Silvia Visentin 1 , Ambrogio Pietro Londero 2 , Beatrice Bellamio 1 , Grazia Giunta 1 , Chiara Cosma 3 , Diego Faggian 3 , Mario Plebani 3 , Erich Cosmi 4 . Show Affiliations »
Abstract
BACKGROUND: Recent studies reveal that offspring of pregnancies complicated by hypertensive disorders may have an increased cardiovascular risk. Genetic and nongenetic factors seem to play an important role in premature arterial disease. Endothelium may be significant for long-term remodeling of the arterial wall. The aim of the study was to assess fetal endothelial and renal function in late-onset gestational hypertension. MATERIALS AND METHODS: This was a case-controlled study. Singleton pregnancies affected by late-onset gestational hypertension (after 34 weeks' gestation) and controls were included. Ultrasound examinations (fetal biometry, fetal Doppler, fetal aorta intima media thickness (aIMT), fetal kidney volumes, maternal Doppler, presence of uterine arteries protodiastolic notching from anomaly scan) and clinical data were collected. A sample of amniotic fluid was taken at delivery. RESULTS: Fifty patients with late-onset hypertension and 50 controls were included. At growth scan (weeks 29-32) we found in the study group significantly higher fetal aIMT, umbilical artery pulsatility index (PI), fetal aorta PI, and mean uterine arteries PI with persistent bilateral notch. In the case group microalbuminuria levels were significantly higher than controls (1.32±0.11 vs. 1.10±0.13g/l, P < 0.0001), and there was a negative correlation between renal fetal volume at growth scan and amniotic microalbuminuria (r: -0.95, 95% C -0.97 to -0.90, P < 0.0001). CONCLUSIONS: Gestational hypertension should be considered as one of the adverse early risk factors that might predispose to impaired fetal cardiovascular development during intrauterine life; therefore, this study provides further evidence to better understand the origins of cardiovascular diseases. © American Journal of Hypertension, Ltd 2015. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
BACKGROUND: Recent studies reveal that offspring of pregnancies complicated by hypertensive disorders may have an increased cardiovascular risk. Genetic and nongenetic factors seem to play an important role in premature arterial disease . Endothelium may be significant for long-term remodeling of the arterial wall. The aim of the study was to assess fetal endothelial and renal function in late-onset gestational hypertension . MATERIALS AND METHODS: This was a case-controlled study. Singleton pregnancies affected by late-onset gestational hypertension (after 34 weeks' gestation) and controls were included. Ultrasound examinations (fetal biometry, fetal Doppler, fetal aorta intima media thickness (aIMT), fetal kidney volumes, maternal Doppler, presence of uterine arteries protodiastolic notching from anomaly scan) and clinical data were collected. A sample of amniotic fluid was taken at delivery. RESULTS: Fifty patients with late-onset hypertension and 50 controls were included. At growth scan (weeks 29-32) we found in the study group significantly higher fetal aIMT, umbilical artery pulsatility index (PI), fetal aorta PI, and mean uterine arteries PI with persistent bilateral notch. In the case group microalbuminuria levels were significantly higher than controls (1.32±0.11 vs. 1.10±0.13g/l, P < 0.0001), and there was a negative correlation between renal fetal volume at growth scan and amniotic microalbuminuria (r: -0.95, 95% C -0.97 to -0.90, P < 0.0001). CONCLUSIONS: Gestational hypertension should be considered as one of the adverse early risk factors that might predispose to impaired fetal cardiovascular development during intrauterine life; therefore, this study provides further evidence to better understand the origins of cardiovascular diseases . © American Journal of Hypertension , Ltd 2015. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
Entities: Chemical
Disease
Species
Keywords:
blood pressure; late onset hypertension; renal failure; vascular remodeling.
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Year: 2015
PMID: 26150542 DOI: 10.1093/ajh/hpv103
Source DB: PubMed Journal: Am J Hypertens ISSN: 0895-7061 Impact factor: 2.689