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Ann Thorac Surg 1996;61:840-844
© 1996 The Society of Thoracic Surgeons
Divisions of Cardiothoracic Surgery and Pediatric Cardiology, University of California, San Francisco, California
Accepted for publication November 3, 1995.
| Abstract |
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Methods. To address these issues, we have used a technique of coarctation resection and extended anastomosis of the descending aorta to the undersurface of the aortic arch. The salient features of this approach include extensive mobilization of the aortic arch and neck vessels, careful trimming of all ductal tissue, ligation of the isthmus just beyond the left subclavian artery, and end-to-side anastomosis of the descending aorta to a separate incision in the undersurface of the aortic arch proximal to all tubular hypoplasia. Between July 1992 and January 1995, 19 consecutive neonates (median age, 13 days) and 4 consecutive infants under 3 months of age (median age, 69 days) with a mean peak systolic upper to lower extremity resting gradient of 27.9 ± 16.9 mm Hg underwent repair of aortic coarctation and tubular hypoplasia of the arch. Other procedures performed at the time of repair included ligation of a patent ductus arteriosus (n = 19), pulmonary artery banding (n = 3), and closure of ventricular septal or atrial septal defect (n = 3).
Results. There were no perioperative deaths. Early postoperative complications included a recurrent laryngeal nerve injury and a transient focal tonic clonic seizure. There was one late death, after a subsequent intracardiac surgical procedure, at a median follow-up of 16 months (range, 1 to 29 months). Twenty-one of 22 late survivors were free of recurrent aortic coarctation by echocardiography findings and clinical examination, with a median upper to lower extremity gradient of 0 mm Hg. Reintervention for recurrent aortic coarctation was not required in any survivor.
Conclusions. The technique described herein completely removes all potentially abnormal tissue from the aorta, including ductal tissue and all tubular hypoplastic tissue proximal to the coarctation site.
| Introduction |
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| Patients and Methods |
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Definitions
AORTIC ARCH HYPOPLASIA.
The size of the aortic arch relative to that of the ascending aorta was assessed by echocardiography, and the arch diameter was confirmed by the operating surgeon. Hypoplasia of the proximal aortic arch was defined as a cross-sectional diameter of the aortic arch segment between the innominate artery and the left common carotid artery equal to or less than 60% of that of the ascending aorta. Hypoplasia of the distal aortic arch was judged to be present when the cross-sectional diameter of the arch segment between the left common carotid artery and the left subclavian artery was equal to or less than 50% of that of the ascending aorta [6].
RECURRENT AORTIC COARCTATION.
At the end of the operation, the pressures proximal and distal to the coarctation repair site were measured directly by a catheter pull-back method and recorded. The gradient between the two was defined as the immediate postrepair gradient. Recurrent coarctation was defined as the presence of a gradient of 20 mm Hg or greater at follow-up.
HYPERTENSION.
Patients were considered hypertensive when systolic blood pressure in the right arm exceeded the 95th percentile for blood pressure as defined by the American Task Force for Blood Pressure Control in Children [7].
Patient Population
Between July 1992 and January 1995, 19 consecutive neonates (median age, 13 days; range, 3 to 34 days) and 4 infants (median age, 69 days; range, 61 to 78 days) underwent operative repair of aortic coarctation complex. The median weight was 2.9 kg (range, 1.3 to 5.0 kg), and 20 patients (86.9%) had associated hypoplasia of the aortic arch. Associated intracardiac anomalies were present in 22 of 23 patients at the time of operation. Other morphologic lesions included patent ductus arteriosus in 19 (82.6%), atrial septal defect/patent foramen ovale in 15 (65.2%), ventricular septal defect in 15 (65.2%), Shone's complex in 5 (21.7%), complete atrioventricular canal defect in 1 (4.3%), and Taussig-Bing anomaly in 1 (4.3%). Two patients had hypertension, and 21.7% required inotropic agents. The preoperative upper to lower extremity peak systolic gradient at rest was 27.9 ± 16.9 mm Hg. A preoperative prostaglandin E1 infusion was given in 15 patients (65.2%).
Operative Technique
All patients underwent the following repair. Using a left posterolateral thoracotomy through the third intercostal space, the aorta, ductus arteriosus, left subclavian artery, left carotid artery, and innominate artery were dissected and mobilized. Extensive mobilization of the aortic arch was accomplished by dissecting circumferentially at least to the base of the innominate artery; the descending aorta was mobilized to at least the second set of intercostal vessels (Fig 1A
). Intercostal vessels were not ligated in the course of the dissection. An angled vascular occlusion clamp was placed across the distal transverse arch at the level of the undersurface of the aortic arch and opposite the origin of the innominate artery (Fig 1B
), while unobstructed forward blood flow to the innominate artery was documented by a radial arterial line or pulse oximetry. This clamp isolated the left carotid and subclavian arteries as well. A second angled cross-clamp was placed across the descending aorta approximately 1.5 cm below the insertion of the ductus arteriosus and was used to control intercostal arteries if possible. Additional intercostal arteries were temporarily clipped.
