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Importance of an Intact Growth Hormone/Insulin-Like Growth Factor 1 Axis for Normal Post-Infarction Healing: Studies in Dwarf Rats¹

From the Charles A. Dana Research Institute and the Harvard-Thorndike Laboratory, Department of Medicine (Cardiovascular Division) of Beth Israel Hospital (A.C., J.D.G., H.S., S.E.K., J.P.M., P.S.D.), Harvard Medical School, Boston, Massachusetts 02215

Address all correspondence and requests for reprints to either: Antonio Cittadini, M.D., Department of Clinical Medicine and Cardiovascular Sciences, University Federico II, Via Sergio Pansini, 5, 80131 Naples, Italy. E-mail: cittadin{at}unina.it Or Pamela S. Douglas, M.D.,

Treatment with GH attenuates remodeling and improves left ventricular function in the setting of experimental heart failure following coronary ligation. This study was designed to test the hypothesis that an intact GH/insulin-like growth factor 1 (IGF-1) axis is required for normal myocardial infarction healing. Myocardial infarction was induced by coronary ligation in GH-deficient dwarf rats and in age-matched controls. In dwarf rats, serum IGF-1 levels were reduced by 50%, and grow rate was 50% less than normal littermates, although no differences in myocardial IGF-1 messenger RNA levels were observed compared with controls. All rats underwent transthoracic echocardiography at baseline, 2 weeks, and 6 weeks after myocardial infarction. Left ventricular end-diastolic pressure was obtained by in vivo closed chest catheterization. At 6 weeks, both infarcted groups exhibited similar myocardial infarction size at transthoracic echocardiography and at morphometric histology. In both groups with myocardial infarction, there was significant left ventricular dilation and reduced systolic function. However, the extent of remodeling as assessed by the increase in end-diastolic dimension (% + 36 ± 5 vs. +19 ± 4; P < 0.01) and depression of function (% fractional shortening -12 ± 2 vs. -7 ± 1; P < 0.01) were both greater in the dwarf group. Furthermore, dwarf rats failed to develop compensatory hypertrophy of noninfarcted posterior wall (% posterior wall +5 ± 1 vs. +15 ± 3; P < 0.01). Therefore, pathologic left ventricular remodeling and functional loss following myocardial infarction is more marked in conditions of GH deficiency. An intact GH/IGF-1 axis appears necessary for a normal response to myocardial infarction injury in the rat.

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