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J Thorac Cardiovasc Surg 1994;107:1374-1375
© 1994 Mosby, Inc.
LETTERS TO THE EDITOR |
King Faisal Specialist Hospital and Research Center
Riyadh, Saudi Arabiaa
To the Editor:
Right ventricular (RV) outflow conduits are known to have a high risk of calcification, fibrosis, and obstruction Although false aneurysm formation has been described, rupture has rarely been reported. We report here the case of a patient who had an intracardiac rupture of a false aneurysm after a homograft reconstruction of the RV outflow tract for tetralogy of Fallot with pulmonary atresia.
An 18-year-old woman, whose condition had been palliated with bilateral systemic-pulmonary shunts in early childhood for tetralogy of Fallot with pulmonary atresia and nonconfluent pulmonary arteries, underwent definitive correction in 1987 at the age of 14 years. At the definitive operation, the ventricular septal defect was closed with bovine pericardium and the pulmonary arterial confluence was established by a 16 mm Dacron polyester fiber tube between the left and right hila of the lungs. The RV continuity was obtained with an aortic homograft. RV pressures continued to be suprasystemic after the correction.
The patient's condition was reevaluated by cardiac catheterization in May 1990. This revealed a hypertensive RV (140/2 mm Hg). There was a gradient of 55 mm Hg between the conduit and right pulmonary artery (RPA), with severe stenosis at the left hilar anastomosis. Multiple balloon dilations of the RPA were carried out. These did not change the gradient. The left pulmonary artery (LPA) anastomosis could not be crossed. Further surgical intervention was not undertaken in view of the high risk.
In January 1992, the patient was admitted with hemoptysis, for which she underwent restudy. Cardiac catheterization showed a hypertensive RV (131/15 mm Hg), with a gradient of 73 mm Hg between the conduit and the RPA. The LPA could not be entered. RV cineangiogram showed narrowing of the RPA and LPA. There was a pulsating false aneurysm originating at the junction of the homograft with the Dacron conduit, impinging on the aorta to the front. A thin, downward-directed leak could be detected, but its outlet could not be identified. The patient was referred for operation, on the assumption that the false aneurysm was leaking into the bronchus to mitigate imminent rupture.
The operation was performed with femorofemoral bypass, with core cooling to 20° C and circulatory arrest. The wall of the homograft was extensively calcified and fibrotic; the valve cusps were calcified and adherent to it. There was extensive peel formation in the Dacron tube, with a leak at the Dacron tube homograft suture line leading to a false aneurysm. This false aneurysm (2 cm) was surrounded by a thick, fibrinous capsule. A probe showed a patent rupture into the left ventricular outflow tract (Fig. 1). The Dacron tube was excised with the homograft. Continuity between the hila was established with a 14 mm ringed polytetrafluoroethylene tube and the RV was connected to the polytetrafluoroethylene tube by a fresh aortic homograft.
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The use of an aortic homograft to establish continuity from RV to pulmonary artery has gained widespread clinical application. Concern has been expressed, however, about calcification of these homografts in the pulmonary position.
1 The prevalence can be as high as 92% when homografts are used for cyanotic congenital heart defects. False aneurysms of the aortic homografts have been reported in both the pulmonary and aortic positions 2, 3 and can occur both at the proximal and at the distal anastomosis. In the first reported case in the literature, 4 the false aneurysm occurred proximal to the valve and the patient died of rupture into the left hemithorax. In our patient, the site of rupture was the distal homograft anastomotic site with the Dacron conduit. This rupture presumably occurred as a result of a combination of distal obstruction and high proximal pressure leading to the anastomotic leak and false aneurysm formation. There was also a hemodynamically insignificant rupture of the false aneurysm into the left ventricular outflow tract near the superior edge of the ventricular septal defect patch. This was not visualized in the angiographic study, possibly because of the nearly equal pressures in the two ventricles. As far as we are aware, there is no documentation of such a complication in the literature. The cause of hemoptysis in this patient remains unexplained.
Properly sized branched pulmonary artery homografts would probably avoid the intimal proliferation seen in Dacron tubes 5 and decrease the number of anastomotic suture lines. Long-term problems of such homografts, however, would still remain.
References
This article has been cited by other articles:
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  M. Ono, N. Fukushima, S. Ohtake, and H. Matsuda Infectious false aneurysm of the right ventricular outflow tract after repair of congenital heart defect treated with Freestyle(R) aortic bioprosthesis Interactive CardioVascular and Thoracic Surgery, June 1, 2003; 2(2): 105 - 107. [Abstract] [Full Text] [PDF]
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