Chemical Elements and Structural/Molecular Properties of Myocardium in Infants with Transposition of Great Arteries

The imbalance of chemical elements (CE) during the prenatal development of a foetus might cause foetal heart abnormalities and even miscarriages (Skalny, 1999; Kudriyn, 2000), while the deficit of many vital CE during the gestation period could lead to congenital heart diseases. The deficiency of Cu in the course of this period might provoke the development of aortic aneurysms and impairment of vessel elasticity (Panchenko, 2004), while the lack of Zn could bring about transposition of the great arteries (TGA) (Shankar & Prasad, 1998; Beerli et al., 2000). The content of Fe, Cu, Zn, Se and Mn in optimal quantities is indispensable for adequate support of the cellular cycle, growth and differentiation of cells, including cardiomyocytes (Ruff, 1999). TGA comprises a special group of congenital heart diseases (CHD) with concordant atrioventricular and discordant ventricular-arterial junctions (Fozzard et al., 1986; Hoffman, 2006). This complicated disease occurs in newborns with CHD in an excess of 10 % of cases, with significant mortality and morbidity (Bokeria & Gorbachevsky, 1996). This is because it is yet unclear why this disease occurs, how this pathology progresses during the growth and development of newborns and, most importantly, which metabolic processes get impaired in cardiomyocytes that lead to the death of myocardium. Nowadays, a high level of immunofluorescent methods allows for identifying the cardiomyocytes that are involved in DNA replication (Re, 1987; Bolli, 2002). The main difficulty encountered in treating this disease is to correctly evaluate the ventricular function providing an adequate cardiac output (Castaneda, 1993, 1998). Age is also an important factor in determining the speed and functional reaction of the myocardium to pressure overload (Isoyama et al., 1987; Re, 1987; Scholzen & Gerders, 2000). Further research is needed to answer the following questions: 1. How is CE distribution disrupted in different parts of the heart and how is this disruption related to pathomorphological abnormalities? 2. How are morphology and the molecular structure of cardiomyocytes changed in the course of growth and development of infants with TGA,