Myofibrillar adaptations during cardiac hypertrophy.

The main purpose of this study was to determine the transmural adaptive changes that occur in cell size, myofibrils, and myosin isoforms from the endocardium (ENDO) to the epicardium (EPI) of the left ventricle (LV) of the rat heart during compensatory hypertrophy. Hypertrophy was induced by supra-renal aortic constriction for periods of 2, 7, 15 and 30 days. Percent left ventricular hypertrophy averaged 63 +/- 9.7% at 30 days following constriction. A significant (p < 0.05) transmural gradient in the V3 myosin isoform (9 +/- 0.7% ENDO vs. 5 +/- 1.8% EPI) was initially observed at 7 days and was still evident by 30 days (25 +/- 3.6% ENDO vs 15 +/- 2.0% EPI). Cell cross-sectional area was also greater (p < 0.05) in the ENDO than in the EPI at 7, 15 and 30 days. MF diameter was determined only at 30 days and was found to be similar to control values in both the hypertrophied ENDO (sham 1.24 +/- 0.05 vs hyp 1.18 +/- 0.09 microns) and EPI (sham 1.17 +/- 0.08 vs hyp 1.06 +/- 0.08 microns). The combined effects of cardiac myocyte hypertrophy with no change in MF diameter resulted in a calculated increase of approximately 70% in the number of myofibrils per myocyte both in the ENDO and EPI. It was concluded that the adaptive strategy of the left ventricular free wall to pressure overload was to initially increase myocyte cross-sectional area and then switch myosin expression from V1 to V3, both of which proceeds transmurally from the sub-endocardium towards the sub-epicardium.(ABSTRACT TRUNCATED AT 250 WORDS)