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Ann Thorac Surg 1995;59:33-41
© 1995 The Society of Thoracic Surgeons
Divisions of Cardiac Surgery and Pediatric Cardiology, The Johns Hopkins Medical Institutions, Baltimore, Maryland
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Abstract |
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Introduction |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
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Since 1945 when the first successful repair for coarctation of the aorta (CoA) was performed [1, 2], surgical repair has remained the preferred and primary therapy for CoA. Despite satisfactory results with end-to-end anastomosis (ETE) [3–6], a small but persistent rate of restenosis [3–5] has prompted the further development of repair techniques, such as the subclavian flap aortoplasty (SFA) [7] and patch angioplasty [8, 9], as well as the use of absorbable suture [10] and the application of balloon angioplasty for the treatment of restenosis [11]. Concurrently, there have been advances in the surgical management of the associated cardiac abnormalities, as well as improvements in the approach to perioperative management. The use of prostaglandin E1 (PGE1) to maintain ductal patency has led to an improvement in the preoperative condition in certain patients [12]. Improvements in diagnostic technology have made possible a more accurate evaluation of each patient and a better understanding of the contribution of associated cardiac anomalies to the patient's condition. Despite these changes, significant perioperative morbidity and mortality still attend CoA repair, particularly in neonates [13–16]. This population is at higher risk for complications because of the acute nature of the presentation, the presence of heart failure, and a higher prevalence of other cardiac malformations.
We reviewed three decades' worth of experience with CoA repair in infants and neonates at The Johns Hopkins Hospital to identify changes in the management of patients with CoA and the technique of repair, and to determine whether these changes have resulted in improved survival and restenosis rates.
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Material and Methods |
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). For the purpose of comparison, patients were divided into three groups: group I, 1962 to 1971, 19 patients; group II, 1972 to 1981, 57 patients; and group III, 1982 to 1991, 103 patients. The proportion of neonates (<30 days old at the time of operation) was similar among the groups, making up 60% of group I, 57% of group II, and 70% of group III (p = not significant [NS]). The mean age at diagnosis increased over the three decades, from 19 ± 25 days in group I to 22 ± 41 days in group II and 27 ± 53 days in group III (p = NS). However, the mean age at the time of operation decreased from 58 ± 93 days in group I to 54 ± 89 days in group II and 45 ± 67 days in group III (p = NS). The mean patient weight at the time of operation was not significantly different among the three groups: group I, 4.2 ± 1.7 kg; group II, 3.8 ± 1.7 kg; and group III, 3.9 ± 1.5 kg (p = NS). The frequency of associated cardiac abnormalities varied among the groups (Table 2). Isolated CoA was present in 13% (2 patients) in group I, 19% (10 patients) in group II, and 18% (19 patients) in group III (p = NS). Patent ductus arteriosus (PDA) was more prevalent in group I (27%, 4 patients) than it was in groups II (19%, 10 patients) or III (17%, 17 patients) (p = NS). The frequency of ventricular septal defects (VSDs) with or without PDA decreased over the three decades from 53% (8/15) in group I to 38% (20/53) in group II and 26% (27/103) in group III (p < 0.05). The proportion of patients with complex congenital cardiac abnormalities increased from 7% (1/15) in group I to 25% (13/53) in group II and 39% (40/103) in group III (p < 0.05). A bicuspid aortic valve was present in 35% (60/171) of all the patients. A family history of coarctation or congenital heart disease existed in 68 patients, of whom 17 (25%) had first-degree or second-degree relatives with congenital cardiac abnormalities.
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). The mean gradient between the systolic blood pressure in the upper and lower extremities was similar among the groups: group I, 65 ± 31 mm Hg; group II, 77 ± 52 mm Hg; and group III, 55 ± 30 mm Hg (p = NS). The preoperative use of PGE1 was begun in early 1976; relatively few patients in group II (9%, 5/57) received prostaglandin treatment, compared with group III (55%, 57/103) (p < 0.01). Digoxin and diuretics were the mainstay of therapy in groups I and II.
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). Resection of the CoA with ETE was the primary mode of repair in group I, accounting for 89% (17/19) of the procedures, compared with 58% (33/57) of the repairs performed in group II and 14.5% (15/103) of those done in group III (p < 0.05). Subclavian flap aortoplasty was first performed in our institution in 1978, and constituted 23% (13/57) of the repairs done in group II and 70% (72/103) of the repairs done in group III (p < 0.05). The remaining procedures consisted of patch angioplasty (18 patients), a flap-patch combination (7 patients), or extraanatomic bypass (4 patients). Absorbable suture was introduced into use during the group III period and was used in 39% (39/100). All procedures were performed through a left thoracotomy.
