Morphopathology of myocardial hypoxic-ischemic injuries in newborns at 22-27 weeks' gestation

Abstract

To determine the parameters of myocardial structural injuries developed in chronic intrauterine hypoxia conditions in newborns at 22-27 weeks' gestation. A battery of morphological techniques, including organometry studies and separate weighing of the heart; 3D histology; morphometry with the determination of the area of cardiomyocyte nuclei, the specific area of the muscular and interstitial components of the right ventricular myocardium; immunohistochemistry with monoclonal antibodies to transforming growth factor βı (TGF-βı), cardiac troponin T (cTnT), and transmission electron microscopy, was used to examine heart samples from 30 deceased newborns at 22-27 weeks' gestation who developed in chronic intrauterine hypoxia conditions. A control group consisted of hearts from 20 extremely low body weight (ELBW) newborns, the main cause of whose death was asphyxia caused by the premature detachment of a normally positioned placenta. Analysis of the organometric parameters of heart samples from newborns at 22-27 weeks' gestation, who had experienced chronic intrauterine hypoxia, revealed right ventricular hypertrophy with increases in the area of cardiomyocyte nuclei and in the specific area of the muscle component compared to the control group. Impaired myocardial microcirculation and destructive changes in cardiomyocytes were diagnosed in conjunction with the decreased troponin T and increased TGF-β1 expressions. Incomplete differentiation of cardiomyocytes and their myofibrillar component was revealed at the myocardial ultrastructural level in ELBW newborns who had experienced chronic intrauterine hypoxia. The parameters of myocardial structural rearrangement in ELBW newborns who had experienced chronic intrauterine hypoxia are compensatory right ventricular hypertrophy, microcirculatory disorders, destructive changes in cardiomyocytes, decreased cTnT and increased TGF-β1 expressions in conjunction with impaired cardiomyocyte differentiation.