Literature DB >> 23537971

The association of fetal cerebrovascular resistance with early neurodevelopment in single ventricle congenital heart disease.

Ismee A Williams1, Carlen Fifer, Edgar Jaeggi, Jami C Levine, Erik C Michelfelder, Anita L Szwast.   

Abstract

BACKGROUND: Children with congenital heart disease are at risk for impaired neurodevelopment (ND). We investigated the association of fetal cerebrovascular resistance with ND in patients with single ventricle lesions.
METHODS: In the Single Ventricle Reconstruction (SVR) and Infant Single Ventricle trials, 14-month ND was assessed using the Bayley Scales of Infant Development II. We investigated associations between ND scores and fetal middle cerebral artery pulsatility index (MCA-PI) z-scores, a Doppler-derived estimate of cerebrovascular resistance in a subset of those infants.
RESULTS: Neurodevelopment assessments were performed at age 14.3 ± 1 months in 170 (74%) of 230 Infant Single Ventricle and 321 (58%) of 555 SVR subjects. Fetal echocardiographic data were available in 119 subjects, 72 (61%) of which had ND testing. Mean Psychomotor Development Index (PDI) (76 ± 20) and Mental Development Index (MDI) (89 ± 17) scores were lower than normative means (100 ± 15, P < .001). Mean MCA-PI z-score was -0.95 ± 1.52. Middle cerebral artery pulsatility index z-score correlated negatively with PDI (r = -0.27, P = .02) but was not associated with MDI. When MCA-PI z-score was added to a multivariable model controlling for factors identified in the SVR trial to predict PDI, the percentage of explained variation increased from 23% to 30%, and MCA-PI z-score remained an independent predictor (r = -3.864, P = .03). Middle cerebral artery pulsatility index z-score was not an independent predictor in a model adjusting for site.
CONCLUSIONS: Among fetuses with single ventricle anomalies, lower cerebrovascular resistance was associated with higher ND scores. This relationship is opposite to that observed with advanced intrauterine growth retardation and may represent a unique ability of these congenital heart disease fetuses to compensate for diminished cerebral oxygen delivery.
Copyright © 2013 Mosby, Inc. All rights reserved.

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Year:  2013        PMID: 23537971      PMCID: PMC3644301          DOI: 10.1016/j.ahj.2012.11.013

Source DB:  PubMed          Journal:  Am Heart J        ISSN: 0002-8703            Impact factor:   4.749


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