Objectives—The aim of this study was to determine if early gadolinium enhancement (EGE) by cardiovascular magnetic resonance (CMR) imaging in a canine model of reperfused myocardial infarction depicts the area at risk (AAR) as determined by microsphere blood flow analysis.

Background—It remains controversial whether only the irreversibly injured myocardium enhances when performing CMR imaging in the setting of acute myocardial infarction. Recently, EGE has been proposed as a measure of the AAR in acute myocardial infarction as it correlates well with T2-weighted imaging of the AAR, but still requires pathological validation.

Methods—Eleven dogs underwent 2 hours of coronary artery occlusion and 48 hours of reperfusion prior to imaging at 1.5T. EGE imaging was performed 3 minutes after contrast administration with coverage of the entire left ventricle. Late gadolinium enhancement (LGE) imaging was performed between 10 and 15 minutes after contrast injection. AAR was defined as myocardium with blood flow (mL/min/g) < 2SD from remote myocardium determined by microspheres during occlusion. The size of infarction was determined using triphenyltetrazolium chloride (TTC).

Results—There was no significant difference in the size of enhancement by EGE compared to the size of AAR by microspheres (44.1± 15.8% vs. 42.7± 9.2%, p=0.61) with good correlation (r=0.88, p < 0.001) and good agreement by Bland-Altman analysis (mean bias 1.4± 17.4%). There was no difference in the size of enhancement by EGE compared to enhancement on native T1 and T2 maps. The size of EGE was significantly greater than the infarct by TTC, (44.1± 15.8% vs. 20.7± 14.4%, p < 0.001) and LGE (44.1± 15.8% vs. 23.5± 12.7%, p < 0.001).

Conclusion—At three minutes post-contrast, EGE correlated well with the AAR by microspheres and CMR, and was greater than infarct size. Thus, EGE enhances both reversibly and irreversibly injured myocardium.

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Notes/Citation Information

Published in JACC: Cardiovascular Imaging, v. 10, issue 2, p. 130-139.

© 2017 by the American College of Cardiology Foundation. Published by Elsevier.

This manuscript version is made available under the CC‐BY‐NC‐ND 4.0 license https://creativecommons.org/licenses/by-nc-nd/4.0/.

The document available for download is the author's post-peer-review final draft of the article.

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Funding Information

This work was supported by the Intramural Research Program of the National Heart, Lung, and Blood Institute, National Institutes of Health, USA [Z01 HL006136-04 and HL004607-16]. Dr. Arai is a principal investigator on a US government Cooperative Research and Development Agreement (CRADA) with Siemens Medical Solutions (HL-CR-05-010).