Why is neonatal myocardium more prone for heart failure?
Contractile elements form 30% of the fetal heart while it forms 60% in the adult. Immature myocytes lack sufficient sarcoplasmic reticulum and mitochondria. There is also a decreased level of cellular transport. This makes the neonatal myocardium more prone for heart failure. When the number of mitochondria increase, the myocardium matures to utilize fatty acids instead of carbohydrates as the major energy source.
There is structural difference between the neonatal myocyte and the mature myocyte. The neonatal myocyte is short, rounded and not well organized intracellularly, while the mature myocyte is slender, longer and well organized intracellularly. Though neonatal myocardium has lower ability to develop tension, its function can be augmented by inotropic support. This factor is of great help in managing neonatal heart failure.
But the Frank-Starling mechanism whereby cardiac output increases on increasing the preload is intact in the neonatal myocardium. Hence cardiac output can increase with higher filling and inotropy as well as with increase in heart rate.
After birth, the left ventricular myocytes proliferate faster than the right ventricular myocytes because of increase in the systemic vascular resistance. Ventricular acidic fibroblast growth factor released locally contributes to this hyperplastic growth. After the initial few weeks, it is more of hypertrophy rather than hyperplasia which contributes to increase in left ventricular mass. This is in response to the higher hemodynamic workload as well as circulating growth factors and catecholamines.