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All surviving patients had postoperative clinic visits every month for 3 months, and then every 3 months for 1 year. Thereafter, most were seen on a yearly or twice-yearly basis. Follow-up information was obtained from clinical records, as well as from direct contact with the patient or local physician.
Twenty-eight clinical variables were subjected to an initial univariate analysis to screen for positive or negative predictors of restenosis and mortality. Variables identified by univariate testing with a p value of less than 0.15 were subjected to a Cox proportional hazards regression analysis. The following variables were examined:
Actuarial survival was determined by the Kaplan-Meier method. Comparisons between groups were performed by an analysis of variance of repeated measures and 
2 tests. All data are represented as the mean ± the standard deviation or as percentages. Actual numbers are included in parentheses. Statistical significance was assigned to differences with a p value of less than 0.05.
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Results |
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). In groups I and II, 100% (10/10) and 81% (44/54), respectively, were given digitalis treatment preoperatively, compared with only 15% (15/100) in group III (p < 0.05, group III versus groups I and II). Diuretic use was similar in the groups (group I, 20%, 2/10; group II, 40%, 17/42; and group III, 36%, 36/100) (p = NS). Prostaglandin E1 was administered in 9% (5/57) of the group II patients and 57% (55/103) of the group III patients (p < 0.01).
Operative and Postoperative Data
In the total series, the intraoperative mortality rate was 3.9% (7/179) and the postoperative mortality rate was 8.9% (16/179), for a total perioperative mortality of 12.8%. The perioperative mortality was 21% (4/19) for group I, 21% (12/57) for group II, and 7% (7/103) for group III (p < 0.05, group III versus groups I and II). All intraoperative deaths were the result of cardiac arrest; all postoperative deaths were due to low cardiac output or sepsis. There were no operative deaths among the patients with an isolated CoA. Pulmonary artery banding was performed in 36% (19/53) of the patients with CoA and VSD; 79% (15/19) of these patients survived. Of the 34 patients with CoA and VSD who did not undergo banding, 88% (30/34) survived the postoperative period (p = NS).
POSTOPERATIVE COMPLICATIONS.
Persistent congestive heart failure after CoA repair occurred in 27% (47/174). Minor complications occurred in 21% (4/19), 26% (15/57), and 23% (24/103) of groups I, II, and III, respectively (p = NS). Twenty-four (14%, 24/174) patients had hypertension postoperatively. Left hemidiaphragm paralysis occurred in 6 patients; right-sided paralysis opposite the CoA was observed in 1. One patient had vocal cord paralysis. Chylothorax developed in 4 and reoperation to manage it was required in 2. Two patients required reoperation for the control of postoperative bleeding. There were no episodes of extremity necrosis on the side of the subclavian artery ligation. There were 21 infections (9 cases of pneumonia, 6 cases of systemic sepsis, and 6 cases of wound infection). There were no cases of paraplegia in this series.
There were no intraoperative or postoperative deaths nor postoperative complications among the patients undergoing isolated CoA repair. Two patients with CoA and PDA died postoperatively. All other deaths occurred in patients with VSD or complex cardiac abnormalities, or with a combination of both.
Among the patients receiving preoperative PGE1 therapy, the operative mortality was 11% (7/62), compared with 15% (23/72) among those not given PGE1 therapy during the same period (p = NS). Of the 62 patients treated with PGE1, 8% (5 patients) had an isolated CoA, 16% (10 patients) had CoA and PDA, 23% (14 patients) had VSD (with or without PDA), and 53% (33 patients) had additional complex intracardiac abnormalities. During the same period, 72 patients were not treated with PGE1 preoperatively. Twenty-six percent (19 patients) had an isolated CoA, 15% (11 patients) had PDA, 42% (30 patients) had an isolated VSD, and 17% (12 patients) had additional complex cardiac abnormalities. The preoperative use of PGE1 was not found to be a predictor of survival (Table 4).
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Forty percent of the group I patients (4/10) required subsequent operations, as did 32% (17/52) of those in group II and 33% (34/103) of those in group III. There were one intraoperative and four postoperative deaths associated with these procedures in group II and two intraoperative and four postoperative deaths in group III. The mean interval between the time of the initial CoA repair and the subsequent secondary procedure was 61.5 ± 43.5 months in group I, 41.8 ± 45.5 months in group II, and 10.3 ± 13.7 months in group III (p < 0.001).
