Abstract
Background CHD represents the most important component of pediatric cardiovascular diseases. It has a high risk of morbidity and mortality in newborns and infants. were considered as multifactorial diseases. However genetic factors were considered as a corner stone of their etiology. The DNA content represents the nuclear genomic concentration. It is affected by several multifactors. Objective The aim of our study was to determine the DNA content in particular common congenital heart disease. To detect the correlation between their DNA content and the chromosomal pattern as well as with the hemodynamic aspect of CHD. Material and methods The present study was subjected on 30 children suffering from the most common CHD and accordingly classified into three groups; 1St (VSD) 2nd (TOF), 3’ (D-TGA), each included 10 cases with specific criteria and equally gender distribution, and ten healthy age matched children as control group. All studied groups were subjected to thorough clinical, functional, structural and hemodynamic cardiac assessment as investigated via electrocardiogram, cardiac X rays, full echocardiography, and cardiac catheterization studies. Also full chromosomal, cytogenetic and DNA content studies were applied. Results The value of structural and numerical chromosornal aberrations was found to be significantly higher in cyanotic congenital heart disease (CCHD) than that of acyanotic congenital heart disease (ACCHD). Current study revealed that there was a highly significant correlation between the incidence of the chromosomal aberrations both structural and numerical as well as the aging and the mean values of DNA content of CHD. Also there was highly significant decreased in DNA content values in CHD in comparison to control group and the affection in DNA content of (CCHD), was more aggressive than in (ACCHD). However there was non significant relation between DNA content and the hemodynamic and function aspect of CHD. Conclusion DNA content of CHD was highly significant reduced. It is affected by the incidence of chrornosomal aberrations, aging and the cardiomyocytic apoptosis.
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