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Ann Thorac Surg 1996;62:199-206
© 1996 The Society of Thoracic Surgeons
Department of Cardiothoracic Surgery, Laënnec Hospital, Paris, France
Accepted for publication March 2, 1996.
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Abstract |
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 TopFootnotes Abstract IntroductionPatients and MethodsResultsCommentAcknowledgmentsReferences |
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Methods. From 1974 to 1994, 52 patients underwent a classic complete repair of lesions associated with congenitally corrected transposition. They were divided into two groups: ventricular septal defect plus left ventricular outflow tract obstruction (group I, 37 patients) and isolated ventricular septal defect (group II, 15 patients). Tricuspid plasty or replacement was performed primarily in 1 patient of group I (3%) and in 8 patients of group II (53%).
Results. The overall operative mortality was 15% (8/52 patients), and the incidence of postoperative atrioventricular block was 27% (14/52 patients). Eight patients died secondarily, 5 of heart failure. Survival rates were 83% ± 6% at 1 year and 55% ± 14% at 10 years for group I and 86% ± 9% at 1 year and 71% ± 12% at 10 years for group II (not significant). Redo tricuspid plasty or replacement was performed in 12 patients.
Conclusions. Results of classic complete repair of lesions associated with congenitally corrected transposition are not satisfactory in our experience because (1) the operative mortality and the incidences of tricuspid valve replacement and atrioventricular block are high and (2) secondary heart failure is frequent. However, a retrospective review of morphologic findings shows that "anatomic" complete repairs would not have been feasible in 6 of our patients.
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Introduction |
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TopFootnotesAbstractIntroductionPatients and MethodsResultsCommentAcknowledgmentsReferences |
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The "classic" complete repair of cardiac malformations associated with congenitally corrected transposition of the great arteries (CCTGA) leaves the right ventricle (RV) in a systemic position (in this article, ventricles are named exclusively according to their morphology, and not to their spatial situation). Long-term function of the RV is of major concern after such surgical corrections. Tricuspid insufficiency is present at the time of complete repair in 25% to 40% of patients [1–4], and may contribute to secondary RV failure. Doubts about the ability of the RV to maintain systemic RV function over a long-term period have led to the conception [5] and realization [6–8] of "anatomic" repairs for corrected transposition, connecting the aorta to the left ventricle (LV). The aims of the present study are (1) to specify the results of classic complete repairs after long-term follow-up and (2) to evaluate retrospectively morphologic situations that could have made difficult or impossible an anatomic repair.
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Patients and Methods |
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TopFootnotesAbstractIntroductionPatients and MethodsResultsCommentAcknowledgmentsReferences |
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Corrected Transposition Associated With Ventricular Septal Defect and Pulmonary Stenosis: 37 Patients (Group I)
Mean age at the date of complete classic repair was 12.0 ± 1.2 years (range, 15 months to 33 years). Twenty-one patients had a previous systemic–pulmonary shunt. A second Blalock-De Leval shunt was implanted in 6 patients and a second central shunt in 1 patient.
ANATOMY.
The situs and the spatial position of the heart are given in the list above. Azygos continuation was present in 4 patients, partial anomalous pulmonary venous return in 1 patient, and bilateral superior venae cavae in 7 patients. The LVOTO was a pulmonary atresia in 8 patients and a pulmonary stenosis in 29 patients. Two patients had mild pulmonary stenosis with systolic gradients less than 25 mm Hg; they have not been included in this group, but in group II. Patients with pulmonary stenosis had valvular lesions in 3 cases, subvalvular lesions in 7 cases (5 fibromuscular stenosis, 2 bulging anomalous valvular fibrous tissue), and mixed lesions in 19 cases. Pulmonary artery branch stenosis was present in 7 patients, bilateral in 2 patients, and located at the site of a previous systemic–pulmonary shunt in 6 patients. A sole VSD was perimembranous in 33 patients, extending toward the inlet septum in 2 patients and the muscular-infundibular junction in 1 patient. Multiple VSDs were present in 1 patient. In no case was the VSD flow-limiting. Only 1 patient had preoperative significant tricuspid insufficiency (TI) quoted as moderate (2/4), and due to valvular dysplasia. Tricuspid chordae tendineae were abnormally inserted onto the inferior edge of the VSD in 3 patients, whereas chordae crossed the VSD to insert onto a tricuspid papillary muscle located in the LV (straddling) in only 1 patient.
Congenital mitral anomalies were observed in 4 patients. In these cases, the subvalvular apparatus was always altered: shortness or absence of chordae in 3 patients, absence of anterior papillary muscle in 2 patients, and parachute valve in 1 patient. The septal or "anterior" mitral leaflet (which is in fact posterior in most cases) was divided by a cleft in 2 patients. Atrioventricular valve insufficiency was graded angiographically, echocardiographically, or by both methods. Doppler color flow imaging is now most frequently used for this purpose.
