Evaluation of cardiac functions in term small for gestational age newborns with mild growth retardation: A serial conventional and tissue Doppler imaging echocardiographic study

Altın, Hakan; Karaarslan, Sevim; Karataş, Zehra; Alp, Hayrullah; Şap, Fatih; Baysal, Tamer

doi:10.1016/j.earlhumdev.2012.04.003

Cited by 42 publications

(46 citation statements)

References 38 publications

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“…The MPI has been shown to progressively increase with fetal deterioration (7) and it appears to have a negative association with perinatal outcome (including 5-min Apgar score, cord pH, and perinatal mortality) (7,46). An increased MPI has also been found in neonates following IUGR (37,40,43) and has even been reported in infants born growth restricted up to 3 mo of age (40), suggesting that cardiac dysfunction, although subclinical, can persists beyond the fetal and neonatal period. …”

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confidence: 93%

“…The ratio of the left ventricular wall thickness to diastolic diameter ("relative wall thickness") has been found to be decreased in infants born growth restricted compared to their AGA peers, indicating dilation of the ventricle (eccentric hypertrophy) (37,39). Another measure that is used to detect ventricle dilation, the left ventricular end diastolic internal diameter, has been found to be greater in infants born growth restricted than in AGA controls (38,40), although this finding has not been consistently reported (6,41). Dilation of the left atrium has been demonstrated by an increased left atrium/aortic root ratio in comparison to AGA controls (26).…”

Section: Cardiac Morphologymentioning

confidence: 99%

“…They are however more likely to result from increased afterload in relation to high placental resistance, since most growth-restricted fetuses are capable of maintaining their cardiac output (7,48,50) and the majority of studies also report normal postnatal systolic function (10,(36)(37)(38)(39)(40)(41)51). Fractional shortening and ejection fraction, both measurements that give an indication of left ventricular pump function, have been found to be similar in growth-restricted and AGA neonates and infants (10,(36)(37)(38)(39)(40)(41). In most studies, cardiac output of neonates and infants born growth restricted has also been found comparable to controls (36)(37)(38)40,51).…”

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confidence: 99%

“…Dilation of the left atrium has been demonstrated by an increased left atrium/aortic root ratio in comparison to AGA controls (26). Cardiac changes in IUGR are thus most often described as cardiomyopathy-like, with dilated ventricles and a more globular cardiac shape compared to controls (10,26,32,34,(37)(38)(39)(40)42). …”

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confidence: 99%

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Intrauterine growth restriction: impact on cardiovascular development and function throughout infancy

et al. 2016

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Intrauterine growth restriction (IUGR) refers to the situation where a fetus does not grow according to its genetic growth potential. One of the main causes of IUGR is uteroplacental vascular insufficiency. Under these circumstances of chronic oxygen and nutrient deprivation, the growth-restricted fetus often displays typical circulatory changes, which in part represent adaptations to the suboptimal intrauterine environment. These fetal adaptations aim to preserve oxygen and nutrient supply to vital organs such as the brain, the heart, and the adrenals. These prenatal circulatory adaptations are thought to lead to an altered development of the cardiovascular system and "program" the fetus for life long cardiovascular morbidities. In this review, we discuss the alterations to cardiovascular structure, function, and control that have been observed in growth-restricted fetuses, neonates, and infants following uteroplacental vascular insufficiency. We also discuss the current knowledge on early life surveillance and interventions to prevent progression into chronic disease. Intrauterine growth restriction (IUGR) refers to the situation where a fetus does not grow according to its genetic growth potential. The main cause of IUGR in developed countries is uteroplacental vascular insufficiency (1), which drives the fetus to redistribute its cardiac output to preserve oxygen and nutrient supply to the brain, heart, and adrenals. Although these adaptive circulatory changes are beneficial during intrauterine life, they are thought to cause dysfunctional development of the cardiovascular system and "program" the fetus for life long cardiovascular morbidities (2). This is also known as the Developmental Origins of Health and Disease hypothesis, which postulates that insults during intrauterine and early postnatal development can permanently change the body's structure, function, and metabolism and influence susceptibility to adult noncommunicable diseases (2). Despite their increased risk of cardiovascular disease, infants born growth restricted usually do not receive long-term cardiovascular follow-up. Depending on the definition used, IUGR can occur in up to 10% of pregnancies, and as cardiovascular disease is the number one cause of death worldwide (3), early identification of cardiovascular risk factors and targeted interventions in this high-risk population are of major clinical importance. In this review, we discuss the alterations of cardiovascular structure, function, and control that have been observed in infants born growth restricted and their implications for surveillance and intervention to prevent progression into chronic disease. CHALLENGES IN IDENTIFYING IUGRThe current literature uses many different definitions of IUGR, which may explain some of the contradicting findings discussed in this review. Traditionally, and most commonly, IUGR is defined as a birth weight below the 10th percentile for gestational age on the normative population growth curve (4). This definition, however, merely describes those who ...

