Distal Aortic Arch Hypoplasia and Coarctation Repair: A Tailored Enlargement Technique

Abstract

Background:

Several techniques have been described to correct coarctation associated with distal arch hypoplasia. However, in neonates, residual gradients are frequently encountered and influence long-term outcome. We reviewed our experience with an alternative technique of repair combining carotid–subclavian angioplasty and extended end-to-end anastomosis.

Methods:

From 1998 through 2014, 109 neonates (median age, 9 days) with coarctation and distal arch hypoplasia (n = 106) or type A interrupted aortic arch (n = 3) underwent repair using this technique. Thirty patients had isolated lesions (group 1), 44 associated ventricular septal defect (group 2), and 35 associated complex cardiac lesions (group 3). Median follow-up was 98 months.

Results:

Repair was performed via left thoracotomy in 97%. There was one procedural-related death (0.9%) and overall five patients died during index admission (4.6%). Ten deaths were recorded at follow-up. Actuarial five-year survival was 86% (100% in group 1, 91% group 2, and 66% in group 3). Recurrent coarctation (clinical or invasive gradient >20 mm Hg) developed in 15 patients, all but 2 successfully treated by balloon dilatation. Freedom from any reintervention (dilatation or surgery) at five years was 86%. Only two patients were on antihypertensive drugs at last follow-up.

Conclusions:

This combined technique to correct distal arch hypoplasia and isthmic coarctation results in low mortality and acceptable recurrence rate. It preserves the left subclavian artery and allows enlargement of the distal arch diameter. Late outcome is excellent with very low prevalence of late arterial hypertension.

Keywords

surgery (incisions/exposure/ techniques)aortic arch coarctation neonate outcomes (including mortality morbidity survival etc)survival analysis

Introduction

Coarctectomy with extended end-to-end anastomosis is commonly the preferred technique of repair in neonates and young infants.¹ Recoarctation rate varies from 3.6% to 18%.^2,3 Varying degrees of aortic arch hypoplasia are frequently encountered in infants with isthmic coarctation and may contribute to recurrence.³

In neonates presenting with underdevelopment of the transverse arch, the “relative” stenosis within this proximal segment after repair increases the risk of reintervention⁴ and is associated with impaired exercise performance at older age despite acceptable transaortic gradients at rest.⁵ Therefore, additional arch aortoplasty has been advocated for those anatomical variants, including carotid–subclavian angioplasty. Since 1998, our center has used selectively a modified approach⁶ to the carotid–subclavian angioplasty initially described by Amato⁷ for all patients with distal arch hypoplasia.

Herein, we report the long-term results in 109 patients operated over a 16-year period. Outcomes were analyzed for survival, recurrent obstruction requiring any reintervention, and the presence of late hypertension.

Materials and Methods

Definitions

Transverse arch: Segment between the brachiocephalic artery and the left subclavian artery (LSCA), divided into the proximal arch (between the brachiocephalic artery and the left common carotid [LCC]) and the distal arch (between LCC and LSCA). The isthmus corresponds to the segment between the LSCA and the ductus arteriosus.

Distal arch hypoplasia was defined as (a) < −3 Z-score (Zsc) based on echocardiographic measurements (n = 80/109), (b) if the diameter was <1 mm/kg + 1⁸ (n = 77/109), or (c) if long narrow distal arch was noted at surgery (n = 29/109).

Recurrent coarctation: Clinical or invasive gradient of greater than 20 mm Hg (undetected after initial repair) or any reintervention for arch/aortic obstruction.

Hypertension: Systolic or diastolic blood pressure (BP) that exceeds 95th percentile for age, gender, and height.⁹

Early death: Death within 30 days of operation or before hospital discharge.

Patient Demographics

Between 1998 and 2014, out of 280 infants, 109 (67 boys and 42 girls; median age, 9 days) underwent coarctation repair using a technique combining carotid–subclavian angioplasty and extended end-to-end anastomosis (see below). The other 171 patients underwent coarctation repair either using an end-to end (n = 20) or an extended end-to-end anastomosis (n = 151). Patients with proximal arch hypoplasia were excluded from this study.

