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J Thorac Cardiovasc Surg 2005;130:942-944
© 2005 The American Association for Thoracic Surgery


Brief Communication

Long-term outcome of left ventricular outflow tract after biventricular repair using Damus-Kaye-Stansel anastomosis for interrupted aortic arch and severe aortic stenosis

Shin Takabayashi, MD * , Hideaki Kado, MD, Yuichi Shiokawa, MD, Kouji Fukae, MD, Toshihide Nakano, MD

Department of Cardiovascular Surgery, Fukuoka Children's Hospital, Fukuoka, Japan.

Received for publication January 16, 2005; accepted for publication January 26, 2005.

* Address for reprints: Shin Takabayashi, MD, Department of Thoracic and Cardiovascular Surgery, Mie University School of Medicine, 2-174, Edobashi, Tsu, Mie 514-8507, Japan (Email: shin1111{at}clin.medic.mie-u.ac.jp).

Interrupted aortic arch (IAA) with a ventricular septal defect (VSD) is rare but lethal in association with subaortic stenosis. The primary biventricular repair for this lesion consists of left ventricular outflow tract (LVOT) reconstruction by Damus-Kaye-Stansel (DKS) anastomosis and intracardiac rerouting through the VSD, along with concomitantly performed right ventricular outflow tract (RVOT) and aortic arch reconstruction (Yasui procedure 1 Go; Figure 1, A). In this study, we reported long-term follow-ups in 2 patients and estimated the transition of LVOT diameter.


Figure 1
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Figure 1. A, Drawing of the Yasui procedure; B, 9.4 years after the biventricular repair.

 
Clinical Summaries

Patient 1
An IAA (type B) was diagnosed in a 36-day-old boy weighing 3.4 kg, as was a perimembranous VSD. The subaortic diameter was 2.6 mm, and the aortic valve (diameter, 3.9 mm) was bicuspid. In primary biventricular repair, LVOT reconstruction consisted of intracardiac rerouting from the VSD (8 mm) to the pulmonary artery by using a Teflon patch and a DKS anastomosis. RVOT reconstruction was performed by the Rastelli procedure with a 14-mm Hancock valved conduit (Medtronic, Inc, Minneapolis, Minn). Aortic arch reconstruction was performed with an 8-mm expanded polytetrafluoroethylene (ePTFE) graft anastomosis between the ascending and descending aorta. When the patient was aged 5 years 9 months, a conduit replacement for a re-RVOT reconstruction with a 16-mm ePTFE graft was required because of weight gain. When he was 7 years old, we performed an additional 12-mm ePTFE graft anastomosis between the left common carotid artery and the descending aorta. The follow-up period is now 16 years, and New York Heart Association is class I.

Patient 2
An IAA (type B) was diagnosed in a 42-day-old boy weighing 2.8 kg, as was a perimembranous VSD. The subaortic diameter was 2.8 mm, and the aortic valve (diameter, 3.5 mm) was bicuspid. In primary biventricular repair, LVOT reconstruction consisted of intracardiac rerouting from an enlarged VSD (9 mm) to the pulmonary artery with a polyester patch and DKS anastomosis. RVOT reconstruction was performed by the Rastelli procedure with a 12-mm Carpenter-Edwards valved conduit (Edwards Lifesciences, Irvine, Calif). Aortic arch reconstruction was performed by direct anastomosis. When the patient was aged 7 years 9 months, a conduit replacement for re-RVOT reconstruction with an 18-mm nonvalved ePTFE graft was necessary. The follow-up period is now 10 years, and the patient is in New York Heart Association class I.

Angiocardiograms were performed after the initial operation 4 times in patient 1 and 5 times in patient 2. The latest examinations revealed morphologically that there was no LVOT stenosis on a lateral view (Figure 1, B). Furthermore, there was no regurgitation of semilunar valves and no pressure gradient between the left ventricle and the ascending aorta. We also show the transitions of LVOT consisting of each of the parameters (Figure 2, A) and by each parameter/normal aortic diameters 2 Go (Figure 2, B).


Figure 2
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Figure 2. DKS, Damus-Kaye-Stansel anastomosis; VSD, ventricular septal defect; sub AS, subaortic stenosis.

 
Discussion

Although operative results of IAA have improved, mortality from IAA with severe subaortic stenosis remains high. 3 Go We previously reported primary biventricular repair of IAA and severe aortic stenosis in neonates. 1 Go Although good late survival of biventricular repair for patients with aortic hypoplasia and VSD was reported, 4 Go detailed outcomes of LVOT over a long-term follow-up have not been previously reported.

In this study, our results showed no progressive LVOT stenosis, as was indicated by linear growth in each site of DKS, VSD, and the subaortic stenosis. Although, in these biventricular repairs, the intracardiac patch insertion between the LVOT and the right ventricle is different from DKS anastomosis in single-ventricle patients, there was no LVOT stenosis over long-term follow-up with the patch used in our patients. It is interesting to note that after another routing, the subaortic stenosis reduced without regression of the original aortic route. No pressure gradient across the reconstructed LVOT and preserved semilunar valve function indicated that our primary biventricular repairs, which added an LVOT route, resulted in excellent outcomes. Although reoperations due to relative stenosis of the artificial graft accompanied patient growth, this possibility would be reduced by the aortic arch and RVOT reconstruction by a modification that used only autologous tissues without conduits. 5 Go A limitation of this study is that measurements of angiocardiography in a lateral view to assess the LVOT and the area through which the systemic flow passes are unknown.

In conclusion, LVOT constructed by DKS anastomosis and intracardiac rerouting through the VSD for IAA and VSD with severe aortic stenosis was stable, without progressive stenosis or regurgitation in long-term follow-up. Linear growth of the main route by the systemic flow passages is expected.

References

  1. Yasui H, Kado H, Nakano E, Yonenaga K, Mitani A, Tomita Y, et al. Primary repair of interrupted aortic arch and severe aortic stenosis in neonates. J Thorac Cardiovasc Surg. 1987;93:539-545.[Abstract]
  2. Rowlatt UF, Rimoldi HJA, Lev M. The quantitative anatomy of the normal child's heart. Pediatr Clin North Am. 1963;10:499-588.
  3. McCrindle BW, Tchervenkov CI, Konstantinov IE, Williams WG, Neirotti RA, Jacobs ML, et al. Risk factors associated with mortality and interventions in 472 neonates with interrupted aortic arch. a Congenital Heart Surgeons Society study. J Thorac Cardiovasc Surg. 2005;129:343-350.[Abstract/Free Full Text]
  4. Ohye RG, Kagisaki K, Lee LA, Mosca RS, Goldberg CS, Bove EL. Biventricular repair for aortic atresia or hypoplasia and ventricular septal defect. J Thorac Cardiovasc Surg. 1999;118:648-653.[Abstract/Free Full Text]
  5. Black MD, Smallhorn JF, Freedom RM. Aortic atresia with a ventricular septal defect. modified single-stage neonatal biventricular repair. Ann Thorac Surg. 1999;67:751-755.[Abstract/Free Full Text]



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