SURGICAL METHODS.
The LVOTO was corrected by an LV-to-pulmonary artery (PA) nonvalved bypass tube in 17 patients, by a valved one in 15 patients (bioprosthesis in 14, aortic homograft with Dacron extension in 1), by a pulmonary commissurotomy in 3, and by a posterior pulmonary annulus enlargement in 2 patients. This latter technique (F. Leca, Laënnec Hospital, and S. Chauvaud, Broussais Hospital, Paris, France) is very similar to that described by Doty and associates [9], but differs from it because the pulmonary incision is not posterior but rather posterolateral and can be extended into the septal (anatomically posterior in CCTGA) leaflet of the mitral valve.
The VSD was approached via the morphologic LV side of the septum in 28 patients (right atrium in 13 patients, left ventricle in 15 patients). The technique described by De Leval and colleagues [5] consisting of a right ventricular insertion of a patch on the anterosuperior margin of the VSD was used in 10 of these 28 patients. The situs was solitus for all of them. The VSD was approached via the morphologic RV side of the septum in 9 patients (through the left atrium in 3 patients having situs solitus and dextrocardia, through the RV in 2 patients both having situs inversus, and through the aorta in 4 patients).
Primary tricuspid valve replacement was performed in 1 patient (moderate TI and dysplasia). Primary mitral valve replacement was performed in 2 patients (severe mitral malformation and mitral insufficiency in both). The LV was undersized in 2 patients who underwent complete repair and concomitant cavobipulmonary shunt.
Corrected Transposition Associated With Ventricular Septal Defect: 15 Patients (Group II)
Mean age at the date of complete classic repair was 5.8 ± 2.0 years (range 4 months to 26 years). Previous coarctation repair and pulmonary artery banding were performed in 4 neonates, and previous pulmonary artery banding was performed in 3 patients at ages of 4, 8, and 21 months.
ANATOMY.
The situs was solitus and the heart position was levocardia in all cases. A sole VSD was perimembranous in 7 patients, extended to the inlet septum in 2 patients, and was muscular-trabecular in 2 patients. In 2 patients who had undergone previous pulmonary artery banding, multiple trabecular VSDs were closed, and only one perimembranous VSD was found at the time of complete repair. In 2 other patients, multiple VSDs were only diagnosed after complete repair, due to persisting VSD at echocardiographic controls. A sole VSD was restrictive in 3 patients aged 4 months, 7 months, and 5 years (partial occlusion by fibrous atrioventricular [AV] valvular tissue). Preoperative TI reported as moderate to massive was found in 9 patients. Its mechanism was septal leaflet joining with restrictive motion, with or without minimal RV atrialization (pseudo-Ebstein) in 5 patients, dysplasia in 2 patients, and annular distention in 2 patients. Tricuspid chordae tendineae were abnormally inserted onto the edge of the VSD in 4 patients, whereas chordae crossed the VSD to insert onto a tricuspid papillar muscle located in the LV (straddling) in 3 patients. No congenital mitral anomalies were observed. A significant functional mitral insufficiency was only observed in 1 patient.
SURGICAL METHODS.
The VSD was closed with a patch in 14 patients and by five separate felt-buttressed stitches in 1 patient. It was approached via the right atrium in 10 patients and via the LV in 5 patients (fibrous tissue). The technique of De Leval and associates [5] was used in only 1 patient. The banding was simply withdrawn in 2 patients; in other 3 patients, an enlarging pulmonary trunk plasty was performed using a patch, and was extended to the right branch in 1 patient. Tricuspid valve replacement was performed at the same time as VSD closure in 6 patients, a tricuspid plasty in 1 patient, and a double mitral and tricuspid plasty in 1 patient. A pacemaker was implanted primarily in 1 patient who was suffering from congenital AV block.
Statistical Methods
Means are given with their standard error. Comparison between two qualitative variables were performed using the 
2 test (with the Yates correction when necessary). Survival rates were determined using the Kaplan-Meier method, and were compared with the log-rank test. Statistical significance was determined at p less than 0.05.
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Results |
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TopFootnotesAbstractIntroductionPatients and MethodsResultsCommentAcknowledgmentsReferences |
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). The mean age of patients who died is 17.2 years versus 11.0 years for patients who survived (not significant). Nine patients (24%) had a complete AV block persisting more than 3 weeks after the operation. A pacemaker was implanted in 8 of them, whereas 1 died early. Complete AV block regressed spontaneously in 8 more patients. Univariate analysis did not find any significant risk factor for postoperative AV block, partly because only a few patients were included. However, only 1 of 10 patients with situs inversus versus 8 of 27 patients with situs solitus experienced early AV block; similarly, none of the 8 patients with pulmonary atresia had early AV block versus 9 of 29 patients with pulmonary stenosis. In our experience, the use of the de Leval technique did not lower the incidence of postoperative AV block. The RV approach for VSD closure led to an AV block in only 1 of 9 patients (Table 2).
