Differential Growth Rates, Rather Than Compaction, Determine Left Ventricular Wall Formation

Trabecular muscle makes up most of the ventricular wall of the human embryo. It is presumed that compaction in the foetal period changes ventricular wall morphology by converting weaker trabeculae to stronger compact muscle. Using developmental series covering the embryonic and foetal periods of human, mouse and chicken, we show ventricular morphology is determined by differential rates of positive growth of trabecular and compact layers rather than compaction. In mouse, foetal cardiomyocytes are relative weak, but adult trabecular and compact cardiomyocytes are equally strong. In foetal and adult humans, trabecular and compact myocardium exhibit a similar abundance of immunohistochemically detected vascular, mitochondrial and sarcomeric proteins. Even in human noncompaction, a congenital malformation characterized by excessive trabeculation, the trabecular and compact muscle are similar. In conclusion, trabecular and compact myocardium are equally equipped for force production and their proportions are determined not by compaction, but by differential growth rates.