These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Abnormal maternal cardiac function and morphology in pregnancies complicated by intrauterine fetal growth restriction. Author: Vasapollo B, Valensise H, Novelli GP, Larciprete G, Di Pierro G, Altomare F, Casalino B, Galante A, Arduini D. Journal: Ultrasound Obstet Gynecol; 2002 Nov; 20(5):452-7. PubMed ID: 12423481. Abstract: OBJECTIVE: To explore maternal cardiac function through an echocardiographic evaluation, in a group of nulliparous patients with intrauterine fetal growth restriction during the third trimester of pregnancy. METHODS: Twenty-one consecutive nulliparous pregnant women who had fetuses with intrauterine growth restriction (IUGR) and abnormal umbilical artery Doppler pulsatility index (PI) underwent maternal echocardiographic examination during the third trimester of gestation. The data were then compared with those obtained from 21 normal nulliparous women who had fetuses with an estimated fetal weight > 10th percentile and a normal umbilical artery Doppler PI who were considered as the control group. RESULTS: Heart rate was slightly lower in the IUGR group, whereas blood pressure and total vascular resistance were higher compared with the control subjects. End-diastolic volume, stroke volume and cardiac output were lower in the IUGR patients compared with normal patients. The IUGR group had smaller left atrial maximal dimensions and greater left atrial minimal areas compared with the control subjects. Left atrial function was depressed in the IUGR group. A smaller left ventricular mass was present in the IUGR patients compared with the control subjects. Isovolumetric relaxation time (IVRT) was prolonged in the IUGR patients compared with the controls. CONCLUSIONS: The absence of a 'correct' maternal cardiovascular compensatory response to abnormal trophoblastic invasion, might be one of the factors that slowly determine the conditions of reduced placental perfusion and eventually of the development of fetal growth restriction.[Abstract] [Full Text] [Related] [New Search]