title: Ventricular remodeling in a mouse model of myocardial infarction.
abstract: We investigated the suitability of studying ventricular remodeling in a mouse model of myocardial infarction (MI). We performed left coronary ligation (n = 22) or a sham procedure (n = 21) on normal C57BL/6J mice. Six weeks later, animals underwent echocardiography and hemodynamic evaluation. Left ventricular (LV) volume at a common distending pressure was calculated from passive pressure-volume curves. The MI group exhibited lower systolic blood pressure (P < 0.05), higher LV end-diastolic pressure (P < 0.05), and lower peak first derivative of LV pressure (dP/dt, P < 0.05) than the sham group. Mice with moderate (< 40%, n = 11) and large (> or = 40%, n = 11) MIs displayed increased LV mass-to-body weight ratio (P < 0.02 and P < 0.01, respectively, vs. sham group), whereas only the large-MI group exhibited increased right ventricular mass-to-body weight ratio (P < 0.01). LV volumes were increased in the moderate-MI group (P = 0.059 vs. sham group) and to a much greater extent in the large-MI group (P < 0.0001 vs. sham group). The moderate- and large-MI groups also exhibited increases in LV end-diastolic diameter (P < 0.03 and P < 0.0001, respectively, vs. sham group) and LV end-systolic diameter (P < 0.01 and P < 0.0001, respectively, vs. sham group) with decreased fractional shortening (P < 0.01 for both). These data demonstrate ventricular remodeling in a mouse model of MI and confirm the feasibility of quantifying indexes of remodeling in vivo and postmortem. This model will be of particular usefulness when applied to transgenic strains.
authors.affiliation: Division of Cardiology, Molecular Cardiology Research Institute, New England Medical Center, Boston, Massachusetts, USA.
authors.forename: R D
authors.initials: RD
authors.lastname: Patten
authors.forename: M J
authors.initials: MJ
authors.lastname: Aronovitz
authors.forename: L
authors.initials: L
authors.lastname: Deras-Mejia
authors.forename: N G
authors.initials: NG
authors.lastname: Pandian
authors.forename: G G
authors.initials: GG
authors.lastname: Hanak
authors.forename: J J
authors.initials: JJ
authors.lastname: Smith
authors.forename: M E
authors.initials: ME
authors.lastname: Mendelsohn
authors.forename: M A
authors.initials: MA
authors.lastname: Konstam
mesh_terms: D000818:Animals; D001835:Body Weight; D004195:Disease Models, Animal; D006352:Heart Ventricles / Q000473:pathology* / Q000503:physiopathology*; D006439:Hemodynamics; D017379:Hypertrophy, Left Ventricular / Q000473:pathology* / Q000503:physiopathology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009203:Myocardial Infarction / Q000473:pathology* / Q000503:physiopathology*