Natriuretic peptides in the pathogenesis of cardiac dysfunction in the recipient fetus of twin-twin transfusion syndrome
Objective: Although serial amnioreduction has substantially improved the prognosis of twin-twin transfusion syndrome, the majority of recipient twins develop cardiac dysfunction in utero and some have structural abnormalities in the neonatal period. The mechanism of cardiac dysfunction is unclear. T...
Gespeichert in:
Veröffentlicht in: | American journal of obstetrics and gynecology 2002-01, Vol.186 (1), p.121-127 |
---|---|
Hauptverfasser: | , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | Objective: Although serial amnioreduction has substantially improved the prognosis of twin-twin transfusion syndrome, the majority of recipient twins develop cardiac dysfunction in utero and some have structural abnormalities in the neonatal period. The mechanism of cardiac dysfunction is unclear. To test the hypothesis that this occurs as a result of preload or pressure overload, we determined atrial natriuretic peptide and brain natriuretic peptide levels and their association with endothelin-1 in monochorionic pregnancies with or without chronic twin-twin transfusion syndrome. Patients And Methods: Matched maternal and fetal blood samples were obtained in utero from monochorial twin pregnancies complicated with (n = 14) and without twin-twin transfusion syndrome (n = 6). Serial fetal echocardiography assessment included cardiac anatomy, chamber size, cardiothoracic ratio, ventricular thickness, and the presence and severity of atrioventricular valve regurgitation. Postnatal echocardiograms were obtained on the surviving twins. The plasma levels of atrial natriuretic peptide, brain natriuretic peptide, and endothelin-1 were measured by use of radio-immunoassay. Results: Levels of fetal atrial natriuretic peptide (P |
---|---|
ISSN: | 0002-9378 1097-6868 |
DOI: | 10.1067/mob.2002.118845 |