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(Circulation. 2006;113:183-185.)
© 2006 American Heart Association, Inc.

Editorial

Brain Injury in Congenital Heart Disease

Jane W. Newburger, MD, MPH; David C. Bellinger, PhD, MSc

From the Departments of Cardiology (J.W.N.) and Neurology (D.C.B.) at Children’s Hospital Boston and the Departments of Pediatrics (J.W.N.) and Neurology (D.C.B.), Harvard Medical School, Boston, Mass.

Correspondence to Jane W. Newburger, MD, MPH, Department of Cardiology, Children’s Hospital, 300 Longwood Ave, Boston, MA 02115. E-mail jane.newburger@cardio.chboston.org

Key Words: Editorials • cerebral infarction • embolism • heart defects, congenital • stroke

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Mortality rates for virtually all forms of congenital heart disease have declined with dramatic advances in medical, transcatheter, and surgical therapies.¹ As the population of congenital heart disease survivors has burgeoned, however, their long-term functional morbidities have become the focus of increasing concern. Among the foremost morbidities are adverse neurodevelopmental outcomes, with their profound personal and societal costs.²

Article p 280

Neurological and developmental outcomes of congenital heart patients are influenced by many factors, both innate and acquired, with cumulative effects. Genetic syndromes such as trisomy 21 or 22q11 microdeletion^3–5 may affect both the heart and the brain. Cerebral dysgenesis is reported to occur in 10% to 29% of children with congenital heart disease in autopsy series, with the incidence varying by lesion^6–8; findings may range from microdysgenesis to gross abnormalities such as agenesis of the corpus callosum, incomplete operculization, and microcephaly. During fetal life, congenital heart lesions may be associated with changes in cerebrovascular blood flow distribution and resistance. For example, fetuses with hypoplastic left heart syndrome, whose cerebral perfusion is supplied retrograde through the ductus arteriosus, have lower cerebrovascular resistance than normal.⁹

Postnatal neurodevelopmental risk factors may derive from the sequelae of congenital heart disease itself—eg, chronic severe hypoxemia, failure to thrive, arrhythmias with cardiac arrest or hypotension—or from the procedures used for cardiac correction or palliation.¹⁰ Neuropathological studies have revealed both focal and diffuse infarction. Focal infarction has been ascribed to thromboembolic events, whereas a diffuse pattern of cerebral injury has been attributed to hypotension and . . . [Full Text of this Article]

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