Patient’s characteristics are provided in Table 1. The median weight was 3.2 kg. The cohort was divided into three groups: group 1 had simple coarctation (n = 30 or 27.5%), group 2 had coarctation associated with ventricular septal defect (VSD; n = 44 or 40.3%), and group 3 coarctation associated with complex congenital heart disease (n = 35 or 32.2%). Details of group 3 are given in Table 2.

Table 1.

Patient Characteristics.^a

Characteristics	Number (%)
Age (days) median (range)	9 (1-1,277)
Neonate	92 (84.4)
Sex (M/F)	67/42
Weight (kg) median (range)	3.2 (1.2-18.8)
Chromosomic anomaly	12 (11)
Preoperative PGE1	87 (80)
Preoperative heart failure	40 (37)
Preoperative ventilation	34 (31)
Preoperative inotrope	21 (19)
Preoperative renal failure	10 (9)
Preoperative balloon atrial septostomy	8 (7)

Abbreviation: F, female; M, male; PGE, prostaglandin E₁.

^a n = 109.

Table 2.

Details of Congenital Heart Diseases in Group 3.

Condition	Number of Patients, n = 35
DORV	7
TGA-VSD	6
AVSD	7
Shone syndrome	9
Univentricular hearts	5
Major aortic valve dysfunction	1

Abbreviations: AVSD, atrioventricular septal defect; DORV, double outlet right ventricle; TGA-VSD, transposition of the great arteries ventricular septal defect.

By transthoracic echocardiography, median distal transverse arch diameter was 0.38 cm (Zsc = −3.4) and median isthmus diameter was 0.21 cm (Zsc = −4.1). Alternatively, 72.5% of patients had a distal transverse arch < (1 mm/kg +1).⁸

Prostaglandin E₁ infusion was present in 87 (80%) patients preoperatively. Thirty-four (31%) neonates received ventilatory support and 10 (9%) had impaired renal function (creatinine level higher than 100 µmol/L).

Data Collection and Follow-Up

Information about preoperative, operative, and postoperative variables was retrospectively collected by reviewing a computerized patient database, hospital charts, operative notes, and autopsy reports, if appropriate. Clinical and echocardiography follow-up was obtained from outpatient clinics records or from referring pediatric cardiologists.

Patients with arm–leg gradients greater than 20 mm Hg or discrepant pulse examinations on repeated visits were evaluated by echocardiography. Patients with flow acceleration across the site of repair, persistence of flow in the descending thoracic aorta during diastole, or evidence of anastomotic narrowing by means of 2-D imaging were referred for cardiac catheterization.

Clinical follow-up was 92% complete (95/104 patients). The median follow-up was 98 months. The study protocol was approved by our institutional ethical board.

Statistical Analysis

Continuous data are presented as mean (standard deviation) or median (interquartile range [IQR]) for nonparametric data. Normality of the distribution was assessed with the Shapiro-Wilk test. As variables of interest (Table 3) for group comparison were not normally distributed, we used the Kruskal-Wallis analysis of variance. Categorical data are presented as proportion and compared with the χ² test or the Fisher exact test if appropriate. Failure time data on survival, recurrent coarctation, and need for reintervention (balloon dilatation or stenting or reoperation) are presented using Kaplan-Meier survival curves. Differences between the groups were tested by the “log-rank test.”

Table 3.

Hospital and Follow-Up Details.

Characteristics	Number (%), n = 109	Group 1 (%), n = 30	Group 2 (%), n = 44	Group 3 (%), n = 35	P Value
ICU LOS (days)	4	3	4	6	<.001
Hospital LOS (days)	16	9	14.5	23	<.001
Follow-up (months)	97.7	102	110	31.7	<.001
Overall mortality	15 (13.7)	0 (0)	4 (9)	11 (31.4)	.001^a
Cardiac reoperation (any causes)	55 (50.4)	3 (2.7)	26 (59)	26 (74.3)	.003

Abbreviations: ICU, intensive care unit; LOS, length of stay.

^a Fisher exact test.

Pre- and intraoperative variables (Table 1 and Table 4) were tested in univariate analysis for the end points of “survival” and “need for reintervention,” using the proportional hazard model (Cox regression). Statistical analysis was made using the IBM SPSS statistic version 22.

Table 4.

Analysis Between Recoarctation versus No Recoarctation Patients.

