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Ann Thorac Surg 1996;61:234-237
© 1996 The Society of Thoracic Surgeons

Case Report

Early Pulmonary Homograft Failure From Dilatation Due to Distal Pulmonary Artery Stenosis

Serafin Y. DeLeon, MD, J. Michael Tuchek, MD, Timothy J. Bell, MD, Joanne Hofstra, MS, Dolores A. Vitullo, MD, Jose A. Quinones, MD, Elizabeth A. Fisher, MD

Departments of Thoracic and Cardiovascular Surgery and Pediatrics, Loyola University Medical Center, Maywood, Illinois

Accepted for publication July 10, 1995.


   Abstract
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 Abstract
Introduction
 Comment
 References
 
Early progressive pulmonary homograft insufficiency developed in an 11-month-old infant after repair of truncus arteriosus because of dilatation secondary to the presence of residual distal pulmonary artery stenosis and hypoplasia. Before repair, the pulmonary artery branches were discontinuous, with the right pulmonary artery being somewhat hypoplastic and originating from the trunk, and the left pulmonary artery supplied by a modified Blalock-Taussig shunt created in the newborn period. At repair, a pulmonary homograft was used to connect the branches. Progressive cardiomegaly and oxygen dependance occurred 3 weeks postoperatively. Cardiac catheterization showed systemic right ventricular pressure, severe homograft insufficiency, and residual distal pulmonary artery stenosis and hypoplasia. On reoperation at 3 months postoperatively, the homograft annulus diameter increased from 14 mm to 16 mm. Dilatation and insufficiency probably occurred because the right ventricle and homograft distal to the obstruction functioned as a unit during systole. The problem might have been minimized with the use of aortic homograft, which is thicker, or annular reinforcement with a synthetic material.


   Introduction
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 Abstract
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Comment
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See also page 236.

Homografts are preferred for reconstruction of the right ventricular outflow tract [1, 2]. They are especially useful in infants and young children because of better hemostasis, easier handling, and moldability within the chest cavity, minimizing compression of coronary arteries in contrast to the less-forgiving porcine valve conduits.

Homografts, like any biologic valve prosthesis, will eventually degenerate and calcify. Accelerated degeneration has been reported and attributed to possible immunologic rejection [3]. Although mild incompetence is commonly present in the early months postoperatively, severe incompetence in the absence of degeneration is exceedingly rare [4].

We report an 11-month-old infant who had a total repair of truncus arteriosus and in whom early severe pulmonary homograft valve incompetence developed because of dilatation due to presence of distal pulmonary artery stenosis.

As a newborn, the patient had a modified Blalock-Taussig shunt to the left pulmonary artery that was supplied by a patent ductus arteriosus. The right pulmonary artery had stenosis at its origin from the left side of the truncus arteriosus.

Cardiac catheterization before total repair showed a well-functioning Blalock-Taussig shunt and somewhat hypoplastic right pulmonary artery (Fig 1Go) with a mean pressure of 11 mm Hg. At operation a 14-mm pulmonary homograft was implanted uneventfully using the branches to connect the discontinuous pulmonary artery branches. The homograft had intact adventitia and epicardium. Because of systemic right ventricular pressure, high central venous pressure (21 to 22 mm Hg), and impaired cardiac output after weaning from cardiopulmonary bypass, a 1-cm atrial fenestration was created, after which the cardiac output improved.



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  		Fig 1. . Preoperative angiograms showing a somewhat hypoplastic right pulmonary artery with stenosis at its origin from the truncus arteriosus. The left pulmonary artery is supplied by the Blalock-Taussig shunt.

 
The oxygen saturation initially ranged from 68% to 78% but gradually improved to 95% by the fifth postoperative day. The central venous pressure gradually decreased to 9 to 12 mm Hg by the fifth postoperative day. However, although oxygen administration was finally stopped on the 15th postoperative day, it had to be restarted because of arterial desaturation and diaphoresis. The patient finally was discharged receiving 1 L/min of oxygen on the 28th postoperative day. Because of continued problems, cardiac catheterization was performed 2 months postoperatively, which showed systemic right ventricular pressure, right ventricular enlargement and severe dilatation, and insufficiency of the pulmonary homograft with hypoplastic right pulmonary artery and stenosis of the left pulmonary artery (Fig 2Go). The pressures in the right ventricle and homograft proximal to the pulmonary artery branches were similar (100/15 mm Hg), indicating severe insufficiency.



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  		Fig 2. . Angiogram 2 months postoperatively showing stenosis of the left pulmonary artery (white arrow) and hypoplasia of the right (white arrows). The homograft annulus is dilated (black arrows).

