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Eur J Cardiothorac Surg 2005;28:508-509
© 2005 Elsevier Science NL
Letter to the Editor |
Ospedale Bambino Gesù, Roma, Italia
Received 29 March 2005; accepted 6 June 2005.
* Corresponding author. Address: Dipartimento Medico-Chirurgico di Cardiologia Pediatrica, Ospedale Bambino Gesù, Roma, Italia, Piazza S. Onofrio 4, 00165 Roma, Italia. Tel.: +39 06 6859 4265; fax: +39 06 6859 2257. (Email: d.dicarlo{at}mclink.it).
Key Words: Congenital heart defects • Aortic regurgitation • Aortic valve surgery
In their article, Ishizaka and co-workers [1] provide further information on prevalence, causes and management of acquired aortic regurgitation (AR) after repair of Fallot's Tetralogy; they recommend aortic valve repair unless the valve is obviously dysplastic and we strongly agree with them. In the Authors' experience, older age at repair and a bulboventricular VSD acted as risk factor for development/progression of AR.
By reading this paper and other relevant literature [2,3], one is led to think that acquired AR in children/adolescents is almost exclusively related to abnormalities of the left ventricular outflow tract and thoracic aorta or Fallot's Tetralogy. This, in our mind, is not the case. This serious complication may follow other types of ‘corrective’ congenital heart operations as well.
It is well known that dilatation of the ascending aorta may be followed by loss of coaptation of the aortic leaflets and central regurgitation. In the last 10 years, we have replaced the ascending aorta in 22 patients with congenital heart defects for a variety of reasons. Fifteen patients (68%) had a degree of aortic regurgitation (mean 2.8, range 1–4); a constant feature of this sub-group was dilatation of ascending aorta and loss of the normal aortic shape at the sino-tubular junction. Three patients, two with Truncus Arteriosus and one with sub-aortic obstruction as the original diagnosis, had an abnormal aortic/truncal valve.
Along with David and colleagues [4], we elected to treat AR in these patients by restoring a ‘normal’ sino-tubular junction, which required replacement of the ascending aorta with a downsized tubular prosthesis. Only the three patients with abnormal aortic/truncal valve underwent a direct valvuloplasty.
In the whole group, the degree of AR was reduced from average 2.8 to 1.7; specifically, 10 patients (68%) were improved, four unchanged and one worse.
In a mean follow-up of 55 months, two patients required aortic valve replacement (100% actuarial survival, 72% reoperation-free proportion at 5 years).
Our series includes an important diagnostic group; patients with Univentricular Heart (UVH) physiology. Four patients underwent repair of AR by the described method simultaneously with BCPA or TCPC for various anatomic types of UVH. Results were not satisfactory, as in only one patient was AR reduced, in two unchanged and in one worse.
Aortic valve repair in patients with UVH physiology has been rarely reported on [3,5]. Indeed, there is lack of information regarding the long-term effect on clinical status and survival of patients with an already abnormal circulation plus this complication, whenever progressive. Our small experience suggests that aggressive valve repairs, together with replacement of an abnormal ascending aorta, should be employed in these high-risk patients; the technique suggested by Ishizaka and co-workers (a sub-annular plication suture) in their paper may prove very useful.
In summary, we congratulate the Authors for an interesting paper. We wish to emphasize that the problem of AR may emerge as persistent or recurrent morbidity in patients following several operations, otherwise deemed ‘corrective’. The pathophysiology of acquired AR is multi-factorial and may require an individualized surgical approach.
References
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