Abstract
The aim of this study was to assess the capability of MRI to characterize
systolic and diastolic function in normal and chronically failing
mouse hearts in vivo at rest and during inotropic stimulation. Applying
an ECG-gated FLASH-cine sequence, MRI at 7 T was performed at rest
and after administration of 1.5 microgram/g IP dobutamine. There
was a significant increase of heart rate, cardiac output, and ejection
fraction and significant decrease of end-diastolic and end-systolic
left ventricular (LV) volumes (P<0.01 each) in normal mice during
inotropic stimulation. In mice with heart failure due to chronic
myocardial infarction (MI), MRI at rest revealed gross LV dilatation.
There was a significant decrease of LV ejection fraction in infarcted
mice (29%) versus sham mice (58%). Mice with MI showed a significantly
reduced maximum LV ejection rate (P<0.001) and LV filling rate (P<0.01)
and no increase of LV dynamics during dobutamine action, indicating
loss of contractile and relaxation reserve. In 4-month-old transgenic
mice with cardiospecific overexpression of the beta(1)-adrenergic
receptor, which at this early stage do not show abnormalities of
resting cardiac function, LV filling rate failed to increase after
dobutamine stress (transgenic, 0.19+/-0.03 microL/ms; wild type,
0.36+/-0.01 microL/ms; P<0.01). Thus, MRI unmasked diastolic dysfunction
during dobutamine stress. Dobutamine-stress MRI allows noninvasive
assessment of systolic and diastolic components of heart failure.
This study shows that MRI can demonstrate loss of inotropic and lusitropic
response in mice with MI and can unmask diastolic dysfunction as
an early sign of cardiac dysfunction in a transgenic mouse model
of heart failure.
Users
Please
log in to take part in the discussion (add own reviews or comments).