	No Recoarctation (n = 92)	Recoarctation (n = 17)	P Value
Gender	58 M/34 F	9 M/8 F	.43
Group 1 and 2 vs Group 3	60/32	11/6	.76
Age (days)	34.4	14.7	.55
Weight (kg)	3.4	3	.28
Preoperative isthmus Z-score	−4	−4	.85
Preoperative distal transverse aorta Z-Score	−3.3	−3.4	.74
Postoperative isthmus Z-score	−1.2	−2	.004
Gradient postoperative (mm Hg) TTE	8.7	19	.002
Total aortic CCT (minutes)	57	59	.80

Abbreviations: CCT, cross-clamp time; F, female; M, male; TTE, transthoracic echocardiography.

Surgical Technique

For the upper body, invasive BP monitoring was used, whereas a noninvasive method was applied for the lower body. There was no attempt to control patient’s body temperature throughout the procedure. Our technique was described by Kalangos et al in 2001.⁶ Briefly, after thoracotomy, the aortic arch, brachiocephalic vessels, ductus arteriosus, and the descending thoracic aorta were completely mobilized. The site of coarctation was first ligated allowing the ductus to perfuse the distal aorta during arch enlargement. A curved clamp occluded altogether the LCC, the LSCA, and the transverse arch proximal to the LCC. An incision was made on the superior aspect of the distal aortic arch between the origins of the LCC and LSCA and extended to the facing aspects of both vessels (Figure 1A). Apposition surfaces between the LCC and distal arch on one side and between the LSCA and the distal arch on the other side were sewn together starting from the midpoint of the posterior lip of the aortotomy (Figure 1B).

The same procedure was repeated between the anterior lips. The descending aorta was then clamped, the ductus ligated, the coarctation excised, and the undersurface of the aortic arch incised to allow an extended end-to-end anastomosis (Figure 1C and D).

Results

Thirty-Day Mortality and Morbidity

Repair was performed via left thoracotomy in 97% of the patients. The mean total cross-clamp time (arch enlargement and coarctation repair) was 55 (30-105) minutes with a distal cross-clamp time of 29 (15-74) minutes. In case of unrestrictive VSD (23 patients in group 2 and 18 patients in group 3), a pulmonary artery band (PAB) was placed. Median invasive ventilation time was 1.9 days (IQR 25th percentile-75th percentile: 1-3.8). Thirty-seven percent of patients needed inotropic support. Following the pRIFLE criteria,¹⁰ ten patients had some degree of acute kidney injury.The median intensive care unit (ICU) stay was 4 days (IQR 25th percentile-75th percentile: 3-8.5) and hospital stay was 16 days (IQR 25th percentile-75th percentile:10-23).

There was one procedural-related death (0.9%) in group 2. The patient died of severe low cardiac output (LCO) after single-stage repair performed under deep hypothermic circulatory arrest (DHCA). He additionally suffered severe brain ischemic damage.

Four patients from group 3 (double outlet right ventricle–transposition of the great arteries [TGA] n = 3, TGA-VSD n = 1) died during the same hospitalization following their coarctation repair. Two deaths unrelated to the coarctation repair occurred following surgical repair of intracardiac anomalies. Two patients died prior to intracardiac repair. One patient with TGA-VSD had a restrictive patent foramen ovale. He suffered LCO and subsequent severe brain ischemia. One patient had fulminant Clostridium-necrotizing enterocolitis (NEC) and abdominal compartment syndrome 12 days after initial repair and pulmonary artery banding. Overall, five (4.6%) patients died during index hospitalization.

Two patients needed early reinterventions, one for a descending aorta thrombosis and one for migration of the PAB. Chylothorax developed in seven (6%) patients. Phrenic nerve and recurrent nerve palsy developed in one patient each.

Six patients had neurological complications (ischemic or hemorrhagic stroke): one in group 2 (the only death) and five patients in group 3 (four deaths). One was procedure related. No patient suffered from paraplegia.

Among the six patients suspected of developing NEC, only three had a confirmed diagnosis by imaging studies. All but one were treated conservatively.

Late Mortality and Morbidity

Late mortality

Ten (9%) patients died during follow-up. All deaths were unrelated to their coarctation repair surgery (Table 3).

