myocardium in the control animal [808.2 ms (796.3, 811.0)]. IMH- animals exhibited significantly higher myocardial T 1 than IMH+ animals in both non-hemorrhagic reperfused [807.8 ms (786.1, 830.3); P <0.001] and remote myocardium [805.6 ms (786.1, 825.5); P <0.001]. A mixed-effects model confirmed significant cohort-specific T 1 decrease within hemorrhagic reperfused tissue of IMH+ animals (estimate= -0.49±0.15; P =0.001), with a significant time-dependent effect (β= -0.125±0.03; P <0.001). Remote myocardial and left ventricular blood pool T 1 did not differ between groups (both P >0.05). Gross and microscopic findings confirmed extravasated erythrocytes and disrupted myocardial architecture, consistent with hemorrhagic injury.
CONCLUSIONS: This proof-of-concept study demonstrates the feasibility and potential of T 1 -weighted FE-MRI as a unique approach for detecting IMH immediately after ischemia-reperfusion injury. Early identification of IMH by FE-MRI may facilitate translational efforts to develop and evaluate targeted therapies that reduce IMH burden and improve post-AMI outcomes.
MATERIALS AND METHODS: IMH was induced in 22 Yorkshire swine using a closed-chest ischemia-reperfusion model with intracoronary collagenase administration. FE-MRI was performed immediately after reperfusion using T 1 -weighted cine imaging and serial T 1 mapping with a modified Look-Locker inversion recovery (MOLLI) pulse sequence. Imaging findings were compared among IMH-positive (IMH+), IMH-negative (IMH-), and control animals. Results were validated through gross pathology, histology, and electron microscopy.
RESULTS: Nine animals completed imaging, of which 5 were IMH+ and 4 IMH- based on histopathology and FE-MRI. In IMH+ animals, the T 1 within hemorrhagic reperfused myocardium was significantly lower than remote myocardium [420.8 ms (380.5, 656.3) vs. 806.0 ms (781.0, 818.8); P <0.001], and lower than healthy myocardium in the control animal [808.2 ms (796.3, 811.0)]. IMH- animals exhibited significantly higher myocardial T 1 than IMH+ animals in both non-hemorrhagic reperfused [807.8 ms (786.1, 830.3); P <0.001] and remote myocardium [805.6 ms (786.1, 825.5); P <0.001]. A mixed-effects model confirmed significant cohort-specific T 1 decrease within hemorrhagic reperfused tissue of IMH+ animals (estimate= -0.49±0.15; P =0.001), with a significant time-dependent effect (β= -0.125±0.03; P <0.001). Remote myocardial and left ventricular blood pool T 1 did not differ between groups (both P >0.05). Gross and microscopic findings confirmed extravasated erythrocytes and disrupted myocardial architecture, consistent with hemorrhagic injury.
CONCLUSIONS: This proof-of-concept study demonstrates the feasibility and potential of T 1 -weighted FE-MRI as a unique approach for detecting IMH immediately after ischemia-reperfusion injury. Early identification of IMH by FE-MRI may facilitate translational efforts to develop and evaluate targeted therapies that reduce IMH burden and improve post-AMI outcomes.