Ostadal B.,1*Kolar F.,1 Ostadalova I.,1 Sedmera D.,1,2 Olejnickova V.,1,2 Hlavackova M.,1 Alanova P.1
1Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic,
2 Institute of Anatomy, First Faculty of Medicine, Charles University, Prague, Czech Republic
Abstract
The heart is capable of extensive adaptive growth in response to the demands of the body. When the heart is confronted with an increased workload over a prolonged period, it tends to cope with the situation by increasing its muscle mass. Adaptive growth response of the cardiac muscle changes significantly during phylogenetic and ontogenetic development. Cold-blooded animals maintain the ability of cardiomyocyte proliferation even in adults. On the other hand, the extent of proliferation during ontogenetic development in warm-blooded species shows significant temporal limitations: whereas fetal and neonatal cardiac myocytes express proliferative potential (hyperplasia), after birth proliferation declines and heart grows almost exclusively by hypertrophy. It is, therefore, understandable that also regulation of the cardiac growth response to the increased workload differs significantly during development. The pressure overload (aortic constriction) induced in animals before the switch from the hyperplastic to hypertrophic growth leads to a specific type of the left ventricular hypertrophy which, in contrast with the same stimulus applied in adulthood, is characterized by hyperplasia of cardiomyocytes, capillary angiogenesis and biogenesis of collagenous structures, proportional to the growth of myocytes. These studies suggest that timing may be of crucial importance in neonatal cardiac interventions in humans: early definitive repairs of selected congenital heart disease may be more beneficial for long-term results of surgical treatment.