Three patients died in group 2. One patient with a borderline left ventricle died of pulmonary infection with underlying pulmonary hypertension, one patient died of septicemia, and one following surgical repair for biliary atresia.

In group 3, five patients died following a second cardiac surgical procedure for correction of associated malformations (4-26 months after coarctation repair). One died following percutaneous balloon aortic valve angioplasty complicated by brain hemorrhage and one patient died of respiratory syncytial virus infection. Overall survival at one year and five years was 100% and 100% in group 1, 93.2% and 90.9% in group 2, and 72.6% and 65.7% in group 3 (P < .001).

By univariate analysis, preoperative prognostic factors for death were the need for balloon atrial septostomy prior to repair (hazard ratio [HR]: 7.3, 95% confidence interval [CI]: 2.3-23.3), associated complex cardiac anomalies (HR: 7.3, 95% CI: 2.3-23.3), and weight <2.5 kg (HR: 3.8, 95% CI: 1.2-12). Perioperative prognostic factors were prolonged ventilation time (HR: 4.5, 95% CI: 1.2-16), ICU stay (HR: 7.6, 95% CI: 1.7-33), and a delayed metabolic homeostasis as defined by a return to baseline lactate level beyond the first postoperative day (HR: 3.2, 95% CI: 1-10.3; Table 5).

Table 5.

Univariable Analysis of Predictors of Death.

	HR	95% CI	P Value
Inotrope preop	0.3	0.04-2.1	.21
Ventilation preop	0.8	0.25-2.5	.69
Renal failure preop	0.04	0.001-68.2	.40
Rashkind preop	7.3	2.3-23.3	.001
Age (neonate)	1	0.2-4.3	.97
Weight (2.5 kg)	3.8	1.2-12	.02
Complex vs others	7.3	2.3-23.3	.001
Assoc PAB	1.9	0.7-5.3	.20
Ao CCT (IQR 50)	1.4	0.5-3.9	.52
Ventilation post (IQR 50)	4.5	1.2-16	.02
PICU LOS (IQR 50)	7.6	1.7-33	.007
Max lactate (IQR 50)	3.1	1-9.73	.05
Normal lactate <24 hours postoperative	3.2	1-10.3	.04

Abbreviations: Ao CCT, aortic cross clamp time; Assoc PAB, associated pulmonary artery banding; HR, hazard ratio; IQR, interquartile range; Max lactate, maximal level of lactate; PICU LOS, pediatric intensive care unit length of stay.

Recoarctation

Fifteen (13.7%) patients presented with a recoarctation during follow-up. Fourteen had a clinical arm–leg gradient (or invasive gradient) >20 mm Hg and echographic signs of recoarctation, whereas one patient had more than 50% reduction in the aortic diameter at the site of repair together with left ventricular dysfunction. Most recurrences (13/15 patients) were located at the distal anastomosis.

Fourteen patients underwent balloon angioplasty, with one failure requiring repeat surgery (see below). Most of the balloon angioplasties (87.5%) were performed within the first year. Repeat angioplasty was required in three patients.

Two patients required reoperations to treat proximal aortic arch stenosis. At the time of their initial repair, both patients had underestimated proximal arch hypoplasia (−3.4 Zsc and −2.7 Zsc, respectively) and that segment failed to grow at follow-up. Proximal arch enlargement was performed under cardio-pulmonary bypass (CPB) on a beating heart using antegrade cerebral perfusion 28 and 130 months later.

Overall, freedom from recurrence of coarctation at one year, five years, and ten years were 88%, 86%, and 86% (Figure 2). For patients operated after 2006 (n = 59), five-year freedom from recurrence was 91%.

By univariate analysis, none of the preoperative variables could predict recurrence of coarctation. However, a small postoperative aortic diameter at the site of repair (neo-isthmus <2 Zsc; HR: 10.2, 95% CI: 3.2-32.8) and the presence of an arm–leg pressure gradient greater than 10 mm Hg at discharge (HR: 3.5, 95% CI: 1.1-11.4) were found to be prognostic of recurrence (Tables 4 and 6).

Table 6.

Univariable Analysis of Predictors of Recoarctation (percutaneous transluminal angioplasty, PTA) or Surgery.