RESTENOSES.
Twenty-five clinically significant restenoses (arm-leg gradient >30 mm Hg in the resting state) occurred in 23 patients, for an overall restenosis rate of 16.4% (23/140). (The threshold arm-leg gradient for repeat intervention at our institution is 30 mm Hg.) Fifty-six percent (5/9) of the group I patients suffered restenoses. Restenoses occurred in 18% (7/39) of the group II patients, but group III had the lowest rate of 12% (11/94) (p < 0.05). The mean time to the diagnosis of restenosis was 6.0 ± 5.3 years in group I, 7.0 ± 4.3 years in group II, and 0.39 ± 0.26 years in group III (p < 0.05).
In group I, 4 patients with restenoses required operation: 2 underwent re-resection with an ETE, 1 had an extraanatomic bypass, and 1 underwent patch repair with prosthetic material. One patient refused reoperation and was lost to follow-up. The patient with restenosis repaired by the ETE technique suffered a second restenosis 10 years later at 24.3 years of age and underwent successful balloon angioplasty. Successful balloon angioplasty was defined by the following two features: no angiographically apparent stenosis, and a residual gradient between the ascending and descending aorta of less than 30 mm Hg. Among the patients in group II, 3 patients with restenoses underwent surgical repair with a patch technique and 4 underwent balloon angioplasty. Balloon angioplasty was used for dilation of eight of the 11 restenoses in group III. Seven balloon procedures were successful; the 1 patient in whom it failed required patch angioplasty for surgical repair 3 months later. Overall, the ages of the patients undergoing balloon angioplasty ranged from 58 days to 24.3 years. Three group III patients with restenosis underwent surgical repair (two patch repairs and one ETE procedure) because the length of the stenosis or aortic tortuosity precluded the performance of balloon angioplasty. No patient in the series required a third CoA repair.
There were no early deaths among those patients who underwent reoperation or balloon angioplasty for the relief of restenosis. One late death occurred during a completion Fontan procedure 5 years after the patient had undergone an operation for relief of the restenosis.
From the standpoint of the risk of restenosis in relation to the surgical repair technique, restenosis occurred a mean of 6.5 ± 5.1 years postoperatively in 23% (12/52) of the patients who underwent ETE repair; this compares with 11% (9/77; p < 0.1) of those who underwent SFA at 0.63 ± 1.0 years and 27% (3/11; p < 0.01) of those who had patch angioplasty at 2.2 ± 2.4 years. From 1962 to 1978 (before SFA was introduced into use at our institution), the restenosis rate was 30% (10/33) among long-term survivors of ETE. Although the overall restenosis rate was lower in association with SFA than with ETE (p < 0.1), neither proved to be significant predictors of freedom from restenosis based on the results of multivariate analysis. However, patch aortoplasty was significantly associated with a risk of restenosis (p < 0.01) (see Table 4).
All but 1 patient with restenosis who had undergone SFA were originally operated on when they were less than 20 days of age, and the great majority of restenoses occurred within 1 year of operation. The only late restenosis among the patients who underwent SFA occurred at 3.4 years in a patient operated on at 18 days of age. Although the follow-up was longer in the ETE group, only three restenoses developed within 1 year of repair (69, 171, and 323 days postoperatively). Younger age at operation was shown by multivariate analysis to be significantly associated with restenosis (p < 0.02) (see Table 4). Also examined was the risk of restenosis in relation to the type of suture used.
The types of suture used for repair in group I were silk and braided polyester. The two types of suture used over the past two decades have been polydioxanone absorbable suture and polypropylene. The restenosis rate by suture type was 18% (6/33) for absorbable suture (4 cases after SFA and 2 after ETE) versus 11% (9/82) for polypropylene (5 cases after SFA, 2 after ETE, and 2 after patch angioplasty, and 42% (8/19) for braided nonabsorbable suture (7 cases after ETE and 1 after patch angioplasty). The use of monofilament nonabsorbable suture (polypropylene) was significantly associated with freedom from restenosis (p < 0.02). The era of operation did not affect the restenosis rate (see Table 4).
Follow-up Findings
In group I, early follow-up information was obtained in 15 patients, and late follow-up data in 10 patients, of whom 9 were long-term survivors. The mean follow-up was 13.8 ± 10.4 years. Three patients had persistent hypertension, and 2 of them required medication. One of these patients suffered leg cramping with exercise, but exhibited no upper-to-lower extremity systolic blood pressure gradient. There was one late mortality (11.3 years postoperatively) stemming from ventricular fibrillation in a patient with aortic valve disease and third-degree heart block.
