J A avides-Serralde

Bio: J A avides-Serralde is an academic researcher. The author has an hindex of 1, co-authored 1 publications receiving 223 citations.

Fetal Growth Restriction Results in Remodeled and Less Efficient Hearts in Children

Abstract: Background—Fetal growth restriction (FGR) affects 5% to 10% of newborns and is associated with increased cardiovascular mortality in adulthood. The most commonly accepted hypothesis is that fetal metabolic programming leads secondarily to diseases associated with cardiovascular disease, such as obesity, diabetes mellitus, and hypertension. Our main objective was to evaluate the alternative hypothesis that FGR induces primary cardiac changes that persist into childhood. Methods and Results—Within a cohort of fetuses with growth restriction identified in fetal life and followed up into childhood, we randomly selected 80 subjects with FGR and compared them with 120 normally grown fetuses, matched for gender, birth date, and gestational age at birth. Cardiovascular assessment was performed in childhood (mean age of 5 years). Compared with control subjects, children with FGR had a different cardiac shape, with increased transversal diameters and more globular cardiac ventricles. Although left ejection fraction was similar among the study groups, stroke volume was reduced significantly, which was compensated for by an increased heart rate to maintain output in severe FGR. This was associated with subclinical longitudinal systolic dysfunction (decreased myocardial peak velocities) and diastolic changes (increased E/E ratio and E deceleration time). Children with FGR also had higher blood pressure and increased intima-media thickness. For all parameters evaluated, there was a linear increase with the severity of growth restriction. Conclusions—These findings suggest that FGR induces primary cardiac and vascular changes that could explain the increased predisposition to cardiovascular disease in adult life. If these results are confirmed, the impact of strategies with beneficial effects on cardiac remodeling should be explored in children with FGR. (Circulation. 2010;121:2427-2436.)

Fetal growth restriction: current knowledge.

Abstract: Fetal growth restriction (FGR) is a condition that affects 5–10% of pregnancies and is the second most common cause of perinatal mortality. This review presents the most recent knowledge on FGR and focuses on the etiology, classification, prediction, diagnosis, and management of the condition, as well as on its neurological complications. The Pubmed, SCOPUS, and Embase databases were searched using the term “fetal growth restriction”. Fetal growth restriction (FGR) may be classified as early or late depending on the time of diagnosis. Early FGR (<32 weeks) is associated with substantial alterations in placental implantation with elevated hypoxia, which requires cardiovascular adaptation. Perinatal morbidity and mortality rates are high. Late FGR (≥32 weeks) presents with slight deficiencies in placentation, which leads to mild hypoxia and requires little cardiovascular adaptation. Perinatal morbidity and mortality rates are lower. The diagnosis of FGR may be clinical; however, an arterial and venous Doppler ultrasound examination is essential for diagnosis and follow-up. There are currently no treatments to control FGR; the time at which pregnancy is interrupted is of vital importance for protecting both the mother and fetus. Early diagnosis of FGR is very important, because it enables the identification of the etiology of the condition and adequate monitoring of the fetal status, thereby minimizing risks of premature birth and intrauterine hypoxia.

Neonatal Morbidities of Fetal Growth Restriction: Pathophysiology and Impact.

Abstract: Being born small lays the foundation for short-term and long-term implications for life. Intrauterine or fetal growth restriction describes the pregnancy complication of pathological reduced fetal growth, leading to significant perinatal mortality and morbidity, and subsequent long-term deficits. Placental insufficiency is the principal cause of FGR, which in turn underlies a chronic undersupply of oxygen and nutrients to the fetus. The neonatal morbidities associated with FGR depend on the timing of onset of placental dysfunction and growth restriction, its severity, and the gestation at birth of the infant. In this review, we explore the pathophysiological mechanisms involved in the development of major neonatal morbidities in FGR, and their impact on the health of the infant. Fetal cardiovascular adaptation and altered organ development during gestation are principal contributors to postnatal consequences of FGR. Clinical presentation, diagnostic tools and management strategies of neonatal morbidities are presented. We also present information on the current status of targeted therapies. A better understanding of neonatal morbidities associated with FGR will enable early neonatal detection, monitoring and management of potential adverse outcomes in the newborn period and beyond.

Fetal growth restriction - from observation to intervention.

Abstract: Fetal growth restriction (FGR) due to placental dysfunction has important short- and long-term impacts that may reach into adulthood. Early-onset FGR before 34 weeks' gestation shows a characteristic sequence of responses to placental dysfunction that evolves from the arterial circulation to the venous system and finally to biophysical abnormalities. In this form of FGR safe prolongation of pregnancy is a primary management goal, as gestational age at delivery, birth weight and iatrogenic premature delivery have an important impact on short-term outcome and neurodevelopment. Surveillance intervals should be adjusted based on umbilical artery and venous Doppler studies. Intervention thresholds need to be based on the balance of fetal vs. neonatal risks and therefore critically depend on gestational age. Late-onset FGR presents with subtle Doppler and biophysical abnormalities and therefore poses a diagnostic dilemma. Often unrecognized, term FGR contributes to a large proportion of adverse perinatal outcome. Monitoring intervals should be adjusted based on middle cerebral artery Doppler and fetal heart rate parameters. Delivery timing thresholds can be low. In both forms of FGR neurodevelopmental impacts of placental disease occur before clinical decisions regarding delivery timing arise. This places special emphasis on future preventative studies.