Cardiac Maturation

Cardiac development and function are completed by week 11. The fetal and neonatal heart continues to grow and mature rapidly. During fetal development the heart grows primarily by the process of cell division, whereas cardiac growth after birth proceeds by the mechanism of cell hypertrophy. Recent research refutes the hypothesis that mature cardiac cells lose the ability to divide, and instead suggests that a limited amount of cell division occurs in adult hearts that have been damaged by ischemia.

Maturational changes in the composition of the cardiac myocytes, differences in energy production and/or maturation of the contractile function in the fetal and neonatal heart, and changes in hemodynamics affect the treatment of newborns, especially those with congenital heart defects that require interventional procedures or cardiac surgery.

After birth, left ventricular cardiac output increases to meet the growing metabolic needs of the newborn. Neonatal myocardium has less muscle mass and less cellular organization than the adult myocardium. Fetal myocytes are also rounded, with both myocytes and myofibrils lacking a consistent orientation. During maturation, those cells increase in size and orient themselves. Fetal myocardial cells contain higher amounts of glycogen than the mature myocardium which indicates an increased dependence on glucose for energy production, in contrast to the adult heart which prefers long-chain fatty acids.

Immature myocardium requires high levels of extra-cellular calcium and has a decreased sensitivity to beta-adrenergic inotropic agents. Furthermore, neonates and infants are more sensitive to calcium channel blocking drugs than older individuals. Sensitivity to beta-agonist agents in immature and older children with congenital heart disease is significantly decreased and requires alternative treatment.