Cardiac changes in fetuses secondary to immune hemolytic anemia and their relation to hemoglobin and catecholamine concentrations in fetal blood

Citation
R. Oberhoffer et al., Cardiac changes in fetuses secondary to immune hemolytic anemia and their relation to hemoglobin and catecholamine concentrations in fetal blood, ULTRASOUN O, 13(6), 1999, pp. 396-400
Citations number
21
Categorie Soggetti
Reproductive Medicine
Journal title
ULTRASOUND IN OBSTETRICS & GYNECOLOGY
ISSN journal
09607692 → ACNP
Volume
13
Issue
6
Year of publication
1999
Pages
396 - 400
Database
ISI
SICI code
0960-7692(199906)13:6<396:CCIFST>2.0.ZU;2-R
Abstract
Objectives Immune hemolytic anemia in the fetus may cause cardiac decompens ation and intrauterine death. Postnatally, norepinephrine (noradrenaline) i s released in chronic heart failure and may lead to myocardial hypertrophy The aim of this study was to determine fetal cardiac changes associated wit h immune hemolytic anemia by means of echocardiography, and to relate them to fetal hemoglobin and norepinephrine levels. Design Thirty anemic fetuses underwent a total of 76 umbilical venous trans fusions. Before the procedure, fetal echocardiography was performed, Lend e nd-diastolic myocardial wall thicknesses and ventricular dimensions togethe r with Doppler flow patterns at the atrioventricular and semilunar valves w ere measured Fetal hemoglobin, epinephrine and norepinephrine concentration s were determined before the transfusion. Statistical analysis of this pros pective study comprised descriptive statistics including linear regression and correlation analyses. Two samples of measurements were compared by the Mann-Whitney U test. Results The mean hemoglobin concentration before the first transfusion was 6.9 g% at a mean gestational age of 26.8 weeks. Norepinephrine values were elevated in comparison to a reference range, and were higher than epinephri ne values. The most striking echocardiographic finding was myocardial hyper trophy of all ventricular walls. Mean blood flow velocities were increased; at the left ventricle, they were negatively related to the hemoglobin conc entrations, and positively to the norepinephrine values. Conclusions Fecal myocardial hypertrophy in anemia may be the result of an augmented cardiac workload, indicated by the increased left ventricular mea n velocities. This reaction reflects the redistribution of blood flow that may depend on hemoglobin and norepinephrine concentrations.