Premium
Serial MRI evaluation of cardiac structure and function in mice after reperfused myocardial infarction
Author(s) -
Ross Antwone J.,
Yang Zequan,
Berr Stuart S.,
Gilson Wesley D.,
Petersen William C.,
Oshinski John N.,
French Brent A.
Publication year - 2002
Publication title -
magnetic resonance in medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.696
H-Index - 225
eISSN - 1522-2594
pISSN - 0740-3194
DOI - 10.1002/mrm.10166
Subject(s) - cardiology , ejection fraction , medicine , myocardial infarction , cardiac function curve , end diastolic volume , infarction , ventricular remodeling , pathophysiology , stroke volume , heart failure
This study evaluated the utility of cardiac MRI for assessing the impact of myocardial infarction (MI) on cardiac structure and function in mice following reperfused 1‐ or 2‐hr occlusions of the left anterior descending coronary artery (LAD). When assessed 1 day after MI, the left ventricular ejection fraction (LVEF) had declined by more than half, and remained depressed for the duration of the study. Furthermore, MI initiated dramatic increases in both LV end‐systolic volume (LVESV) and end‐diastolic volume (LVEDV), with a greater than threefold increase in LVESV and a twofold increase in LVEDV by 4 weeks post‐MI. Transmural LV wall thickening (WTh) analysis revealed that noninfarcted myocardium in the remote septal region exhibited an early deficit in contractile function after MI that transiently resolved by day 7, only to be followed by a late phase of dysfunction that became fully manifest by day 28 post‐MI. In conclusion, MRI allows the serial assessment of cardiac structure and function after MI in mice, with a resolution adequate to document both regional and temporal changes. The application of these imaging techniques in transgenic and knock‐out mice will greatly expedite research aimed at defining the functional roles of individual genes in the pathophysiology of LV remodeling (LVR) after reperfused MI. Magn Reson Med 47:1158–1168, 2002. © 2002 Wiley‐Liss, Inc.