Abstract

Since the initial report of coarctation balloon angioplasty in 1982, several groups have used this technique for native coarctations in neonates, infants, and children and for postoperative recoarctations. However, recommendations for use of balloon angioplasty as a treatment procedure of choice are clouded by reports of aneurysm development at the site of coarctation. Here we review our experience as well as that published in the literature, including Valvuloplasty and Angioplasty of Congenital Anomalies Registry data, and present evidence in support of balloon angioplasty as a therapeutic procedure of choice for treating native and recurrent postoperative aortic coarctations. Balloon angioplasty of native aortic coarctations in 20 neonates and infants 1 year old or less reduced peak systolic pressure gradient across the coarctation from 40 ± 12 mm Hg (mean ± standard deviation) to 11 ± 8 mm Hg ( p < 0.001); no patient required immediate surgical intervention. The residual gradient at follow-up (mean follow-up, 12 months) in 16 infants was 18 ± 16 mm Hg, a significant improvement ( p < 0.01) compared with preangioplasty values. In none of the patients did an aneurysm develop. Recoarctation developed in 5 (31%) of the 16 infants and was successfully treated either by surgical resection (in 2) or by repeat balloon angioplasty (in 3). A comparison of mortality and recurrence rates between the balloon angioplasty and surgical groups was made with the help of data pooled from the literature published since 1980. The initial (7% versus 23%) and late (2% versus 25%) mortality and recoarctation (11% versus 18%) rates were higher ( p < 0.025) after surgical intervention than after balloon therapy. When only reports in which patients were operated on after 1979 were included in this type of analysis, the initial and late mortality rates remained higher ( p < 0.01) after operation than after angioplasty, and the recoarctation rates became similar ( p > 0.1). Thirty-two children (>1 year old) underwent balloon angioplasty of native coarctation with a resultant reduction in peak systolic pressure gradient from 48 ± 19 mm Hg to 10 ± 9 mm Hg ( p < 0.001), which continued to remain low (14 ± 11 mm Hg; p < 0.001) at follow-up catheterization in 24 children 13 months (mean) later. There were no immediate or late deaths. A small aneurysm developed in 1 patient (4%) but did not require intervention. Recoarctation developed in 2 patients (8%), and in both, repeat balloon angioplasty was performed with good results. Hypertension decreased. Comparison with pooled surgical data revealed that initial (0% versus 1.6%; p < 0.025) and late (0% versus 8%; p < 0.001) mortality rates were lower after balloon angioplasty and that rates of recoarctation (6% versus 5.5%) and aneurysm formation (12% versus 13%) were similar ( p > 0.1). Postoperative aortic recoarctation in 10 children was treated by balloon dilation. The coarctation gradient was reduced from 52 ± 21 mm Hg to 15 ± 7 mm Hg ( p < 0.001), which decreased to 6 ± 6 mm Hg ( p < 0.01) at a mean follow-up of 17 months. There were no deaths, recoarctation, or aneurysm formation in this small group of patients. Compared with pooled data of repeat operation from the literature, the balloon angioplasty group had a lower mortality rate, but the recoarctation rates were similar. Although we have compared pooled surgical data with pooled balloon therapy data in all three groups presented, we recognize that there are limitations to the comparison of “older” surgical studies with “current” balloon angioplasty experience. Based on our experience and that in the literature, we surmise that coarctation balloon angioplasty is the treatment of choice for symptomatic native coarctation and recoarctation, especially in neonates and infants 1 year old or less.

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