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J Thorac Cardiovasc Surg 2001;122:518-523
© 2001 The American Association for Thoracic Surgery

Surgery for Congenital Heart Disease (CHD)

Angiogenic proteins in the lungs of children after cavopulmonary anastomosis

From The Division of Cardiac Surgery,^a Children's Hospital and Regional Medical Center and the Department of Surgery, the University of Washington School of Medicine, the Division of Cardiology,^b Children's Hospital and Regional Medical Center and the Department of Pediatrics, the University of Washington School of Medicine, and the Department of Pathology,^c Children's Hospital and Regional Medical Center, Seattle, Wash.

This work was supported by a grant from the Howard Hughes Medical Institute.

Received for publication Sept 12, 2000. Revisions requested Dec 15, 2000; revisions received Feb 15, 2001. Accepted for publication Feb 28, 2001. Address for reprints: Brian W. Duncan, MD, Cleveland Clinic Children's Hospital, Division of Pediatric and Congenital Heart Surgery, 9500 Euclid Ave/M-41, Cleveland, OH 44195 (E-mail: duncanb{at}cff.org)

Abstract

Objective: Pulmonary arteriovenous malformations may cause progressive cyanosis after cavopulmonary anastomosis and may develop as a result of abnormal angiogenesis. We used immunohistochemistry to determine whether angiogenic proteins are increased in the lungs of children after cavopulmonary anastomosis.
Methods: Lung specimens were obtained from 13 children after cavopulmonary anastomosis and from 6 control subjects. Specimens were stained with antibodies against vascular endothelial growth factor and its receptor (flk-1/KDR), basic fibroblast growth factor, -smooth muscle actin, CD31, collagen IV, fibronectin, and proliferating cell nuclear antigen. Staining was graded on a scale of 0 to 3. Vessels positive for proliferating cell nuclear antigen were counted in 10 fields per specimen, and the results were averaged.
Results: After cavopulmonary anastomosis, patients demonstrated increased staining for vascular endothelial growth factor (P = .03) and its receptor (P = .03) and decreased staining for CD31 (P = .004). Proliferating cell nuclear antigen staining in patients was equivalent to that for control subjects (P = .9).
Conclusions: Lung biopsy specimens from children after cavopulmonary anastomosis demonstrate increased expression of vascular endothelial growth factor and its receptor. These data confirm earlier findings that blood vessels forming after cavopulmonary anastomosis may have reduced intercellular junctions (decreased CD31 staining). Despite the increased numbers of pulmonary vessels that are present in these patients, these vessels are not highly proliferative (proliferating cell nuclear antigen staining equivalent to that of control subjects). These results suggest that vascular endothelial growth factor may be a mediator of angiogenesis in the lungs of children after cavopulmonary anastomosis; however, other factors, such as vascular dilation and remodeling, may also be important.

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