LEFT-VENTRICULAR FUNCTION AND REMODELING AFTER MYOCARDIAL-INFARCTION IN AGING RATS

Adaptations of the aging left ventricle (LV) to hemodynamic overload a re functionally and structurally distinct from those of the young orga nism. This study describes the influence of aging on LV hemodynamics a nd remodeling late after myocardial infarction (MI) in Fischer 344 Bro wn Norway rats. In sham rats at 23 mo, LV weight, myocyte cross-sectio nal area (CSA), and myocardial fibrosis were increased, whereas LV dP/ dt, LV relaxation, and maximal LV systolic function declined with resp ect to younger rats (7, 12, and 18 mo of age). Isometric myocardial fu nction was evaluated in papillary muscles of 12- and 23-mo-old sham ra ts. Myocardial systolic function was decreased in older rats. To deter mine 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 s ize was similar in each group. Right ventricular weight, LV end-diasto lic pressure, and volume index were increased, whereas LV dP/dt, peak cardiac index, and peak developed LV pressure declined after MI. Howev er, there were no significant differences between young and older rats in any variable of LV systolic function or remodeling after MI. Myocy te CSA increased in younger rats after MI but was unchanged in 23-mo-o ld rats. After MI, myocardial fibrosis was significantly increased fro m baseline only in younger rats. The negative interaction of aging and MI on myocyte hypertrophy and fibrosis was highly significant. The fi ndings indicate that baseline LV and myocardial function decline with age. In the aging rat after MI, despite limited compensatory hypertrop hy and more advanced baseline myocardial fibrosis, the long-term funct ional and structural adaptations to MI are similar to those of the mat ure adult heart.