QF1-004 - Serial and Quantitative Evaluation of T1, T2, and T2* Mapping Kinetics during Ischemia and Early after Reperfusion in a Myocardial Infarction in Pig Model

Thursday, February 13, 2020

2:54 PM – 2:57 PM

Location: Sabal/Sago (Meeting Room in Exhibit Hall)

Background:
While starting to occur early during ischemia, and abruptly increasing after reperfusion, edema was believed to remain stable during the first week after myocardial/infarction. Recent experimental work has been shifting the paradigm by showing that edema was following a bimodal pattern over the first week, with an initial wave appearing upon reperfusion while dissipating at 24h(1). The time-resolved dynamics of edema as measurable by quantitative mapping during ischemia and within hours following reperfusion are unknown.

The purpose of this study is to describe acute myocardial changes occurring during ischemia and after reperfusion in an ischemia-reperfusion (IR) pig model using quantitative T1, T2, and T2* CMR imaging techniques.

Methods: Serial acquisitions were performed in an open-chest total 40min LAD occlusion pig model (30-35kg; n=20). Quantitative Magnetic Resonance Imaging (QMRI) was performed at baseline, at multiple times points during ischemia, and starting immediately after reperfusion then repeated during 120min. CMR was done on a 1.5T magnet (Aera, Siemens healthcare). We acquired a fast QMRI protocol including T1, T2, T2* maps together with LV function quantification from long axis and short axis planes (Dodge). Full function (Simpson) was measured in addition before ischemia and post reperfusion. Post-Gadolinium T1 mapping, early and late Gd enhancement (EGE & LGE) were acquired in all planes. Extracellular volume (ECV) was calculated. The mean values of each index were determined in each compartment: in the lesion (enhanced myocardium on late-gadolinium enhanced, microvascular obstruction or hemorrhage if any), blood and remote myocardium. After reocclusion, animals were euthanized and uniperse blue dye as well as TTC staining were obtained.

Results: We observed an increase of T1, T2, T2* relaxation
times indicating tissue edema during ischemia (+8,7% +5,7% +10%), accentuated after reperfusion (+26.9%, +27.4% and +26.4%) respectively. The values in the remote myocardium slightly increased by 5.4%, 0.6%, and 6% respectively after reperfusion. These post-reperfusion final values were associated with macroscopic wall thickness increase (cell swelling), regional & global dysfunction. We found small correlations between T1 Native post-reperfusion and T1 Native per ischemia.

Conclusion:
Measuring T1, T2, T2* values and CMR function to monitor changes in acute MI is feasible in an experimental model with a QMRI temporal resolution of 5min. Our study demonstrated that inflammatory response (~amount of edema) after reperfusion was not related to the inflammatory status in the tissue pre-reperfusion. Each marker exhibited specific sensitivity to water content and changes in the involved tissue compartments of interest, while also reflecting inter-individual variability. Differences between the MR biomarkers indicate a potential complementarity that deserves further investigations.(1)Fernández-Jiménez, R. JACC 2015

Presenting Author(s)

Magalie Viallon, PhD

Researcher
Univ Lyon, UJM-Saint-Etienne, INSA, CNRS UMR 5520, INSERM U1206, CREATIS

Disclosure: Disclosure information not submitted.

Primary Author(s)

Magalie Viallon, PhD

Researcher
Univ Lyon, UJM-Saint-Etienne, INSA, CNRS UMR 5520, INSERM U1206, CREATIS

Disclosure: Disclosure information not submitted.

Co-Author(s)

LP

Lorena Petrusca, PhD

Univ Lyon, UJM-Saint-Etienne, INSA, CNRS UMR 5520, INSERM U1206, CREATIS, F-42023, Saint-Etienne, France

Disclosure: Disclosure information not submitted.
NM

Nathan Mewton, MD, PhD

Centre d'investigation clinique de Lyon, Hôpital Louis Pradel, Hospices Civils de Lyon, Lyon, France

Disclosure: Disclosure information not submitted.
LA

Lionel Augeul

INSERM UMR-1060, Laboratoire CarMeN, Université Lyon 1, Faculté de Médecine, Rockefeller, Lyon, France

Disclosure: Disclosure information not submitted.
MO

Michel Ovize, MD, PhD

INSERM UMR-1060, Laboratoire CarMeN, Université Lyon 1, Faculté de Médecine, Rockefeller, Lyon, France

Disclosure: Disclosure information not submitted.
Pierre Croisille, MD, PhD

Professor
Jean-Monnet University

Disclosure: Disclosure information not submitted.