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Eur J Cardiothorac Surg 2006;29:636-637
© 2006 Elsevier Science NL
Letter to the Editor |
Kardiocentrum, University Hospital Motol, V Uvalu 84, 150 06 Prague 5, Czech Republic
Received 4 January 2006; accepted 6 January 2006.
* Tel.: +420 224432951; fax: +420 224432920. (Email: tomas.tlaskal{at}lfmotol.cuni.cz).
Key Words: Congenital heart disease • Persistent truncus arteriosus • Interrupted aortic arch • Surgery • Mid-term results • Neonates
We thank Konstantinov for his kind comments regarding our results of primary repair of eight consecutive patients with persistent truncus arteriosus (PTA) and interrupted aortic arch (IAA) [1,2]. It is clear that the studies performed by the CHSS members are most important and reliable because of the high number of centers included into the study, high number of patients, length of follow-up and perfect statistical methods used for outcome analysis. These multicentric studies helped to get relatively objective data concerning long-term results after repair of IAA and associated heart lesions, including PTA. They have also shown that both conditions for and results of surgeries for PTA with IAA are substantially different in individual centers.
In these studies, both mortality and need for reoperation in patients with PTA and IAA were high compared to our experience [2,3]. We must admit, however, the fact that these studies were longer, ended in 1997 and that results improved over the time. In contrary to these studies, we were able to reach 87.5% survival in patients with PTA and IAA at median 2.6 years follow-up [1]. On the other hand, in our series malformation of the truncal valve joined with severe regurgitation or stenosis and the type III influenced the early and mid-term outcomes after repair of PTA more than the presence of IAA.
We had to intervene for aortic arch obstruction in only 14.3% of patients during the follow-up, and during the study period we did not see progression of aortic arch obstruction [2,3]. We think that this could be related to our aggressive method of aortic arch repair, especially in the type B IAA. Extensive mobilization of the aorta and excision of all the ductal tissue is joined with transsection of the left subclavian artery. We do it because in the type B the subclavian artery is nearly completely surrounded by the ductal tissue, which must be excised. Preservation of the left subclavian artery (and anomalous right subclavian artery) in the type B can lead to inadequate mobilization with an increased risk of aortic arch stenosis.
I think that comparison of results of repair of PTA with IAA and APW with IAA is irrelevant. Though PTA and APW are similar from the point of view of embryology and hemodynamics, the surgical treatment is basically different. In APW there is no need for ventriculotomy, VSD closure, and use of a conduit. The procedure is easier and shorter with less risk of myocardial damage. In APW the aortic valve is nearly always normal. After repair of PTA with IAA, there are potential problems related to original anatomy, complexity of surgery, length of aortic cross-clamping, and presence of residual lesions. We believe that any hemodynamically significant residual lesion may accelerate the development of aortic arch anastomosis obstruction, aortic valve regurgitation, and conduit obstruction. Outcome after repair of PTA with IAA is unfavorably affected by all residual lesions and their interactions, though the combination of aortic arch obstruction with aortic regurgitation is probably of specific significance.
References
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