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J Thorac Cardiovasc Surg 2006;132:1426-1432
© 2006 The American Association for Thoracic Surgery

Surgery for Acquired Cardiovascular Disease

Degeneration of the pulmonary autograft: An explant study

^a Department of Cardiothoracic Surgery, University Medical Center Leiden, Leiden, the Netherlands
^b Department of Cardiothoracic Surgery, Erasmus Medical Center, Rotterdam, the Netherlands
^c Department of Pathology, Erasmus Medical Center, Rotterdam, the Netherlands
^d Department of Pathology, University Hospital Maastricht, Maastricht, The Netherlands.

Received for publication April 6, 2006; revisions received June 26, 2006; accepted for publication July 12, 2006.

^_* Address for reprints: Paul H. Schoof, MD, PhD, Department of Cardiothoracic Surgery, D6-50, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, the Netherlands. (Email: P.H.Schoof{at}lumc.nl).

OBJECTIVE: We sought to determine the histologic features of pulmonary autografts explanted after the Ross operation.

METHODS: Histologic sections of 30 explanted autografts and 8 normal heart valves were compared and semiquantitatively scored by a blinded cardiovascular pathologist.

RESULTS: Pulmonary autografts (n = 30) were explanted on average 6.1 ± 0.6 years (median, 6.6 years; range, 0.1-11.7 years) after the Ross operation (n = 28) or removed at autopsy (n = 2). Twelve (43%) of the patients undergoing reoperation had no or negligible autograft insufficiency on early transthoracic echocardiography, 12 (43%) had grade 1 autograft insufficiency, and 4 (14%) had grade 1-2 autograft insufficiency. Valve regurgitation with root dilatation was the most common indication for reoperation after root replacement (n = 26 [93%]) and regurgitation after subcoronary implanted autografts (n = 2 [7%]). Microscopy of the autograft explants revealed normal laminar architecture and cellularity. Wall specimens were characterized by reduced and fragmented elastin and increased collagen levels (fibrosis). Medial elastin changes were associated with the presence of hypertrophic smooth muscle cells. Fibrosis was most severe in the adventitia. Intimal thickening was a common finding. Valve explants showed significant thickening caused by fibrocellular tissue on the ventricular surface and marked thickening of the free margin. An autopsy explant with normal function before death showed similar features.

CONCLUSIONS: Pulmonary autograft explants showed severe aneurysmal degeneration of the wall, which was characterized by intimal thickening, medial elastin fragmentation, and adventitial fibrosis. Valve leaflets were thickened. The presence of these features in a nonfailing explant suggests these changes represent a common mode of remodeling.