	HR	95% CI	P Value
Gender	0.7	0.3-2	.51
Age (neonate)	1.3	0.3-5.7	.75
Weight (2.5 kg)	1.7	0.4-7.4	.50
Weight (2.0 kg)	1.3	0.2-10	.78
Complex vs others	1.1	0.4-3.2	.88
Transverse arc Diam (−3.5 Zsc)	1	0.4-3.2	.97
Isthmus Diam (−4 Zsc)	0.5	0.2-1.5	.20
Ao CCT (IQR 50)	0.7	0.3-2	.53
Isthmus Diam (−2 Zsc)	10.2	3.2-32.8	.001
Arm–leg pressure gradient at discharge (>10 mm Hg)	3.5	1.1-11.4	.03

Abbreviations: Ao CCT, aortic cross clamp time; Diam, diameter; HR, hazard ratio; IQR, interquartile range; Zsc, Z-score.

Late hypertension

Arm–leg pressure was systematically measured in all patients during follow-up. When three successive measures were pathologic, a 24-hour BP monitoring was performed to confirm persistent hypertension. Persistent hypertension was present in four (3.7%) patients: two patients with hypertension only during exercise were not treated and two patients with hypertension at rest required pharmacologic treatment.

Comment

Among surgical techniques, extended end-to-end anastomosis is the procedure of choice for most centers to repair distal arch hypoplasia associated with coarctation,¹ though end-to-side anastomosis, originally designed to correct interrupted aortic arch, is now regularly performed in some centers.^11
-13 In Melbourne’s experience, end-to-side anastomosis compared favorably to extended end-to-end anastomosis, with lower rate of late reintervention (8% vs 21%),¹³ and other studies showed similar results.¹⁴

Several groups have shown that the persistence of a hypoplastic segment after repair is a risk factor for late hypertension, early mortality, and late mortality.^5,8,15 In the current study, we presented our results of a surgical alternative that is designed to enlarge the distal aortic arch in addition to coarctation repair and which adds to the established techniques such as end-to-side anastomosis,⁸ extended end-to-end anastomosis, and reverse subclavian flap angioplasty. The latter is currently seldom used, likely due to the well-described long-term upper limb complications (shortening of the left arm and exercise intolerance).¹⁶

The main advantage of our technique is to enlarge the convexity of the distal arch which eliminates the risk of residual crest-like protrusion in the lumen. Secondly, it obviates the need for the use of cardiopulmonary bypass, low-flow selective antegrade cerebral perfusion, or DHCA. This procedure preserves the LSCA and combines the advantages of the extended end-to-end anastomosis, allowing to resect all ductal tissue and to enlarge the inferior aspect of the aortic arch. The only anatomical limitation to this technique is the presence of a bicarotidian (bovine) aortic arch.

Our early mortality, 4.6% for the entire group, might appear higher than other studies.^1,17 However, all but one in-hospital deaths occurred in patients presenting with complex congenital cardiac anomalies. Considering group 1 and 2 altogether, there was only one death (1.3%). As such, those results are in agreement with Kaushal et al (2%)¹⁷ or Rakhra et al (1.3%)¹³ in their subgroup of isolated coarctation. Controversies exist for neonates with coarctation associated with VSD: one-stage or two-stage repair. In our center, we elected to keep a conservative two-stage repair approach even though more centers were embracing the one-stage repair via sternotomy.^18,19

Few centers compared directly one and two-stage repairs for this subgroup, and none showed advantage for a one-stage repair in terms of mortality and morbidity, while claiming shorter overall hospitalization duration.^18,20 Kaushal et al¹⁷ showed that a one-stage repair was a risk factor for early mortality (P < .05). In Melbourne experience, this subgroup of patients had a mortality of 4.3%, a three-fold increase in comparison to their isolated coarctation group.¹³ In a recent analysis from the Society of Thoracic Surgeons (STS) Congenital Heart Database, in-hospital mortality for one-stage repair of coarctation associated with VSD was 4%.²¹

Our results in this subgroup demonstrate that a two-stage repair was associated with a low rate of morbidity and mortality. None of the patients operated later on for VSD closure died during their hospitalization.

