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Impact of congenital heart disease on cerebrovascular blood flow dynamics in the fetus
Author(s) -
Kaltman J. R.,
Di H.,
Tian Z.,
Rychik J.
Publication year - 2005
Publication title -
ultrasound in obstetrics and gynecology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.202
H-Index - 141
eISSN - 1469-0705
pISSN - 0960-7692
DOI - 10.1002/uog.1785
Subject(s) - medicine , fetus , cardiology , heart disease , cerebral blood flow , blood flow , pregnancy , genetics , biology
Objectives Neurological abnormalities are present in some children after repair of congenital heart disease (CHD). Recently, structural brain abnormalities have been identified in infants prior to cardiac surgery. By altering in utero blood flow patterns, the type of CHD may impact upon cerebrovascular flow dynamics prior to birth. We sought to determine whether left‐ and right‐sided obstructive congenital heart lesions modify cerebrovascular flow dynamics in the fetus. Methods Pulsed Doppler was used to measure blood flow velocities in the umbilical (UA) and middle cerebral (MCA) arteries in 172 fetuses from 20 to 39 weeks' gestational age referred for fetal echocardiography. Pulsatility index (PI), an indicator of downstream vascular resistance, was determined by (peak systolic velocity—end‐diastolic velocity)/mean velocity. Results Fetuses with hypoplastic left heart syndrome (HLHS; n = 28) had decreased MCA‐PI ( P = 0.009) compared to normal fetuses ( n = 114). Fetuses with right‐sided obstructive lesions (RSOL; n = 17) had increased MCA‐PI ( P = 0.001) when compared to fetuses with HLHS. The UA‐PI was elevated in fetuses with RSOLs ( P = 0.045). Conclusions Cerebrovascular resistance is lower than normal in fetuses with HLHS, a condition in which cerebral perfusion occurs retrograde via the ductus arteriosus. Fetuses with RSOL had significantly higher cerebrovascular resistance compared to fetuses with HLHS. The type of CHD impacts upon fetal cerebrovascular blood flow distribution and this may have implications for later development of neurological sequelae. Copyright © 2004 ISUOG. Published by John Wiley & Sons, Ltd.

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