Myocardial growth before and after birth: clinical implications

Perinatal changes in myocardial growth have recently evoked considerable in terest with regard to cardiac chamber development with congenital cardiac l esions and to myocardial development in preterm infants. It is suggested th at cardiac chamber development is influenced by blood flow. Experimental pu lmonary stenosis in fetal lambs may induce either greatly reduced or marked ly increased right ventricular volume. Ventricular enlargement appears to b e associated with a large ventricular volume load resulting from tricuspid valve regurgitation. A small competent tricuspid valve is associated with r educed flow through the ventricle due to outflow obstruction and a small ri ght ventricle. Postnatal growth of the ventricles in congenital heart disea se is discussed. Increase in myocardial mass prenatally is achieved by hype rplasia, both during normal development and when myocardial mass is increas ed by right ventricular outflow obstruction. Postnatally, increases in myoc ardial mass with normal growth, as well as with ventricular outflow obstruc tion, are largely due to hypertrophy of myocytes. Myocardial capillary numb ers do not increase in proportion with myocyte numbers in ventricular myoca rdium in association with outflow obstruction. The postnatal effects of the se changes in congenital heart lesions are considered. Studies in fetal lam bs suggest that the late gestational increase in blood cortisol concentrati ons is responsible for the change in the pattern of myocardial growth after birth. The concern is raised that prenatal exposure of the premature infan t to glucocorticoids, administered to the mother to attempt to prevent hyal ine membrane disease in the infant, may inhibit myocyte proliferation and r esult in a heart with fewer than normal myocytes. This would necessitate th at each myocyte would have to hypertrophy abnormally to achieve a normal ca rdiac mass postnatally.