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Ann Thorac Surg 1999;67:551-553
© 1999 The Society of Thoracic Surgeons
a Department of Cardio-pulmonary Surgery, Heart Center, Dijkzigt Hospital and Erasmus University, Rotterdam, The Netherlands
b Department of Clinical Pathology, Dijkzigt Hospital and Erasmus University, Rotterdam, the Netherlands
Accepted for publication July 30, 1998.
Address reprint requests to Dr Takkenberg, Department of Cardio-pulmonary Surgery, Bd 156, Heart Center, Dijkzigt University Hospital, P.O. Box 2040, 3000 CA Rotterdam, the Netherlands
e-mail: Takkenberg{at}thch.azr.nl
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Abstract |
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A 27-year-old man with a systolic heart murmur since birth was referred to our center with gradually worsening exertional dyspnea and angina. A Ross procedure was performed with aortic root replacement by a pulmonary autograft and right ventricular outflow tract reconstruction with a cryopreserved pulmonary allograft. The native aortic valve was bicuspid and showed severe calcification. There was a moderately enlarged annulus (approximately 30 mm) and moderate dilatation of the aorta (approximately 35 mm). The pulmonary autograft appeared unremarkable. Echocardiographic examination at discharge showed a grade 1 insufficiency of the autograft in the aortic position and good function of the left ventricle.
In the first 5 years after operation the patient was doing well in New York Heart Association class I. But the diameter of the aortic annulus and ascending aorta gradually increased on echocardiographic examination, with an echocardiographic aortic insufficiency of grade 2+ and normal left heart dimensions. Seven years after the Ross procedure the patient started complaining of occasional exertional dyspnea. Echocardiography showed aortic insufficiency of grade 2+ to 3+, left ventricular end-diastolic and end-systolic diameters of 69 mm and 53 mm, with an ascending aorta diameter of 55 mm. The left atrium was dilated and left ventricular function was impaired.
The pulmonary autograft was replaced by a cryopreserved aortic allograft root. At operation a dilated autograft with a diameter of more than 5 cm was found. The procedure and postoperative course were unremarkable. Microscopic evaluation (Fig 1) of the pulmonary autograft revealed focal interruption of the media of the vessel wall with total absence of elastin fibers. Furthermore, the pulmonary artery wall showed intimal proliferation with fibrosis suggestive of chronic exposure to high pressure.
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Ours is not the first report of a patient requiring reoperation for pulmonary autograft root dilatation after a Ross procedure. However, it is the first report on the possible underlying mechanism that may cause the progressive dilatation and consequent failure of the pulmonary autograft in aortic position. The striking histologic features of the pulmonary artery media of this patient are an unknown phenomenon to us, and we can only hypothesize on the possible cause of these lesions. First, they may be common in all pulmonary autograft roots that are exposed to systemic pressures for a longer period of time. We reexamined the histologic features of the explanted pulmonary autograft root of another patient who underwent replacement of the autograft with a homograft 22 months after the initial Ross procedure because of a relapse of rheumatic fever. Surprisingly, the same abnormalities were found in this pulmonary artery. On the other hand, a recently published histologic study of a pulmonary autograft that was explanted 17 months after a Ross procedure revealed no medial abnormalities [6]. Second, our findings could represent a preexisting abnormality. Bicuspid aortic valve disease is associated with aortic wall abnormalities [7, 8], and because both semilunar valves have the same embryologic origin, these lesions may also be present in the pulmonary artery media. Unfortunately, no histologic examination of the aortic wall was done in our patient. However, the second patient in our report did not have a bicuspid aortic valve nor preexisting histologic abnormalities in the media of the excised aortic root. Finally, our findings could also be incidental with no further implications, but only time will tell.
In conclusion, this case report illustrates that a pulmonary autograft root in the aortic position may very well cause clinically significant regurgitation resulting in replacement of the autograft. The histologic abnormalities that were found in 2 patients provide an important new insight into the mechanism that may possibly cause the progressive dilatation in pulmonary autograft roots. Therefore, caution is warranted in the long-term follow-up of patients after the Ross procedure. Careful annual echocardiographic monitoring of the dimensions and function of the autograft is essential. Furthermore, detailed histologic examination of explanted pulmonary autograft roots is recommended to gain more insight into the possible role of pulmonary artery media abnormalities in progressive dilatation of pulmonary autograft roots.
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