In group II, the mean follow-up in 39 long-term survivors was 10.9 ± 5.7 years. Three patients had significant hypertension; 1 had undergone successful balloon angioplasty and none were on medication. One patient had persistent leg claudication 20 years after the CoA repair. One patient had moderate congestive heart failure, defined by a need for medication. One patient suffered minor limb length discrepancy after SFA. Limb length differences were deemed to exist if the physician noted a discrepancy during examination at serial follow-up visits. The smallness of the left upper extremities did not preclude near-normal use of the arm in any of the patients involved. There were five late deaths, occurring an average of 2.7 ± 2 years after initial operation, and all occurred at the time of subsequent cardiac operations. One patient could not be weaned from cardiopulmonary bypass, 1 died from a left atrial monitoring line complication, 1 had fatal postoperative bleeding, and 2 died from cardiac failure.
In group III, the mean follow-up was 3.0 ± 2.9 years for 94 long-term survivors among 99 patients. Three patients had significant hypertension; 1 of whom was on medication. Shortening of the left arm was noticeable in 4 patients (4%, 4/94) who had undergone SFA. Leg claudication remained symptomatic in 10 patients despite the absence of a pressure gradient. One patient remained in congestive heart failure. There were 14 late deaths occurring an average of 0.79 ± 0.63 years after CoA repair. Six were associated with subsequent definitive cardiac surgical procedures; all patients involved had complex cardiac abnormalities. Eight late deaths occurred in patients with complex cardiac abnormalities before a definitive surgical repair procedure could be performed; six were due to cardiac failure.
The overall late mortality was 11% (1/9) in group I, 13% (5/39) in group II, and 15% (14/94) in group III (p = NS). The early and late mortalities were significantly higher in patients with other cardiac abnormalities. In patients with isolated CoA or with CoA and PDA, there was a 1.6% (1/62) hospital mortality and no late deaths. In those with VSD, the early mortality was 21% (11/53) and the late mortality was 1.9% (1/53). In those with complex intracardiac abnormalities, the early mortality was 20% (10/51) and the late mortality was 37% (19/51) (p < 0.05 compared with the other categories). For the patients treated in the most recent decade (group III), the hospital mortality for those with CoA and VSD was 5.1% (2/39) and there have been no late deaths. In those patients with complex malformations, the hospital mortality was 19% (5/26), but the late mortality rose to 54% (14/26). Based on the results of multivariate regression analysis, those variables associated with late mortality were younger age at operation, the concurrent performance of pulmonary banding, and the presence of other complex cardiac anomalies (p < 0.01). Surprisingly, the era of operation was not significantly associated with late survival (see Table 4). The overall actuarial survival was 57.7% ± 0.15% in group I at 27.1 years, 65.7% ± 0.07% at 19.7 years in group II, and 77.5% ± 0.04% in group III at 9.3 years (p = NS). The three survival curves were parallel throughout the long-term follow-up period (Fig 3).
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Comment |
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Our results show that SFA was associated with the lowest rate of restenosis. Almost all of the restenoses in these patients occurred within 1 year of operation, and there were virtually no late restenoses in this group. In contrast, ETE was associated with a high rate of late restenosis. The difference in the timing of restenosis is likely real and not an artifact stemming from the earlier diagnosis now possible in the current era. All patients are monitored by serial blood pressure gradient examinations. Before the advent of ultrasonic technology, when restenoses were suspected, aortography and directly measured pressure gradients were used for confirmation. In the current era, echocardiography is done if a restenosis is suspected. Multivariate analysis revealed that neither type of repair was significantly associated with restenoses, even though the incidence of restenosis tended to be lower in association with SFA. Patch aortoplasty, however, was associated with a significantly higher rate of restenoses. Thus, the findings from our study support SFA and ETE as the preferable repair procedures for infants.
Late symptoms were unrelated to the type of repair performed (except for limb length discrepancy after SFA). The frequency of limb length discrepancy was similar for both infant and neonate repairs. In previous reports, both shorter arm length and brachial plexus injuries have been described as consequences of SFA [24, 25]. The decreased arm length observed in our series was minor and did not interfere with normal use of the arm.
