摘要：SummaryTrabecular myocardium makes up most of the ventricular wall of the human embryo. A process of compaction in the fetal period presumably changes ventricular wall morphology by converting ostensibly weaker trabecular myocardium into stronger compact myocardium. Using developmental series of embryonic and fetal humans, mice and chickens, we show ventricular morphogenesis is driven by differential rates of growth of trabecular and compact layers rather than a process of compaction. In mouse, fetal cardiomyocytes are relatively weak but adult cardiomyocytes from the trabecular and compact layer show an equally large force generating capacity. In fetal and adult humans, trabecular and compact myocardium are not different in abundance of immunohistochemically detected vascular, mitochondrial and sarcomeric proteins. Similar findings are made in human excessive trabeculation, a congenital malformation. In conclusion, trabecular and compact myocardium is equally equipped for force production and their proportions are determined by differential growth rates rather than by compaction.Graphical abstractDisplay OmittedHighlights•The trabecular and compact ventricular layers grow differentially during gestation•Differential growth rates in the embryo result in temporary excessive trabeculation•Normal and excessively trabeculated hearts show no difference in epitope expression•Trabecular and compact cardiomyocytes can generate equal amounts of forceAnatomy; Biology of human development; Developmental anatomy; Developmental biology; Mechanobiology; Medical imaging; Medicine
