Author + information
- Received January 8, 2016
- Revision received March 14, 2016
- Accepted April 14, 2016
- Published online February 6, 2017.
- Sophia Hammer-Hansen, MDa,b,
- Steve W. Leung, MDa,c,
- Li-Yueh Hsu, DSca,
- Joel R. Wilson, MDa,d,
- Joni Taylor, BSa,
- Anders M. Greve, MD, PhDa,
- Jens Jakob Thune, MD, PhDb,
- Lars Køber, MDb,
- Peter Kellman, PhDa and
- Andrew E. Arai, MDa,∗ ()
- aLaboratory for Advanced Cardiovascular Imaging, National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland
- bDepartment of Medicine B, The Heart Center, Rigshospitalet, Copenhagen, Denmark
- cDepartment of Medicine and Radiology, Division of Cardiovascular Medicine, University of Kentucky, Lexington, Kentucky
- dDepartment of Medicine and Radiology, Division of Cardiovascular Medicine, University of California-San Diego, San Diego, California
- ↵∗Address for correspondence:
Dr. Andrew E. Arai, National Heart, Lung, and Blood Institute, National Institutes of Health, Building 10, Room B1D416, MSC 1061, 10 Center Drive, Bethesda, Maryland 20892-1061.
Objectives The aim of this study was to determine whether early gadolinium enhancement (EGE) by cardiac magnetic resonance (CMR) 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 CMR is performed in the setting of acute myocardial infarction. Recently, EGE has been proposed as a measure of the AAR in acute myocardial infarction because it correlates well with T2-weighted imaging of the AAR, but this still requires pathological validation.
Methods Eleven dogs underwent 2 h of coronary artery occlusion and 48 h of reperfusion before imaging at 1.5-T. EGE imaging was performed 3 min after contrast administration with coverage of the entire left ventricle. Late gadolinium enhancement imaging was performed between 10 and 15 min after contrast injection. AAR was defined as myocardium with blood flow <2 SD from remote myocardium determined by microspheres during occlusion. The size of infarction was determined with triphenyltetrazolium chloride.
Results There was no significant difference in the size of enhancement by EGE compared with 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 with enhancement on native T1 and T2 maps. The size of EGE was significantly greater than the infarct by triphenyltetrazolium chloride (44.1 ± 15.8% vs. 20.7 ± 14.4%; p < 0.001) and late gadolinium enhancement (44.1 ± 15.8% vs. 23.5 ± 12.7%; p < 0.001).
Conclusions At 3 min 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.
This work was supported by the Intramural Research Program of the National Heart, Lung, and Blood Institute, National Institutes of Health (Z01 HL006136-04 and HL004607-16). Dr. Wilson is a consultant for Acutus Medical. Dr. Arai is a principal investigator on a U.S. government Cooperative Research and Development Agreement (CRADA) with Siemens Medical Solutions (HL-CR-05-010). All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received January 8, 2016.
- Revision received March 14, 2016.
- Accepted April 14, 2016.
- American College of Cardiology Foundation