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Winfield J. Wells
Ross M. Bremner
Vaughn A. Starnes
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Right arrow Congenital - cyanotic

J Thorac Cardiovasc Surg 2002;124:88-96
© 2002 The American Association for Thoracic Surgery

Surgery for Congenital Heart Disease (CHD)

Homograft conduit failure in infants is not due to somatic outgrowth

Winfield J. Wells, MDa, Hector Arroyo, Jr, MDa, Ross M. Bremner, MDa, John Wood, MDb, Vaughn A. Starnes, MDa

From the Departments of Cardiothoracic Surgerya and Cardiology,b The Heart Institute at Children's Hospital Los Angeles, Keck School of Medicine, University of Southern California, Los Angeles, Calif.

Read at the Eighty-first Annual Meeting of The American Association for Thoracic Surgery, San Diego, Calif, May 6-9, 2001.

Received for publication May 14, 2001; accepted for publication May 18, 2001. Address for reprints: Winfield J. Wells, MD, Associate Professor of Clinical Surgery, The Heart Institute at Children's Hospital Los Angeles, Keck School of Medicine, University of Southern California, Los Angeles, CA 90027 (E-mail: wwells{at}chla.usc.edu).

Objective: It has been assumed that the need for homograft replacement is due to somatic outgrowth, but this has not been adequately studied. Our objective was to identify reasons for homograft conduit failure.
Methods: The records and imaging studies of 40 patients undergoing homograft conduit replacement of the right ventricular outflow tract from 1996 to 2000 were retrospectively reviewed.
Results: The majority of patients had a diagnosis of tetralogy of Fallot (n = 20) and truncus arteriosus (n = 13). The median age at the initial operation was 8 months (0.25-108 months). The initial homograft sizes ranged from 9 to 22 mm, and 28 conduits were of pulmonary origin. When comparing size of the initial homograft with patients' expected pulmonary valve diameter (z = 0), oversizing was noted to be +3 (range, 0.83-5.4). Median interval to conduit failure was 5.3 years (0.83-11.3 years). At homograft replacement, only 12 patients had an existing conduit that was 1 SD below the homograft conduit size needed (z <= -1). Most conduits had important regurgitation, but this was rarely a primary reason for reintervention (n = 1). Reoperation was usually required for stenosis, with a median gradient of 53 mm Hg (20-140 mm Hg). Stenosis was further categorized angiographically as follows: homograft valvular stenosis (shrinkage; 21/40 [53%]), distal anastomotic stenosis (4/40 [10%]), conduit kinking (3/40 [8%]), sternal compression (3/40 [8%]), posterior shelf impingement (2/40 [5%]), and somatic outgrowth (3/40 [8%]). Replacement in 2 patients was for proximal hood aneurysm. Several patients (7/40 [18%]) had stenosis at multiple levels. The average decrease in conduit diameter was 47% (28%-73%).
Conclusions: Somatic outgrowth is seldom a primary reason for homograft conduit replacement of the right ventricular outflow tract. The most common cause for failure is conduit obstruction with thickening and shrinkage at the annular area. Conduit stenosis was responsible for failure in 53% of patients, technical issues were responsible for 30%, and only 8% failed as a result of somatic outgrowth. Placement of a smaller homograft (z = 0) at the initial operation may decrease the incidence of conduit kinking, sternal compression, and posterior shelf impingement.




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