 
At reoperation, the pulmonary homograft valve annulus had increased to 16 mm from 14 mm in diameter. The leaflets were unremarkable. Although we planned to simply narrow the annulus with a strip of polytetrafluoroethylene, adhesions of the homograft to the underlying structure precluded this. The valve was replaced with a porcine valve. A 10-mm stent was placed in the left pulmonary artery at the site of stenosis. A similar stent would not stay in place in the right pulmonary artery as there was no discrete stenosis. The atrial septal defect and a small residual ventricular septal defect were closed. The patient came off cardiopulmonary bypass well but suffered from ventricular arrythmia 12 hours postoperatively and died.


   Comment
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 Comment
References
 
Severe incompetence of the homograft from dilatation due to the presence of distal pulmonary artery stenosis is not a well-recognized problem. Lamberti and colleagues [4] in 1988 reported that 1 of 19 patients with cryopreserved homograft valve in the pulmonary position had early pulmonary insufficiency because of residual stenosis of the right pulmonary artery and pulmonary hypertension in the left lung. At replacement with porcine valve 18 months postoperatively, marked dilatation and distortion of the explanted valve annulus were noted with no evidence of rejection or fibrosis of the leaflets. Based on this patient, Lamberti and colleagues suggested that residual distal obstruction or pulmonary hypertension may be a contraindication to the use of free homograft.

Clarke and Bishop [3], in a series of 137 patients with pulmonary homograft conduit, reported 2 infants with truncus arteriosus requiring reoperation for early homograft stenosis and insufficiency at 1.7 and 2.6 months postoperatively. There was no mention, however, of whether distal pulmonary artery stenosis or hypoplasia was present. They also reported 2 older patients with tetralogy of Fallot requiring reoperation for significant homograft insufficiency and distal pulmonary artery stenosis developing late at 15 and 38 months postoperatively. Clarke and Bishop suggested a possible immunologic cause in the relatively high incidence of early homograft failures in their patients.

Right ventricular outflow tract reconstruction can be accomplished with either aortic or pulmonary homografts. Pulmonary homografts have less elastic tissue, exhibit less tendency to calcify, and appear to have less conduit failure from degeneration compared with aortic homografts [2, 5, 6]. The pulmonary homograft, however, is thinner and may be more susceptible to dilatation in the presence of residual stenosis or hypoplasia of the distal pulmonary arteries, as seen in our patient.

Homografts implanted in the pulmonary position are more susceptible to dilatation and insufficiency because of lack of support, in contrast to homografts used in the aortic position, which are surrounded by the pulmonary valve and mitral valve apparatus [7]. Although Lamberti and colleagues [4] blamed the high diastolic pressure in their patient in whom pulmonary insufficiency developed, the problem in our patient probably resulted from homograft dilatation during systole when the powerful right ventricle and the homograft proximal to the pulmonic stenosis become one unit as shown by the same systolic pressure in the homograft and the right ventricle. It is conceivable that had pulmonary insufficiency not developed, the distal pulmonary arteries would have enlarged.


   References
Top
 Abstract
 Introduction
 Comment
 References
 

  1. Turley K, Turley K, Ebert PA. Aortic allografts: reconstruction of right ventricle-pulmonary artery continuity. Ann Thorac Surg 1989;47:278–81.[Abstract/Free Full Text]
  2. Heinemann MK, Hanley FL, Fenton KN, Jonas RA, Mayer JE, Castañeda AR. Fate of small homograft conduits after early repair of truncus arteriosus. Ann Thorac Surg 1993;55: 1409–12.[Abstract/Free Full Text]
  3. Clarke DR, Bishop DA. Allograft degeneration in infant pulmonary valve allograft recipients. Eur J Cardiothorac Surg 1993;7:365–70.[Abstract/Free Full Text]
  4. Lamberti JJ, Angell WW, Waldman JD, et al. The cryopreserved homograft valve in the pulmonary position: early results and technical considerations. J Cardiac Surg 1988;3:247–51.[Medline]
  5. Allen MD, Shoji Y, Fujimura Y, et al. Growth and cell viability of aortic versus pulmonic homografts in the systemic circulation. Circulation 1991;84 (Suppl 3):94–9.
  6. Bando K, Danielson GK, Schaff HV, Mair DD, Julsrud PR, Puga FJ. Outcome of pulmonary and aortic homografts for right ventricular outflow tract reconstruction. J Thorac Cardiovasc Surg 1995;109:509–18.[Abstract/Free Full Text]
  7. Lupinetti FM, Lemmer JH, Ferguson DW, Stanford W, Behrendt DM. Aortic valve replacement with pulmonary or aortic allografts. Circulation 1991;84 (Suppl 3):89–93.

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