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Eur J Cardiothorac Surg 2006;29:673-674
© 2006 Elsevier Science NL
Cardiac Surgery, Southampton General Hospital, UK
* Corresponding author. Tel.: +44 1794 340266; fax: +44 1794 341090. (Email: monro1711{at}aol.com).
Interrupted aortic arch is a rare condition accounting for about 1% of infants with critical congenital heart disease. The arch interruption may be distal to the left subclavian artery (Type A), between the left carotid and left subclavian arteries (Type B) or between the inomminate and left carotid arteries (Type C) [1]. Type B is the commonest and Type C is very rare. Associated defects such as a Ventricular septal defect (VSD) and Persistent ductus arteriosus (PDA) are almost always present and these constitute a non-complex group. Other associated lesions such as truncus arteriosus, transposition of the great vessels, Taussig-Bing double right ventricle and univentricular heart constitute a complex group. Left ventricular outflow tract obstruction may be present initially or develop later. The aortic valve is bicuspid in about 30% of cases and an aberrant right subclavian artery originating from the descending aorta is quite common, particularly in Type B.
Early in life the duct shuts and this results in severe congestive failure and metabolic acidosis. The great majority of patients present within the first four weeks of life. Before the availability of Prostaglandin, urgent operation was necessary; however, with Prostaglandin the baby can usually be stabilised before surgery. Pre-operative assessment with echocardiography confirms the diagnosis and establishes the presence of associated defects. It is 30 years since Trusler and Izukawa [2] showed how to correct the simple type through the midline with direct anastomosis of the descending to ascending aorta and closure of the VSD. An incresing number of surgeons have used this approach with a lateral thoracotomy approach being reserved for some of the complex group such as univentricular heart.
In that interrupted aortic arch can be considered to be an exagerated type of coarctation, there is some illogicality in that the traditional approach for repair of coarctation and VSD has been through a left lateral thoracotomy together with pulmonary artery banding. In recent years, learning from the experience with interrupted arch repair, more surgeons are starting to treat coarctation and VSD through the midline. It therefore comes as somewhat of a surprise to see a large series of neonates with interrupted aortic arch being treated with a two-stage approach as reported in this journal [3]. They report 52 out of 65 neonates having a staged repair with the initial arch repair and pulmonary banding through the left chest. Their early mortality in the non-complex group is low although there is some cross-over between groups and it is not clear why they used a one-stage repair in 14% of the non-complex group. It is clearly important to end up with live patients, but such an experienced surgeon would probably have had good results with a one-stage procedure in the non-complex group.
It is interesting to see their extensive use of the left carotid turn-down technique which helps to avoid tension. The left carotid artery in a 3.0-kg neonate with Type B interrupted aortic arch is usually about 4.0 mm in diameter and this is adequate for a new aortic arch. Brown et al. have shown that this can be used safely although there is a 33% incidence of late stenosis at the anastomotic site. It has been shown previously that a new arch formed by the left carotid artery grows to about 80% of normal size, which is quite adequate and without a significant gradient across it [4]. Whichever method of repair is used, it is very important to remove all duct tissue as failure to do so predisposes to subsequent aortic narrowing. The use of synthentic tube grafts such as goretex should be avoided as obviously they cannot grow and further surgery is inevitable.
Although the early mortality in the non-complex group of patients undergoing a two-stage approach is low in Brown's series, there is a disconcerting subsequent outcome, as four patients needed their second stage within two weeks and four died before the second procedure. Furthermore there was a significantly lower (49%) 15-year freedom from re-operation with staged repair than with a one-stage approach (67%).
Brown et al. suggest that direct anastomosis is a risk factor for increased mortality. However, this is not a fair conclusion as the patients having direct anastomoses who died were complex (two with truncus arteriosus and one Taussig Bing). Obviously the mortality will be higher in a complex group of patients than in non-complex, most of whom had staged repair.
It is encouraging that the results of surgery for interrupted aortic arch are steadily improving with an early mortality in the region of 10% [5,6]. This improvement relates to many other factors such as improved pre-operative state, anaesthesia, bypass techniques and post-operative care. In particular with modern small aortic cannulae, the ability to continue some perfusion through the innominate artery during repair of the aortic arch rather than having to use deep hypothermia and circulatory arrest is a major advance.
Most surgeons would agree that for the non-complex group, a single stage procedure through the midline which allows for growth is ideal. They would probably be unlikely to wish to enter a controlled trial of a single versus two-stage approach for the non-complex group, which would be the appropriate way to determine which is best. However, as John Brown uses both methods perhaps he could do so. This would be an important study although it would take time to collect sufficient patients.
Whichever method is used there is likely to be a need for further operations. This may be due to left ventricular outflow tract obstruction and aortic valve problems as well as anastomotic stenoses. Therefore, careful follow-up of these patients is important.
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