title: Role of lung biopsy in patients undergoing a modified Fontan procedure.
abstract: Fifty-six patients undergoing a modified Fontan procedure from 1977 to 1985 had lung tissue available from the perioperative period (n = 51) or recent palliative procedure (n = 5) (37 biopsy, 12 autopsy, 7 biopsy and autopsy). Twenty-six patients had tricuspid atresia, and 30 had other causes of functional univentricular heart. Pulmonary arterial structure was classified by both the Heath-Edwards and morphometric scales. Biopsy and autopsy grades were identical except for a minor difference in Heath-Edwards scale in one case. Elevated preoperative mean pulmonary artery pressure (greater than 15 mm Hg) was associated with medial hypertrophy (p = 0.04), although six patients with normal pulmonary artery pressure had medial hypertrophy and six patients with mean pulmonary artery pressure greater than 15 mm Hg did not have medial hypertrophy. Medial hypertrophy was a possible risk factor in patients with univentricular heart: Patients with medial hypertrophy had a ninefold greater risk of death (p = 0.08). Controlling for confounding variables did not alter this result (0.06 less than or equal to p less than or equal to 0.10). Medial hypertrophy was not a risk factor for death in patients with tricuspid atresia: Four had this feature and each survived. Four patients with tricuspid atresia died and none had medial hypertrophy. A mean transpulmonary pressure gradient was measured on the first postoperative day in 45 patients. In patients with medial hypertrophy there was a trend toward a higher gradient (p = 0.13). All patients with medial hypertrophy who had this measurement (n = 9) had a transpulmonary pressure gradient of 7 mm Hg or greater, whereas this was true in only 18 of 36 without medial hypertrophy (p = 0.007). On the basis of an evaluation of medial hypertrophy, we conclude that biopsy does not aid in selection of patients with tricuspid atresia for a Fontan procedure; its role in patients with univentricular heart is uncertain.
authors.affiliation: Department of Pathology, Children's Hospital Center, Boston, Mass.
authors.forename: R L
authors.initials: RL
authors.lastname: Geggel
authors.forename: J E
authors.initials: JE
authors.lastname: Mayer
authors.forename: R
authors.initials: R
authors.lastname: Fried
authors.forename: H
authors.initials: H
authors.lastname: Helgason
authors.forename: E F
authors.initials: EF
authors.lastname: Cook
authors.forename: L M
authors.initials: LM
authors.lastname: Reid
mesh_terms: D000293:Adolescent; D000328:Adult; D001158:Arteries / Q000473:pathology; D001706:Biopsy; D001794:Blood Pressure; D002648:Child; D002675:Child, Preschool; D004108:Dilatation, Pathologic / Q000473:pathology; D005500:Follow-Up Studies; D006330:Heart Defects, Congenital / Q000601:surgery*; D006801:Humans; D006984:Hypertrophy; D007223:Infant; D008168:Lung / Q000098:blood supply* / Q000473:pathology; D011651:Pulmonary Artery / Q000503:physiopathology; D012189:Retrospective Studies; D014261:Tricuspid Valve / Q000002:abnormalities* / Q000601:surgery; D014655:Vascular Resistance