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confidence: 93%

Section: Cardiac Morphologymentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Intrauterine growth restriction: impact on cardiovascular development and function throughout infancy

et al. 2016

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“…For example, impairment of myocardial systolic and diastolic function accompanies intrauterine and secondary infections, and affects preterm neonates with bronchopulmonary dysplasia (BPD), hypoxia, and intrauterine growth retardation [1][2][3][4][5]. Conventional methods of evaluation of myocardial function have limitations in adults, which become even more problematic in the immature myocardium of the preterm neonate.…”

Section: Introductionmentioning

confidence: 99%

Myocardial performance index (Tei index) in term and preterm neonates during the neonatal period

et al. 2016

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A b s t r a c t Background:The myocardial performance index (MPI) is a noninvasive method to measure global systolic and diastolic myocardial function. In both term and premature neonates, changes in the systolic and diastolic function of the left ventricle (LV) and right ventricle (RV) reflect the degree of neonatal myocardial immaturity and the co-existence of foetal circulation. Aim:To assess MPI (or Tei indices) of both ventricles in term and preterm newborns, and to observe MPI trends throughout the neonatal period. Methods:Heart ultrasound imaging was performed on the first day of life (DOL), after patent ductus arteriosus (PDA) closure, and on the 28 th DOL, in 29 term and 29 preterm newborns. RVMPI and LVMPI were measured within the preterm group at 40 weeks of post-conception age (PCA).Results: A statistically significant reduction in RVMPI was observed in both term and preterm newborns. In term newborns, the RVMPI value on the first DOL was 0.42 ± 14, dropping to 0.29 ± 0.09 after PDA closure, and finally reaching 0.22 ± 0.09 on the 28 th DOL. The respective RVMPI values for the preterm newborns were 0.44 ± 0.15, 0.30 ± 0.12, and 0.21 ± 0.08. Little variability in the mean values of LVMPI was observed in both groups throughout the neonatal period. The LVMPI for term neonates in successive measurements was 0.37 ± 0.10, 0.39 ± 0.07, and 0.37 ± 0.11, respectively, and for the preterm neonates it was 0.37 ± 0.10, 0.35 ± 0.09, and 0.36 ± 0.10, respectively. The MPI values from preterm newborns taken at 40 weeks PCA (RVMPI = 0.28 ± 0.09; LVMPI = 0.37 ± 0.05) were comparable to those measured in term newborns after PDA closure. Conclusions:Observed postnatal changes in RVMPI correspond to changes in ventricular function, reflecting the haemodynamic changes of the transitional circulation. The relatively small postnatal changes in LVMPI in term and preterm newborns may reflect an immature myocardium. The RVMPI and LVMPI values at 40 weeks PCA in preterm newborns correlate best with MPI values in term newborns just after PDA closure.

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Perinatal changes in cardiac geometry and function in growth‐restricted fetuses at term

Patey

Carvalho

Thilaganathan

2019

Ultrasound in Obstet & Gyne

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Compared to normal pregnancy, FGR fetuses and neonates at term exhibit altered cardiac indices indicative of myocardial impairment that reflect adaptation to placental hypoxemia and alterations in hemodynamic load around the time of birth. Elucidating potential mechanisms that contribute to the alterations in perinatal cardiac adaptation in FGR could improve the management and evolve better therapeutic strategies to reduce the risk of adverse pregnancy outcome. This article is protected by copyright. All rights reserved.

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Evaluation of cardiac functions in term small for gestational age newborns with mild growth retardation: A serial conventional and tissue Doppler imaging echocardiographic study

Cited by 42 publications

References 38 publications

Intrauterine growth restriction: impact on cardiovascular development and function throughout infancy

Intrauterine growth restriction: impact on cardiovascular development and function throughout infancy

Myocardial performance index (Tei index) in term and preterm neonates during the neonatal period

Perinatal changes in cardiac geometry and function in growth‐restricted fetuses at term

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