PubMed · 7457544
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T J Garite, H D Modaniou, R K Freeman. 1981-01-15. Sinusoidal fetal heart rate pattern.. https://doi.org/10.1016/0002-9378(81)90457-9
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The aim of the study was to determine the morphology of epicardiac ganglia in human fetuses at different stages of their development as these ganglia are considered to be of a pivotal clinical importance. Twenty-one fetal hearts were investigated applying a technique of histochemistry for acetylcholinesterase to visualize the epicardiac neural ganglionated plexus with its subsequent stereoscopic examination on total organs. In all of the examined fetuses, epicardiac neural plexus with numerous ganglia was well recognizable and could be clearly differentiated into seven ganglionated subplexuses, topography and structural organization of which were typical for hearts of adult human. The largest ganglion number comprising 77% of all counted ganglia was identified on the dorsal atrial surface. Fetal epicardiac plexus in gestation period of 15-40 weeks contained 929 +/- 62 ganglia, but ganglion amount did vary substantially from heart to heart. In conclusion, this study implies that the human fetal epicardiac ganglia occupy their definitive location already at gestation period from 15 weeks and their number as well as distribution on heart surface presumably is not age dependent.
OBJECTIVE: The objective of the study was to examine the size and growth of fetal pulmonary artery diameters in congenital diaphragmatic hernia and assess their correlation with postnatal survival and morbidity outcomes. STUDY DESIGN: Prospective antenatal echocardiographic examination of fetal branch pulmonary arteries were correlated with postnatal survival and respiratory morbidity in cases of congenital diaphragmatic hernia. Receiver operator curves were developed to assess their utilization as predictors of respiratory morbidity and survival. RESULTS: Twenty-one cases were diagnosed antenatally over 3 years. Fifteen subjects survived postnatally. The ipsilateral fetal branch pulmonary artery diameter was smaller throughout gestation in left-sided congenital diaphragmatic hernia (P = .008). The small left pulmonary diameter did not correlate with survival but correlated strongly with morbidity outcomes. Progressive ipsilateral fetal pulmonary artery hypoplasia was demonstrated throughout gestation in subjects who died or had severe morbidity. CONCLUSION: Fetal pulmonary artery diameter measurements correlate with respiratory morbidity in postnatal congenital diaphragmatic hernia and may assist with prediction of outcome. Survival has improved, possibly because of improved postnatal management of congenital diaphragmatic hernia, limiting this measurement in assessing survival.
OBJECTIVE: The hypothesis that severe fetal hydrops is caused by an excess of vascular endothelial growth factor (VEGF), mainly produced in the fetal heart, is tested. METHODS: Immunohistochemical VEGF-stained postmortem biopsies from the right ventricle and right atrium of 8 hydropic fetuses were compared to those of 8 nonhydropic fetuses. The endocardium, myocardium, epicardium, endothelium, and vascular smooth muscle cells were scored on intensity of VEGF-staining. The Mann-Witney test was used to test for significancy (p < 0.05) of the differences in staining. Increased vascularization as a result of VEGF was measured in both groups by standard randomization count. RESULTS: The endocardium, epicardium and endothelium of the coronary vessels showed significantly (p < 0.05) more intense VEGF-staining in the hydrops group than in the control group. The atria showed more intense staining than the ventricles in both groups. The hydropic fetuses showed a significantly increased number of coronary vessels in the myocardium. These vessels contained more blood cells than the coronary vessels in nonhydropic fetuses. CONCLUSION: The fetal heart appears to be a major source of excess VEGF in fetal hydrops.