Right ventricular dysfunction in human fetal compromise

Räsänen, Juha; Kirkinen, Pertti; Jouppila, P.

doi:10.1016/0002-9378(89)90250-0

Cited by 16 publications

(3 citation statements)

References 18 publications

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“…Cordocentesis performed in fetuses with absent or reversed end‐diastolic UA flow15 and ADVW3, 16 showed a higher rate of hypoxia and acidemia correlating with poor perinatal and neonatal outcomes5, 17. A number of clinical18 and experimental19 studies have shown an earlier and greater right‐to‐left cardiac output impairment in growth‐restricted fetuses. Weiner et al 20 serially evaluated fetuses with absent end‐diastolic umbilical flow and found that NST remained normal until the MCA lost its vasodilatation, that is primarily related to left heart failure.…”

Section: Discussionmentioning

confidence: 99%

Contraction stress test versus ductus venosus Doppler evaluation for the prediction of adverse perinatal outcome in growth‐restricted fetuses with non‐reassuring non‐stress test

Figueras

Martínez

Puerto

et al. 2003

Ultrasound in Obstet & Gyne

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Section: Discussionmentioning

confidence: 99%

Contraction stress test versus ductus venosus Doppler evaluation for the prediction of adverse perinatal outcome in growth‐restricted fetuses with non‐reassuring non‐stress test

Figueras

Martínez

Puerto

et al. 2003

Ultrasound in Obstet & Gyne

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“…22 It has also been shown that in human fetuses with increased vascular impedance in the descending aorta, RVFS is decreased with no change in the left ventricle. 23 An abnormal fractional shortening could reflect myocardial compromise or an increase in the fetal ventricular workload. In this study, other parameters describing fetal cardiac systolic and diastolic functions did not differ between the groups, suggesting that decreased RVFS reflected increased afterload in these fetuses.…”

Section: Discussionmentioning

confidence: 99%

Ultrasonographic and Biochemical Markers of Human Fetal Cardiac Dysfunction in Placental Insufficiency

et al. 2002

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Background-Placental insufficiency may lead to fetal cardiovascular compromise. We sought to determine whether ultrasonographic parameters of fetal cardiovascular function correlate with umbilical arterial levels of biochemical markers of myocardial dysfunction and damage in placental insufficiency. Methods and Results-In 48 fetuses with placental insufficiency, umbilical artery blood was obtained at delivery for assessment of N-terminal peptide of proatrial natriuretic peptide (NT-proANP) and cardiac troponin-T (cTnT). Group 1 fetuses (nϭ12) had normal NT-proANP and cTnT serum concentrations. Group 2 fetuses (nϭ25) showed increased NT-proANP (Ͼ1145 pmol/L) and normal cTnT values. Group 3 fetuses (nϭ11) had increased NT-proANP and cTnT (Ͼ0.10 ng/mL) levels. The ultrasonographic parameters of fetal cardiovascular function were compared between the groups. Pulsatility indices for veins of the ductus venosus, left hepatic vein, and inferior vena cava correlated significantly with NT-proANP levels. In group 3, ductus venosus, left hepatic vein, and inferior vena cava pulsatility indices for veins were higher (PϽ0.01) than in groups 1 and 2. The proportion of left ventricular cardiac output of combined cardiac output was greater (PϽ0.05) and that of right ventricle was smaller (PϽ0.05) in group 3 than in group 2. In group 3, tricuspid regurgitation was noted most often (PϽ0.05), and right ventricular fractional shortening was less (PϽ0.01) than in group 2. Conclusions-Pulsatility in human fetal systemic veins correlated significantly with the cardiac secretion of ANP. Fetuses with myocardial damage demonstrate increased systemic venous pressure, a change in the distribution of cardiac output toward the left ventricle, and a rise in right ventricular afterload.

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“…Intrauterine growth retardation is associated with increased neonatal mortality, perinatal complications and long-term neurologic sequelae in preterm infants (1), as well as compromised cardiovascular adaptive capacity already in utero (2)(3)(4). However, few data have been reported regarding early circulatory adaptation after intrauterine growth retardation.…”

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confidence: 99%

Cardiac Hypertrophy and Altered Hemodynamic Adaptation in Growth-Restricted Preterm Infants

et al. 2003

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The objective was to elucidate hemodynamic adaptation in very low birth weight (Ͻ1500 g) infants after intrauterine growth retardation. 31 growth-retarded (SGA, birth weight Ͻ-2 SD) and 32 appropriate for gestational age (AGA, birth weight within Ϯ 1 SD range) infants were enrolled. In SGA infants, the diastolic diameters of the interventricular septum and the left ventricle were increased, and serum brain natriuretic peptide (BNP) was elevated. Left ventricular output (LVO) of the AGA infants increased from 150 Ϯ 28 to 283 Ϯ 82 mL/kg/min during the study (p Ͻ 0.01). The SGA infants had a higher initial LVO than the AGA infants (243 Ϯ 47 versus 150 Ϯ 28 mL/kg/min, p Ͻ 0.05), but did not show further LVO increase during the study period. Red cell (RCV) and blood (BV) volume were assessed by Hb subtype analysis, when packed donor red cells were transfused. RCV and BV did not differ between the groups initially, but RCV increased by 18% and BV by 29% in the AGA group during the first 3 d. On day 3, AGA infants had larger BV than the SGA infants (88 Ϯ 5 versus 73 Ϯ 12 mL/kg, p Ͻ 0.05). In conclusion, cardiac hypertrophy, elevated initial LVO and BNP of the SGA infants suggest increased cardiac workload after intrauterine growth retardation. Based on the BV and RCV data, blood volume regulation may also be impaired. The data suggest that SGA preterm infants may be exposed to an increased risk of circulatory failure during early adaptation. Intrauterine growth retardation is associated with increased neonatal mortality, perinatal complications and long-term neurologic sequelae in preterm infants (1), as well as compromised cardiovascular adaptive capacity already in utero (2-4). However, few data have been reported regarding early circulatory adaptation after intrauterine growth retardation. In addition to myocardial performance, adequate intravascular volume is essential for successful postnatal cardiovascular adaptation. Largely due to the lack of applicable methodology, present knowledge on intravascular volume of preterm infants in general is scarce, and the effect of growth retardation on circulating volume has not been studied.The aim of the present study was to test the hypothesis that fetal growth retardation alters the pattern of early hemodynamic adaptation of very low birth weight infants. During the first two weeks of life, left ventricular function and dimensions were assessed by echocardiography in SGA infants and AGA control infants. A circulating indicator of ventricular dysfunction, BNP, was also measured. RCV and BV were determined by a method based on dilution of autologous HbF by donor HbA when red cells were transfused based on clinical judgment. Hemodynamic evaluation was also performed by using indirect indices applied in routine clinical work. METHODS Patients.All infants in the study were born in the maternal unit of the Helsinki University Hospital and treated in the

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Right ventricular dysfunction in human fetal compromise

Cited by 16 publications

References 18 publications

Contraction stress test versus ductus venosus Doppler evaluation for the prediction of adverse perinatal outcome in growth‐restricted fetuses with non‐reassuring non‐stress test

Contraction stress test versus ductus venosus Doppler evaluation for the prediction of adverse perinatal outcome in growth‐restricted fetuses with non‐reassuring non‐stress test

Ultrasonographic and Biochemical Markers of Human Fetal Cardiac Dysfunction in Placental Insufficiency

Cardiac Hypertrophy and Altered Hemodynamic Adaptation in Growth-Restricted Preterm Infants

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