Balloon angioplasty is known to be an effective treatment for restenosis [26–28], but it has proved to be less effective in the treatment of primary CoA [29]. Long-term freedom from restenosis has been demonstrated in patients who undergo balloon angioplasty [11]. In our series, balloon angioplasty was associated with an early success rate of 92% (11/12), a figure comparable to that observed for redo CoA repair. The procedure was effective in achieving restenosis regardless of the type of primary surgical repair performed and over a wide age range (58 days to 24.3 years). The lack of postangioplasty mortality (early or late) and morbidity in our series supports the further use of the technique. Reoperation consisting of patch angioplasty, ETE, or an extraanatomic bypass has also been associated with a 96% success rate without mortality [30]. Similarly, Pollack and colleagues [31] observed no perioperative morbidity or mortality in their series and favored the patch technique. We obtained comparable results with reoperation, with only 1 case of late restenosis among 11 cases (9%). Operations for the relief of restenosis have still been necessary despite the availability of balloon angioplasty, because the length and tortuosity of the stenotic aortic segment can render balloon angioplasty inapplicable.
Elevated early mortality and perioperative complication rates have been associated with CoA repair in infants [13, 18, 32]: an early mortality of 20% to 43% has been reported as well as a significant frequency of postoperative complications such as hypertension, postcardiotomy syndrome, pulmonary insufficiency, infection, bleeding, and neurologic injury [13]. The reasons for this higher complication rate among infants include the acute nature of the presentation in severely ill patients, poor response to attempts at medical management, and the need for emergent repair. Acidosis secondary to poor tissue perfusion distal to the CoA often contributes to causing poor cardiac function. The early mortality rates have been even higher in patients with other cardiac abnormalities (25% to 44%) [33]; in our study, virtually all early deaths occurred in patients with additional cardiac abnormalities. Younger age at operation was also a factor associated with higher mortality, because younger infants were more likely to present in severe distress.
The advent of PGE1 therapy in 1976 was temporally associated with improved perioperative survival, even though the prevalence of complex intracardiac abnormalities was greater in these patients than it was in those treated in the earlier era. However, the long-term survival has remained unchanged because of the deaths from cardiac failure that occur while the patients are awaiting a definitive surgical procedure for the repair of complex cardiac malformations. Because of advances in cardiac surgical procedures for the treatment of congenital heart disease, successful repair in small infants is now possible. The interval between CoA repair and definitive repair has also decreased over the past 30 years. In our study, the early mortality was found to be significantly decreased between the first two decades and the third decade. However, the late mortality was higher in the third decade, resulting in no statistical difference in the overall survival among the patients in the three groups. Fifty percent (7/14) of the late deaths in group III occurred before anticipated definitive repair was performed. This shift points up the continued improvement in operative and perioperative management techniques in the current era.
The most significant recent improvement in late results has been observed in patients with CoA and VSD. There was a marked decrease in early mortality, unrelated to changes in the pulmonary artery banding practice. Other authors have advocated either avoiding pulmonary banding in favor of tolerating a moderate ventricular shunt or proceeding to early definitive repair [16, 34]. Banding procedures were associated with improved survival in the series of patients reported on by Hammon [35] and Penkoske [5] and their co-workers. The present study findings do not allow conclusions to be drawn about the appropriate role of pulmonary artery banding in the treatment of complex malformations; they do, however, demonstrate that early and late mortalities among patients with CoA and complex cardiac malformations remain disappointingly high. That the need for concomitant pulmonary artery banding is a significant predictor of late mortality is corroborating evidence indicating that the severity of associated cardiac disease is the primary determinant of postoperative survival in this group of patients.
The design of this study is limited by the fact that it is retrospective and spans three decades. There is also no comparable control group. These factors raise the possibility that there may have been changes in the definitions of the variables studied and in the precision with which they were measured over the course of the three decades. However, the variables assessed have been largely unaffected by changes in technology. The significant associations with restenosis and mortality therefore need to be interpreted in this light. In addition to documenting the evolution in the treatment of CoA over the course of three decades, the findings in our series confirm the excellent early and late survival rates associated with repair of isolated CoA in neonates and infants; they also suggest that SFA and ETE repairs performed with polypropylene suture achieve results superior to those achieved with patch aortoplasty in terms of preventing late restenosis. In the current era, the early and late mortality in infants and neonates undergoing CoA repair depends mainly on the presence or absence of other cardiac malformations.
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Address reprint requests to Dr Cameron, The Johns Hopkins Hospital, 600 N Wolfe St, Blalock 618, Baltimore, MD 21287.
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