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J Thorac Cardiovasc Surg 2003;126:1053-1060
© 2003 The American Association for Thoracic Surgery


Surgery for congenital heart disease

Pulmonary artery remodeling in transposition of the great arteries: relevance for neoaortic root dilatation

Shirin Lalezari, MDa,b, Mark G. Hazekamp, MD, PhDb, Margot M. Bartelings, MD, PhDa, Paul H. Schoof, MD, PhDb, Adriana C. Gittenberger-de Groot, PhDa,*

a Department of Anatomy and Embryology, Leiden University Medical Center,, Leiden, The Netherlands
b Department of Cardiothoracic Surgery, Leiden University Medical Center, Leiden, The Netherlands

Received for publication September 11, 2002; revisions received January 6, 2003; revisions received March 18, 2003; accepted for publication April 11, 2003.

* Address for reprints: A. C. Gittenberger-de Groot, PhD, Department of Anatomy and Embryology, Leiden University Medical Center, Wassenaarseweg 62, PO Box 9602, 2300 AC Leiden, The Netherlands
ACGitten{at}lumc.nl

OBJECTIVE: Transposition of the great arteries is currently treated by performing the arterial switch operation. Dilatation of the neoaortic root is a late complication with unknown cause. Samples of patients with untreated transposition of the great arteries and patients with normally related great arteries were compared to investigate a possible role for vascular remodeling in the dilatation process.

METHODS: Aortic and pulmonary artery vessel wall and sinus samples were taken from 20 untreated human heart specimens with transposition of the great arteries and 9 age-matched, normal, postmortem human heart specimens, divided into 2 groups according to age. Routine histology and immunohistochemical staining for smooth muscle cell differentiation markers {alpha}-smooth muscle actin, SM22, and calponin were performed.

RESULTS: This study revealed structural differences between the normal aorta and pulmonary artery in the early group, which became more pronounced in the late group. In the early stage in transposition of the great arteries, no marked differences were seen between the aorta and pulmonary artery. With increasing age, however, there was a pronounced down-regulation of all smooth muscle cell markers in the pulmonary artery.

CONCLUSIONS: There is a structural difference between the normal neonatal aorta and pulmonary artery. The great arteries in transposition of the great arteries differ from each other and from normal vessels, indicating a structural vascular difference in transposition of the great arteries. In the pulmonary artery and sinus of untreated transposition of the great arteries, there is a dedifferentiation of smooth muscle cells with increasing age that we could not correlate to altered flow. This structural abnormality might provide an explanation for the neoaortic root dilatation that has been reported as a late complication of the arterial switch operation.





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