Importantly, only 25 (57%) patients of group 2 ultimately required a VSD repair, confirming data from previously published series.²⁰ Among the potential drawback of our technique in comparison to an extended end-to-end repair, we found an increased time of brain perfusion via the right carotid artery only. However, in this series, most neurological complications occurred in the complex coarctation group and none was coarctation repair related.

Using univariate analysis, risks factors for early death were the association of coarctation with a complex cardiac malformation, weight less than 2.5 kg, the need for balloon atrial septostomy, prolonged invasive ventilation, and a prolonged ICU stay together with a longer delay to baseline lactate level following repair. Our results corroborate another study of the STS Congenital Heart Database²² showing that a low weight (<2.5 kg) at operation was a risk factor for mortality.

Recurrence of arch obstruction was found in 15 (13.7%) patients. The reduction of recurrence (9.1%) in the later period of the study favors the hypothesis that there might be a learning curve to the technique.

Importantly, 87% of those recurrences were located at the distal anastomosis and occurred within the first postoperative year. Thirteen patients were successfully treated with balloon angioplasty. Two patients required surgical re-repair, both had underestimated proximal arch hypoplasia at the time of initial repair and underwent successful arch augmentation under CPB later in their follow-up.

Looking at risk factors for recurrence by univariate analysis, we found that a postoperative Zsc at the level of repair < −2 Zsc or an upper–lower limb gradient greater than 10 mm Hg at discharge was a predictor of recurrence. Even though preoperative arch segments have been extensively studied as potential prognostic factors for recurrent obstruction,²³ this report is the first to correlate postrepair dimension with outcome. Similarly, looking at prognostic factor for recurrence after percutaneous balloon angioplasty, Kaine et al found that an isthmus Z value ≤ −2.16 predicted early failure with 91% sensitivity and 85% specificity.²⁴

In contrast to other groups,^4,23 low birth weight was not predictive of recurrence in our study: 2 (18%) out of 11 patients less than 2.5 kg had recurrence. This finding is encouraging, acknowledging that rates of up to 30% to 40% have been reported in the subgroup of neonates with low birth weight.^4,13

Finally, our cohort of patients demonstrated a very low percentage of persisting hypertension after repair (3.7% or 4/109), with only two requiring antihypertensive drugs at follow-up. Pandey et al¹⁶ also reported a 3.3% prevalence in their study using another technique of repair, whereas prevalence of up to 20% has been reported by others.^13,25 The majority of our patients (85%) were operated within 30 days of life; the early repair in this selected group of patients could have positively influence on late outcome.²⁶

Another hypothesis could be that the carotid–subclavian aortoplasty allows to widen the arch at the base of the LCC, so that the thoracic aorta does not always need to be brought up as far into the concavity. Also, the technique widens the convexity of the distal arch and confers a more Romanesque shape to the entire reconstructed arch. This configuration has been shown to positively correlate in terms of vascular remodeling.²⁷

Limitations of the Study

This retrospective study is based on a limited number of patients and spans over 16 years. Another limitation is the absence of a comparative group. In 1998, based on preliminary data from a collaborative center,⁶ one of the surgeons (J.E.R.) elected to operate all patients presenting with distal arch hypoplasia and coarctation using this technique. However, it provided a homogeneous cohort with the same methodology of repair.

Finally, it is likely that the true incidence of persisting hypertension has been underestimated. Indeed, we mostly relied on office BP measurements alone, whereas studies that measured ambulatory and exercise BP reported a much higher incidence of persisting hypertension.

Conclusion

This procedure combines a carotid–subclavian anastomosis to an extended end-to-end anastomosis and allows the enlargement of the distal aortic arch. It is associated with a low mortality rate and an acceptable rate of recoarctation. At long-term follow-up, it is associated with a very low rate of late hypertension.

Patients with an arm–leg gradient >10 mm Hg and/or an isthmus diameter < −2 Zsc after repair should be followed closely. Finally, percutaneous angioplasty is a good technique to relieve obstruction in most of the recurrences.

Footnotes

Authors’ Note

The authors had full control of the design of the study, methods used, outcome parameters, analysis of data, and production of this written report.

Acknowledgments

The authors thank Dr S. Mastrobuoni for his help in statistical reviewing and P. Segers and H. Depasse for their expertise in editorial help.

Declaration of Conflicting Interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

Abbreviations and Acronyms

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