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Ann Thorac Surg 1999;67:1212-1213
© 1999 The Society of Thoracic Surgeons
a Department of Cardiac Surgery, Herzzentrum, University of Leipzig, Russenstrasse 19, D-04289 Leipzig, Germany
To the Editor
With interest I read the article entitled "Coarctation repair: modification of end-to-end anastomosis with subclavian flap angioplasty," by Hovaguimian and colleagues [1], in which they report a combined technique using resection and end-to-end anastomosis and subclavian flap aortoplasty that was applied in 26 neonates and infants. This technique is a modification of the technique originally reported by Dietl and Torres [2].
Historically, surgical repair of coarctation of the aorta in neonates and infants has been associated with substantial perioperative mortality and a high rate of residual or recurrent stenosis at the coarctation repair site with resultant development of systemic hypertension. Inadequate removal of ductal tissue, failure to address tubular hypoplasia of the aortic arch, tension on the suture line, and aneurysm formation have been cited as important factors using standard techniques of resection and end-to-end anastomosis, subclavian flap aortoplasty, or patch aortoplasty. Although, consequently, there still is considerable controversy about the ideal surgical management of coarctation, one observation seems to be clear: there is a distinct trend toward improved outcome in terms of recurrence of coarctation (< 5%) in recent surgical series using complete resection of the coarctation (including the aortic isthmus), with extensive mobilization of the entire thoracic aorta and anastomosis of the descending aorta to the undersurface of the aortic arch [35]. In the case of hypoplasia of the proximal aortic arch, the descending aorta may have to be anastomosed to the distal ascending aorta. This technique allows maximal apposition of normal aortic tissue and an anastomosis free of tension. Nonadherence to these basic principles in coarctation operations were the primary causes for the historically reported high recurrence rates of coarctation.
In the current era, subsequent to the dramatic decrease in perioperative mortality and morbidity, prevention of the development of hypertension has become a key factor in the improvement of the long-term prognosis in coarctation. Brouwer and colleagues [6], who reported a historic series of 120 patients who had coarctation repair at a mean age of 15.5 years, conclude that elective repair of coarctation should be performed around 1.5 years of age because at that age the probability of upper body normotension and long-term survival would be optimal. It is important to realize, however, that the results of their study reflect an older patient population and therefore a suboptimal anatomic substrate that inherently was operated on with partially outdated techniques and suture material. Therefore, the results and inferences of this report and other older series by no means can be extrapolated to the current experience with coarctation repair. Other investigators reported an incidence of chronic hypertension as much as 60% when repair of coarctation is delayed beyond the first year of life [7, 8]. These observations suggest that there is an age beyond which the benefit of coarctation repair in terms of avoidance of the development of hypertension is marginal. This is most likely related to prolonged periods of upper body hypertension and its sequelae, such as the resetting of barometer mechanisms, abnormal compliance of the upper body arterioles, and decreased compliance of the aorta proximal to the coarctation. The results of the report by Hovaguimian and associates [1] and other recently published series [35] indicate that, probably as a result of the still reversible nature of these factors, the incidence of hypertension may be dramatically lower if coarctation is repaired adequately at neonatal age or in early infancy.
Although Hovaguimian and coworkers report excellent results in the surgical treatment of aortic coarctation in a series of 26 neonates and infants, I believe that the addition of subclavian flap aortoplasty to resection and end-to-end anastomosis is not routinely necessary and in most cases even undesirable. In my experience, the routine use of prostaglandin E1 allows the necessary time at operation for careful and extensive mobilization of the entire aortic arch and proximal arch vessels and the descending aorta as far distal as the diaphragm so that tension on the anastomosis can be avoided. Second, in analogy to extensive experience with the neonatal arterial switch operation for transposition of the great arteries, the circumferential suture line after resection and end-to-end anastomosis has proved to grow adequately, especially if absorbable sutures are used. This suggests that the circumferential suture line at the undersurface of the aortic arch will grow equally well if proper care is taken to resect all ductal tissue and resect or bypass all hypoplastic structures in the aortic pathway. As evidenced by histologic examination of coarctation specimens, in the preductal subtype of coarctation, ductal tissue tends to extend only into the descending aorta. In the paraductal subtype, ductal tissue, in addition to extension into the descending aorta, may also extend proximally into the isthmus. The observed pattern of extension of ductal tissue corroborates our belief that the entire coarctation and the isthmus must be resected or bypassed. The knowledge that the majority of restenoses after coarctation repair occur within 1 year of operation and the low incidence of restenosis in the recently reported series attest to this. I believe that the combined approach as advertised by Hovaguimian and associates has the following disadvantages: (1) The ductal tissue is not in all cases completely excised and therefore there may be an increased potential for recurrent obstruction. (2) Sewing of the subclavian flap across the partial end-to-end anastomosis is much more cumbersome than a straightforward anastomosis between the descending aorta and the undersurface of the aortic arch. In addition, it results in the introduction of more suture material with the potential of delayed growth of the anastomosis. (3) The aortic cross-clamp time is increased compared with that during extended end-to-end anastomosis. (4) Subclavian flap aortoplasty has been demonstrated to be associated with hypoperfusion of the left arm and its detrimental sequelae [9].
References
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