Cardiovascular adaptation to extrauterine life after intrauterine growth restriction

Abstract

Neonates with history of intrauterine growth restriction showed cardiac remodelling and signs of systolic and diastolic dysfunction. Overall, there was a significant tendency to worse cardiac function results in the right heart. The adaptation to extrauterine life occurred with more globular hearts, higher stroke volumes but a similar heart rate compared to adequate-for-gestational-age neonates.

Cardiac Measurements of Size and Shape in Fetuses With Absent or Reversed End‐Diastolic Velocity of the Umbilical Artery and Perinatal Survival and Severe Growth Restriction Before 34 Weeks' Gestation

“…Studies in neonates with FGR have also found the RV and LV transverse widths to be increased compared to controls. 2,6 Hobbins et al 13 measured the end-diastolic area of the RV and LV and found no increase in areas in fetuses with an EFW below the 10th centile with a normal UA PI but reported a significant number of fetuses with decreased end-diastolic areas for both ventricles when the UA PI was abnormal. 13 Of interest, decreased LV and RV areas and 24-segment transverse widths were only identified in neonatal survivors in our study.…”

“…The results from the z score computations were classified as above the 95th centile ( z > 1.65) or below 5th centile ( z < −1.65), depending on the measurement. Once the z scores were computed for each of the above measurements, the numbers of fetuses with abnormal z score values were compared to the expected numbers of abnormal values for the 5th and 95th centiles from control populations by the χ 2 analysis or the Fisher exact test (NCSS version 19; NCSS, Kaysville, UT) 8–11,16,25 . In addition, z score values for the above measurements were compared between the two groups by the Student t test if the variables were normally distributed or the Mann–Whitney U test if the measurements were not normally distributed.…”

“…increased fetal cardiac afterload with fetal and neonatal consequences, we were interested in the morphometric changes of the fetal heart in fetuses who had a perinatal death compared to those who survived the neonatal period. [1][2][3][4][5][6][7][8][9][10][11][12][13] Therefore, the purpose of this study was to determine (1) the frequency and z score values of abnormal cardiac morphometric measurements of the 4-chamber view (4CV) and the right ventricle (RV) and left ventricle (LV) in fetuses with AREDV; and (2) differences in the above measurements between fetuses who had a perinatal death and those who did not.…”

“…In a recent meta‐analysis of 31 studies evaluating 336 fetal deaths in growth‐restricted fetuses before 34 weeks' gestation who had absent or reversed end‐diastolic flow of the umbilical artery (UA), ductus venosus (DV), or both, the authors reported odds ratios for fetal death of 6.8 for absent or reversed end‐diastolic velocity (AREDV) of the UA and 11.6 for absent or reversed flow of the DV 1 . Since AREDV is associated with increased placental resistance to blood flow, resulting in an increased fetal cardiac afterload with fetal and neonatal consequences, we were interested in the morphometric changes of the fetal heart in fetuses who had a perinatal death compared to those who survived the neonatal period 1–13 . Therefore, the purpose of this study was to determine (1) the frequency and z score values of abnormal cardiac morphometric measurements of the 4‐chamber view (4CV) and the right ventricle (RV) and left ventricle (LV) in fetuses with AREDV; and (2) differences in the above measurements between fetuses who had a perinatal death and those who did not.…”

Neuron-specific enolase and brain-derived neurotrophic factor levels in umbilical cord blood in full-term newborns with intrauterine growth retardation

“…■ Keywords: newborn; intrauterine growth retardation; neuron-specific enolase; brain-derived neurotrophic factor. недостаточности нарушается генетическая программа развития всех функциональных систем орга низма плода, что затрудняет постнатальную адаптацию и программирует риск небла гоприятных последствий [5][6][7][8][9]. При этом значительные структурно-функциональные изменения на клеточном уровне способствуют возникновению глубоких нарушений гомеостаза мозга, продукции и метаболизма нейромедиаторов, нейромодуляторов и нейрогормонов [10][11][12][13].…”