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) and 3 for residual VSD. Another patient had a chylothorax that relapsed after prolonged chest drainage.
LATE RESULTS.
Five patients were lost to follow-up 1, 10, 23, 57, and 113 months after the complete repair. Mean follow-up is 58 ± 9 months (range, 1 to 198 months). There were six late deaths (Table 3). Five patients were reoperated on for secondary tricuspid valve replacement (4 patients, one redo procedure) or plasty (1 patient) (Table 4). Among them 2 patients died because of tricuspid valve thrombosis due to noncompliance with oral anticoagulation treatment in 1 and global cardiac insufficiency in the other. Actually 2 more patients have moderate TI and have not yet been reoperated on because their RV is not failing.
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A secondary procedure was performed on the pulmonary outflow tract in 4 patients: take-down of the pulmonary bioprosthesis in 1, insertion of a pulmonary bioprosthesis in 1, and percutaneous valvuloplasty in 2. Six more patients had a mean LV-PA gradient greater than 50 mm Hg but underwent no secondary procedure. Implantation of a pacemaker was necessary in 1 patient who suffered from late spontaneous AV block 7 months after the complete repair.
The survival rate is 83% ± 6%, 69% ± 8%, and 55% ± 14%, respectively after 1, 5, and 10 years of follow-up (Fig 1). Freedom from pacemaker implantation and tricuspid valve replacement or repair in survivors is, respectively, 56% ± 8%, 40% ± 9%, and 30% ± 11%.
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). A pacemaker was implanted in 5 patients (33%) who had a complete AV block persisting more than 3 weeks. A complete AV block was spontaneously regressive in 2 other patients. One patient (patient 11, Table 4) underwent early replacement of the tricuspid valve because of a septal leaflet retraction by the VSD patch, which was inserted onto it. Early postoperative complications were severe supraventricular arrhythmia in 2 patients, pneumothorax in 1 patient, cardiac tamponade in 1 patient (surgical drainage), and RV failure necessitating prolonged ventilatory support in 2 patients.
LATE RESULTS.
Two patients were lost to follow-up 6 and 15 months after the complete repair. Mean follow-up is 91 ± 20 months (range 1 to 228 months). Two patients died late (Table 3). Six patients were reoperated on for secondary tricuspid valve replacement (4 patients, three redo procedures), or plasty (2 patients, one redo procedure). One patient underwent orthotopic transplantation 26 months after the VSD closure because of progressive heart failure (patient 17, Table 4). On the whole, 12 of 15 patients in group II have not kept their native tricuspid valve at the end of the follow-up (9 replacements, 2 plasties, and 1 heart transplantation). Among these 12 patients, 3 had cardiac insufficiency, which was the cause of death in 2 of them. Current status is unsatisfactory in both patients treated by plasty: 1 patient is asymptomatic 192 months after the VSD closure (patient 7, Table 4) but moderate TI is observed at echocardiography and the RV is hypokinetic and dilated (echocardiographic telediastolic diameter = 65 mm, telesystolic diameter = 50 mm, shortening fraction = 0.23); the other patient (patient 16, Table 4) has important TI with mild congestive symptoms 245 months after the VSD closure, but the patient refuses reoperation. Moderate TI is present in 2 of the 3 patients who still have their native tricuspid valve without a plasty procedure. No secondary AV block was observed in this group.
The survival rate is 86% ± 9% after 1 year and 71% ± 12% after 5 and 10 years of follow-up (Fig 2). There is no significant difference in the survival rates over the 10-year follow-up between groups I and II. Freedom from death, pacemaker implantation, and tricuspid valve replacement or repair in survivors is 14% ± 9% after 1, 5, and 10 years of follow-up in group II, which is significantly less than in group I (p < 0.05).
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Comment |
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TopFootnotesAbstractIntroductionPatients and MethodsResultsCommentAcknowledgmentsReferences |
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When LVOTO is associated with VSD (group I) (1) situs and heart position abnormalities are frequent, (2) preoperative tricuspid valve insufficiency is unusual, (3) the LV may be underdeveloped as previously reported by others [10, 11], (4) mitral malformation is frequent and can be very severe, and (5) the VSD is large. When CCTGA is associated with VSD but not with LVOTO (group II) (1) patients undergo complete repair at a younger age, (2) situs and position abnormalities are rare, (3) tricuspid malformations and insufficiency are frequent, (4) the VSD may be restrictive, and (5) VSDs may be multiple. Surgical results also differ significantly between these two groups: late tricuspid valve replacement and pacemaker implantation are more frequent when no LVOTO is present.
