Cardiac hypertrophy is the compensatory response of the myocadium to increased workload. Compensatory mechanisms come into play when the hypertrophied heart can no longer accommodate the increased demand or persistent stimuli. Although it has been reported that the molecular changes in hypertrophied hearts that initially mediate enhanced function may contribute to the development of heart failure, the structural/biochemical/molecular basis for myocardial contractile failure is still obscure. This study was aimed to clarify the structural basis for relation between hypertrophy and failure.

Nine pairs of rabbits were sacrificed at 8,12,24,48 hours and 1,2,4,6,8 weeks after experiment aortic constriction. There hearts were studied with routine histopathology. Each heart was weighed and compared with total body weight. Multiple sections were embedded in paraffin, sectioned at 5um, and stained with hematoxylin and cosin and Masson's trichrome and analysed.

The heart weight to body weight ratio(g/Kg) increased progressively with time after aortic banding. Banding of the aorta in the rabbit resulted in multifocal areas of myofiber degeneration, necrosis and fibrosis through the wall of the left ventricle, in the papillary muscles of the left ventricle and in the left ventricular portions of the interventricular septum in rabbit of 6 and 8 weeks after aortic banding. By 4 weeks after banding, the foci of necrosis were not observed.

There findings suggest that the increased necrosis, fibrosis in animals with cardiac hypertrophy induced by banding the aorta may play a role in progression to heart failure.