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J Thorac Cardiovasc Surg 2003;126:1736-1745
© 2003 The American Association for Thoracic Surgery
Surgery for congenital heart disease |
a Division of Cardiothoracic Surgery, The Children's Hospital of Philadelphia, Philadelphia, Pa, USA
b Division of Psychology, The Children's Hospital of Philadelphia, Philadelphia, Pa, USA
c Division of Genetics, The Children's Hospital of Philadelphia, Philadelphia, Pa, USA
d Division of General Pediatrics, The Children's Hospital of Philadelphia, Philadelphia, Pa, USA
e Division of Cardiology, The Children's Hospital of Philadelphia, Philadelphia, Pa, USA
f Division of Neurology, The Children's Hospital of Philadelphia, Philadelphia, Pa, USA
g Department of Anesthesiology, Duke University Medical Center, Durham, NC, USA
h Division of Neurology, Duke University Medical Center, Durham, NC, USA
i Department of Biostatistics, University of Washington, Seattle, Wash, USA
j Division of Cardiothoracic Anesthesia, The Children's Hospital of Philadelphia, Philadelphia, Pa, USA
k Department of Medicine (Medical Genetics), University of Washington, Seattle, Wash, USA
Received for publication November 25, 2002; revisions received March 7, 2003; accepted for publication April 11, 2003.
* Address for reprints: J. William Gaynor, MD, Division of Cardiothoracic Surgery, The Children's Hospital of Philadelphia, 34th and Civic Center Blvd, Ste 8527, Philadelphia, PA, USA 19104
gaynor{at}email.chop.edu
BACKGROUND: There has been increasing recognition of adverse neurodevelopmental sequelae in some children after repair of congenital heart defects. Even among children with the same cardiac defect, significant interindividual variation exists in developmental outcome. Polymorphisms of apolipoprotein E have been identified as a risk factor for worse neurologic recovery after central nervous system injury.
METHODS: A single-institution prospective study of patients 
6 months of age undergoing cardiopulmonary bypass for repair of congenital heart defects was undertaken to evaluate the association between apolipoprotein E genotype and postoperative neurodevelopmental dysfunction. Developmental outcomes were evaluated at 1 year of age by using the Bayley Scales of Infant Development.
RESULTS: One-year evaluation was performed in 244 patients. After adjustment for preoperative and postoperative covariates—including gestational age, age at operation, sex, race, socioeconomic status, cardiac defect, and use of deep hypothermic circulatory arrest—the apolipoprotein E 
2 allele was associated with a worse neurologic outcome as assessed by the Psychomotor Developmental Index of the Bayley Scales of Infant Development (P = .036). Patients with the apolipoprotein E 2 allele had approximately a 7-point decrease in the Psychomotor Developmental Index.
CONCLUSIONS: Apolipoprotein E 2 allele carriers had significantly lower Psychomotor Development Index scores at 1 year of age after infant cardiac surgery. The effect was independent of ethnicity, socioeconomic status, cardiac defect, and use of deep hypothermic circulatory arrest. An effect of the apolipoprotein E 4 allele was not detected. Genetic polymorphisms that decrease neuroresiliency and impair neuronal repair after central nervous system injury are important risk factors for neurodevelopmental dysfunction after infant cardiac surgery.
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