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Department of Pathology, University of Alabama, Birmingham, Alabama 35294-0019; and Department of Internal Medicine, Veterans Affairs Medical Center and University Heart Center, University of Arizona, Tucson, Arizona 85723
Adaptations of the aging left ventricle (LV) to hemodynamic
overload are functionally and structurally distinct from those of the
young organism. This study describes the influence of aging on LV
hemodynamics and remodeling late after myocardial infarction (MI) in
Fischer 344 Brown Norway rats. In sham rats at 23 mo, LV weight,
myocyte cross-sectional area (CSA), and myocardial fibrosis were
increased, whereas LV dP/dt, LV
relaxation, and maximal LV systolic function declined with respect to
younger rats (7, 12, and 18 mo of age). Isometric myocardial function was evaluated in papillary muscles of 12- and 23-mo-old sham rats. Myocardial systolic function was decreased in older rats. To determine how aging affects LV function and remodeling after MI, rats were infarcted at 7 and 18 mo of age and were studied 5 mo later. Infarct size was similar in each group. Right ventricular weight, LV
end-diastolic pressure, and volume index were increased, whereas LV
dP/dt, peak cardiac index, and peak
developed LV pressure declined after MI. However, there were no
significant differences between young and older rats in any variable of
LV systolic function or remodeling after MI. Myocyte CSA increased in
younger rats after MI but was unchanged in 23-mo-old rats. After MI,
myocardial fibrosis was significantly increased from baseline only in
younger rats. The negative interaction of aging and MI on myocyte
hypertrophy and fibrosis was highly significant. The findings indicate
that baseline LV and myocardial function decline with age. In the aging
rat after MI, despite limited compensatory hypertrophy and more
advanced baseline myocardial fibrosis, the long-term functional and
structural adaptations to MI are similar to those of the mature adult
heart.
fibrosis; hypertrophy; myocardial function
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