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  • Title: Evidence of second-trimester changes in head biometry and brain perfusion in fetuses with congenital heart disease.
    Author: Masoller N, Martínez JM, Gómez O, Bennasar M, Crispi F, Sanz-Cortés M, Egaña-Ugrinovic G, Bartrons J, Puerto B, Gratacós E.
    Journal: Ultrasound Obstet Gynecol; 2014 Aug; 44(2):182-7. PubMed ID: 24687311.
    Abstract:
    OBJECTIVES: To evaluate the associations between congenital heart disease (CHD) and head biometry and cerebrovascular blood flow dynamics at the time of diagnosis of CHD in the second trimester of pregnancy. METHODS: This was a study of 95 consecutive fetuses diagnosed with CHD. At the time of diagnosis, fetal biometry was performed and brain perfusion was assessed by middle cerebral artery pulsatility index (MCA-PI), cerebroplacental ratio (CPR) and fractional moving blood volume (FMBV). The results were compared with those of 95 normal fetuses matched for gestational age. RESULTS: Median gestational age at diagnosis was 22 + 3 (range, 20 + 0 to 23 + 5) weeks. Fetuses with CHD showed significantly lower MCA-PI and CPR Z-scores (-0.23 vs 0.34 and -0.37 vs 0.30, respectively; both P < 0.001) and higher FMBV Z-scores (2.35 vs 0.15; P < 0.001). FMBV > 95(th) percentile was observed in 81.1% of cases as compared with 10.5% in controls (P < 0.001). Moreover, cases showed significantly smaller biparietal diameter (BPD) and head circumference (HC) Z-scores (-1.61 vs -0.43 and -0.89 vs 0.09, respectively; both P < 0.001), with a higher proportion of BPD and HC measurements below the 5(th) percentile compared with controls (51.6% vs 13.7% and 26.3% vs 4.2%, respectively; both P < 0.001). These findings were more pronounced in those cases with types of CHD associated with compromised oxygenated blood delivery to the brain, such as left outflow tract obstruction and transposition of the great arteries. CONCLUSIONS: A high proportion of fetuses with CHD have a smaller head and increased brain perfusion already in the second trimester, suggesting an early onset of the mechanisms leading to poorer neurodevelopment later in life.
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