Mechanism od Cardiac Hypertrophy ; The Efficacy of Gene Therapy in Cardiac Hypertrophy

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Myocardial hypertrophy is a basic adaptive mechanism of the heart to compensate for an increased mechanical load. Heart failure is final presentation of cardiovascular disease, such as coronary artery disease, hypertension, valvular heart disease, myocarditis and others. The pathogenetic mechanisms responsible for the transition to cardiac dysfunction and heart failure are not well understood. Volume-overloaded rat hearts were established by A-V shunt between abdominal aorta and inferior caval vein. Immunohistochemical investigations of proto-oncogene proteins were performed in the presence. The myocytes of volume-overloaded hearts were significantly larger in diameter than control hearts on 14th day after A=V shunt. The weight of volume-overloaded hearts was also significantly larger than control hearts. In nuclei of myocytes of volume-overloaded hearts, the maximum expression of Fos and Myc protein was observed on the 2nd day after A-V shunt. After the 2nd day, the expression decreased gradually. In the human heart, however, it has not been clarified whether these proto-oncogenes are related to contractile impairment and structural alteration of the myocardium. The present study is designed to investigate the relationship between the C-Myc protein expression in the myocardium and the myocardial contractile dysfunction in patients with chronic aortic regurgitation. C-Myc was detected in nine of 12 present patients but in none of the normal controls. The degree of C-Myc expression had significant positive correlations with EF and ESS/ESVI and significant negative correlations with ESVI,CD and FC,which suggested that the degree of C-Myc expression may have a significant negative correlation with myocardial contractility and myocardial hypertrophy. Conclusion : C-Myc expression may be related to the pathogenesis of myocardial remodeling in patients with chronic aortic regurgitation.