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Division of Cardiology and The Molecular Cardiology Research Institute, Department of Medicine, New England Medical Center and Tufts University School of Medicine, Boston, Massachusetts 02111
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 (
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.
myocardial hypertrophy; ventricular dilatation; echocardiography; hemodynamics
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