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J Thorac Cardiovasc Surg 1999;117:931-938
© 1999 Mosby, Inc.

SURGERY FOR CONGENITAL HEART DISEASE

A DETAILED HISTOLOGIC ANALYSIS OF PULMONARY ARTERIOVENOUS MALFORMATIONS IN CHILDREN WITH CYANOTIC CONGENITAL HEART DISEASE

From the Divisions of Cardiac Surgery^a and Cardiology,^e Children's Hospital and Regional Medical Center, Seattle; the Departments of Pathology^b and Surgery,^d University of Washington, Seattle, Wash; and the Department of Cardiovascular Surgery,^c The Children's Hospital, Bratislava, Slovakia.

Received for publication Aug 17, 1998. Revisions requested Oct 30, 1998. Revisions received Dec 29, 1998. Accepted for publication Jan 13, 1999. Address for reprints: Brian W. Duncan, MD, Division of Cardiac Surgery, Children's Hospital and Regional Medical Center, 4800 Sand Point Way, NE, PO Box 5371/CM-03, Seattle, WA 98105.

Introduction: Pulmonary arteriovenous malformations are a common cause of progressive cyanosis in children after cavopulmonary anastomoses. We analyzed the pulmonary histologic characteristics from children in whom pulmonary arteriovenous malformations developed after procedures that resulted in pulmonary arterial blood flow devoid of hepatic venous effluent.
Methods: We performed routine histologic studies, immunohistochemical staining, and electron microscopic analysis of peripheral lung biopsy specimens from 2 children with angiographically proven pulmonary arteriovenous malformations. Microvessel density was determined with a computer-assisted, morphometric analysis system.
Results: Histologic examination demonstrated large, dilated blood vessels (“lakes”) and clustered, smaller vessels (“chains”) in the pulmonary parenchyma. Microvessel density was significantly greater in these patients than in age-matched controls (P = .01). Immunohistochemistry demonstrated uniform staining for type IV collagen and -smooth muscle actin, weak staining for the endothelial marker CD31 (cluster of differentiation, PECAM-1), and negative staining for proliferating cell nuclear antigen. Electron microscopy revealed endothelial irregularity, a disorganized basement membrane, and increased numbers of collagen and actin filaments beneath the endothelium.
Conclusions: This study represents an attempt to characterize the histologic features of pulmonary arteriovenous malformations in children with congenital heart disease who have pulmonary arterial blood flow devoid of hepatic venous effluent. The histologic correlate of this condition appears to be greatly increased numbers of thin-walled vessels. Immunohistochemistry suggests that the rate of cellular proliferation is not increased in these lesions. The development of these techniques may provide a standardized histologic approach for this condition and aid in understanding its etiology.

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