**7. References**

346 Congenital Heart Disease – Selected Aspects

possible to observe the appearance of skeletal myosin in the cardiomyocytes. This testifies that, during hypertrophy development, the synthesis changes over from cardiac myosin to a skeletal one. Plain fluorescent microscopy of preparations stained with ethidium bromide revealed a drastic decrease in intensity of the fluorescent marker in infants aged under 6 months, as compared to the control group, and a rapid growth of ethidium bromide incorporation in infants aged 6 months and upward. It indicates a prevalence of the population of cardiomyocytes with diploid nuclei in the hearts of infants aged up to 6 months. In patients aged above 6 months, the heart remodelling process proceeds, with the processes associated with polyploidization of nuclear material and subsequent development of cell hypertrophy dominating. It should be emphasized that the level of polyploidization in LV cardiomyocytes is essentially higher than that in RV. Hence, the hyperplastic processes associated with intensive polyploidization of the genetic material and an increase in the quantity of desoxyribonucleic acid play an important role in the remodelling of the

This study enabled us to come to the following conclusion on the development of a pathological mechanism causing the deaths of TGA patients at an early age. As a result of aorta and pulmonary artery transposition, low-oxygen venous blood flows into the systemic circulation system, limits the growth of newborns. The need for a sufficient volume of oxygen can be met only by increased load on the myocardium, with the development of heart hypertrophy uniform for LV and RV in patients with IVS and more pronounced in RV in patients with VSD. In this case the growth of TGA infants conforms to the age norm and even slightly exceeds it, while the body mass falls far short of the norm by 25-30 %. For hypertrophy and hyperplasia to develop dramatically, there should be an increased supply of nutritional and caloric substances, including CE. As the delivery of CE turns out to be insufficient, or their consumption increases, a 50 % deficiency of such microelements as Cl, Cr, Sr, Zn, Br, Rb and especially Se, which, as an active antioxidant, protects cardiomyocytes from lipid peroxidation, can be seen. As a consequence, structural disorders of the myocardium occur on the morphological/molecular level. Also observed are the following abnormalities: a decrease in the diameter of muscle fibres and the average area of nuclei, a drop in the level of the total calcium ions against the background of intensive polyploidization of genetic material, an increase in the content of the quantity of desoxyribonucleic acid, and change from the cardiac myosin synthesis over to a skeletal one. All these changes lead to alteration of the myocardium, occurrence of cardiosclerosis, development of cardiac insufficiency and reduction of arterial blood saturation down to 32 % and below, which is fatal, and results in death of the organism. This is a picture of TGA development pathogenesis of infants from neonatal age up to 1 year old. In this case, only definitive repair of the disease can break the pathogenetic chain of TGA in an early period, and the best time when effective cardiac surgery could be performed for TGA infants is in

We suppose, that to prevent the development of congenital heart diseases including TGA, pregnant women and nursing mothers should get the optimum quantity of microelements Cr, Zn, Sr, Ni, Rb, Br and most of all Se, protecting the myocardium from lipid

heart in patients aged above 6 months.

**6. Conclusion** 

the neonatal period.

peroxidation.


Trounova, V.A.; Zolotarev, K.V. & Baryshev, V.B. et al. (1998). Analytical possibilities of

Trunova, V. A. & Zvereva, V. V. (2008). Investigation of the distribution macro - and

(1998), pp. 532-536

*Chemistry*, Vol. 49, (2008), pp. 211-216

SRXRF station at VEPP-3 SR source. *Nuclear Instruments and Methods A*, Vol. 405,

traceelements in human myocardium and vessels by SRXRF. *Journal of Structural* 