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At the time of coarctation repair, additional surgical procedures included ligation of patent ductus arteriosus in 19 (82.6%), pulmonary artery banding in 3 (13%), and median sternotomy with closure of atrial septal defect, ventricular septal defect, or both defects in 1 patient (4.3%) each.
| Results |
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Morbidity
There were no intraoperative complications. No permanent neurologic sequelae were observed despite operative clamping of the left common carotid and left subclavian arteries for ESAA. The aortic cross-clamp time was 22.9 ± 11 minutes, and the peak upper to lower extremity systolic pressure difference in the operating room was 2.4 ± 4.8 mm Hg. There were no postoperative complications of intestinal ischemia, hemorrhage, or chylothorax. One transient focal tonic clonic seizure occurred postoperatively in a single patient; however, magnetic resonance imaging of the head failed to reveal any focal lesions, and the patient was subsequently discharged without anticonvulsant medication. No cases of paraplegia occurred. A recurrent left laryngeal nerve injury occurred in 1 patient with laryngomalacia, requiring tracheostomy.
Follow-Up
Detailed follow-up at a median duration of 16 months (range, 1 to 29 months) was obtained on 22 survivors from hospital records, referring pediatric cardiologists, and interviews with family members. During the follow-up period, 6 patients required a subsequent surgical procedure to repair intracardiac defects, and 1 patient underwent balloon aortic valvuloplasty. The success of coarctation repair was appraised by a combination of clinical examination (n = 17), two-dimensional Doppler echocardiography (n = 14), angiographic study (n = 3), or magnetic resonance imaging (n = 1).
Recurrent coarctation was diagnosed in only 1 infant, for an overall recoarctation rate of 4.5%. This patient left the operating room after COA repair with a 15-mm catheter pull-back gradient. Evaluation of the peak systolic pressure gradient in this patient at 6-month follow-up revealed a gradient of 28 mm Hg by clinical examination. Doppler echocardiographic examination demonstrated that the site of obstruction was at the level of the anastomosis, with good growth of the hypoplastic aortic arch. At 9-month follow-up, there has been no increase in the size of the gradient, and no angiographic studies have been performed in this patient. All other 21 survivors had upper to lower extremity gradients equal to 0 at follow-up, determined by some combination of physical examination, echocardiography, or cardiac catheterization. No reoperations or percutaneous transluminal balloon angioplasty procedures have been performed after the initial repair of coarctation.
Blood pressures were measured in the brachial arteries of 22 survivors using a sphygmomanometer, and hypertension was defined as sustained systolic and diastolic blood pressures greater than the 95th percentile for age. Before coarctation repair, 2 (8.9%) of the 23 patients were considered hypertensive. After ESAA, 1 (4.5%) of 22 survivors was hypertensive and required antihypertensive medication for blood pressure control at late follow-up. The postoperative peak systolic gradient was 0 mm Hg in this patient.
| Comment |
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A technique similar to ESAA as described and illustrated in this report has been used to repair interrupted aortic arch and coarctation plus hypoplastic aortic arch through median sternotomy using cardiopulmonary bypass and circulatory arrest [20]. Although ESAA is applicable in the great majority of cases, flexibility must be emphasized, and the full repertoire of techniques should be considered in each individual case. For instance, in the presence of a ``bovine'' innominate trunk with hypoplasia of the distal aortic arch, median sternotomy, cardiopulmonary bypass, and circulatory arrest may be necessary to patch the undersurface of the aortic arch and distal part of the ascending aorta. Patch aortoplasty may be preferred in certain cases of discrete recoarctation that do not respond to balloon dilatation or in infants in poor clinical condition in whom the speed of the operation is of utmost importance. The subclavian flap aortoplasty may be the preferred technique in neonates with borderline left ventricular size in whom it is desirable to preserve temporarily the ductus arteriosus [21]. In addition, extended end-to-end repair [5, 11, 13] may be appropriate in older infants and children in whom the ductus has already closed and further constriction of the ductus is not an issue. These situations are uncommon, and we were able to use ESAA in all cases at our institution over a 2-year period.
Thus, ESAA is the procedure of choice for neonates and infants at our institution. Recurrent aortic coarctation has been identified in only 1 patient (4.5%). The observed gradient in this case was less than 30 mm Hg at 9 months of age. No reoperations or reinterventions have been performed thus far at a median follow-up of 16 months. Although we recognize that the follow-up period of our study is limited, a number of studies have shown that the majority of recoarctations occur within the first year of life regardless of the type of operative repair used [1, 20, 22, 23]. Thus, the results of ESAA when applied to neonates and young infants are compelling and compare favorably with those of other studies [1, 2, 1214]. Further follow-up will be necessary to see whether the freedom from reintervention remains over an extended period and whether a favorable impact on systemic hypertension is achieved.
| Footnotes |
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Address reprint requests to Dr Hanley, Division of Cardiothoracic Surgery, University of California, 505 Parnassus Ave, S-549, San Francisco, CA 94143.
| References |
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