title: Retrospective determination of the area at risk for reperfused acute myocardial infarction with T2-weighted cardiac magnetic resonance imaging: histopathological and displacement encoding with stimulated echoes (DENSE) functional validations.
abstract: BACKGROUND
  The aim of this study was to determine whether edema imaging by T2-weighted cardiac magnetic resonance (CMR) imaging could retrospectively delineate the area at risk in reperfused myocardial infarction. We hypothesized that the size of the area at risk during a transient occlusion would be similar to the T2-weighted hyperintense region observed 2 days later, that the T2-weighted hyperintense myocardium would show partial functional recovery after 2 months, and that the T2 abnormality would resolve over 2 months.
  
  
  RESULTS
  Seventeen dogs underwent a 90-minute coronary artery occlusion, followed by reperfusion. The area at risk, as measured with microspheres (9 animals), was comparable to the size of the hyperintense zone on T2-weighted images 2 days later (43.4+/-3.3% versus 43.0+/-3.4% of the left ventricle; P=NS), and the 2 measures correlated (R=0.84). The infarcted zone was significantly smaller (23.1+/-3.7; both P<0.001). To test whether the hyperintense myocardium would exhibit partial functional recovery over time, 8 animals were imaged on day 2 and 2 months later. Systolic strain was mapped with displacement encoding with stimulated echoes. Edema, as detected by a hyperintense zone on T2-weighted images, resolved, and regional radial systolic strain partially improved from 4.9+/-0.7 to 13.1+/-1.5 (P=0.001) over 2 months.
  
  
  CONCLUSIONS
  These findings are consistent with the premise that the T2 abnormality depicts the area at risk, a zone of reversibly and irreversibly injured myocardium associated with reperfused subendocardial infarctions. The persistence of postischemic edema allows T2-weighted CMR to delineate the area at risk 2 days after reperfused myocardial infarction.
authors.affiliation: National Heart, Lung and Blood Institute, National Institutes of Health, US Department of Health and Human Services, Bethesda, MD 20892-1061, USA.
authors.forename: Anthony H
authors.initials: AH
authors.lastname: Aletras
authors.forename: Gauri S
authors.initials: GS
authors.lastname: Tilak
authors.forename: Alex
authors.initials: A
authors.lastname: Natanzon
authors.forename: Li-Yueh
authors.initials: LY
authors.lastname: Hsu
authors.forename: Felix M
authors.initials: FM
authors.lastname: Gonzalez
authors.forename: Robert F
authors.initials: RF
authors.lastname: Hoyt
authors.forename: Andrew E
authors.initials: AE
authors.lastname: Arai
mesh_terms: D000818:Animals; D004285:Dogs; D004452:Echocardiography / Q000379:methods*; D004489:Edema, Cardiac / Q000175:diagnosis; D006321:Heart / Q000503:physiopathology; D008279:Magnetic Resonance Imaging; D008863:Microspheres; D009203:Myocardial Infarction / Q000175:diagnosis* / Q000503:physiopathology / Q000628:therapy*; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000473:pathology; D020127:Recovery of Function; D015203:Reproducibility of Results; D012307:Risk Factors; D013997:Time Factors