Mortality
Postoperative mortality of classic complete repair (15% for the whole population) is high in our experience as well as for others: 9% to 18% [3–5, 12, 13], and is not different between groups I and II. Changes in operative and perioperative management do not explain this fact: 5 of the 8 early deaths occurred during the last 10 years of the study. Special difficulties due to late referral (patient 3, Table 1), severe postoperative supraventricular arrhythmia (patients 6 and 7), undiagnosed mitral anomaly (patient 4), and irreversible preoperative neurologic lesion (patient 8) for the most part explain these unfavorable courses (Table 1).
Atrioventricular Blocks
The incidence of postoperative complete AV block is also very high (27%) and is not significantly different between groups I and II. However, it is comparable with other published results (26% to 33%) [14, 15].
Various surgical techniques have been propounded to lower the AV block risk during VSD closure in CCTGA with situs solitus [3, 5, 16, 17]. In our experience, 3 of 11 patients (27%) who underwent the De Leval technique [5] had postoperative AV block. Our results concerning the aortic approach [16, 17] are encouraging (no AV block among 4 patients). Unfortunately, this technique is not always feasible, especially in the case of a large conus. Atrioventricular blocks are rare in our experience when the VSD is closed via the morphologically right side of the septum (1/9 patients = 11%). This is a matter of interest concerning anatomic repairs of CCTGA associated with VSD and LVOTO.
Left Ventricular Outflow Tract Obstruction
An LV–PA tube was most often used for the relief of LVOTO. A nonvalved tube was implanted in 17 patients. This decision was grounded on the subpulmonary position of the LV, and aimed at reducing late pulmonary bioprosthesis failure. It was taken from the beginning of our experience and was extended throughout the period under study. No significant differences of early and late outcomes were observed when comparing patients with valved and nonvalved tubes. However, two early deaths would perhaps have been avoided if the LV–PA tubes had been valved. Nevertheless, valve interposition on the LV outflow tract appears to be indicated for us only if (1) the pulmonary tree is deficient (stenosis of arterial branches, lobar amputations, large collaterals), (2) there is PA hypertension, and (3) the mitral valve is not continent. Nonvalvulation does not guarantee the absence of late reoperation for recurrent LVOTO, mainly due to fibrous pannus obstruction of the tube. A posterolateral enlargement of the pulmonary annulus was performed in 2 patients with satisfactory immediate and late results of the LV–PA gradient, but with complete AV block in 1 patient. Before making a posterior pulmonary enlargement, it is necessary to look at the circumflex artery, whose anomalous course behind the PA contraindicates this technique. Unlike with the original technique described by Doty and associates [9], we found that the section of the pulmonary trunk is helpful to perform the pulmonary annulus incision under complete control of the vision.
Tricuspid Valve Replacement
Tricuspid valve plasty or replacement was performed during the complete repair in 9 of 52 patients (17%), which can be compared with the incidence reported by others (16% [12], 26% [11], 33% [18]).
If not primarily corrected, significant TI is a risk factor for early death [3, 14]. Furthermore, tricuspid valve insufficiency has been reported to develop after VSD closure [18]. Our policy was to replace tricuspid valves in the systemic position early, as soon as TI was measured as 2/4 or more. We had to replace those valves because tricuspid plasty is not satisfactory in corrected transposition. Of course, mechanical prosthetic valve replacement cannot be considered a success in children [19]. However, a 25 mm or larger valve was implanted in 9 of 13 patients. Tricuspid replacement may have contributed to stop or prevent RV dysfunction, but our data do not allow us to support such a hypothesis. In the Mayo Clinic experience, tricuspid valve replacement did not prevent death caused by systemic ventricular failure in 12 of 40 patients (30%) [18]. Whether the right systemic ventricle of patients suffering from double discordance will faster and more frequently become insufficient after tricuspid replacement than left systemic ventricle of "normal" patients whose mitral valve has been replaced is a question that has not yet been answered to our knowledge.
The secondary increase or emergence of TI is frequent in our experience (11/44 operative survivors = 25%, 8 of them having been reoperated on), as well as in other studies (8% [12], 13% [13], 17% [14]).
Heart Failure and "Anatomic" Repairs
Heart failure is the most frequent secondary complication after classic complete repair of lesions associated with corrected transposition. Therefore, the main question about such surgical treatment is what will be the late outcome of the systemic RV. The ejection fraction at rest is not considered to satisfactorily reflect the RV function [20–22]. In case of isolated CCTGA, the increase of the RV ejection fraction after exercise has been reported to be adequate in some cases [20] and inadequate in others [22]. Late death is due to cardiac failure in 100% of patients for van Son and associates [18], in 70% of patients for McGrath and co-workers [12], and in 55% (5/9 patients) in our own experience.
The anatomic corrections, which connect the LV to the aorta, have been conceived to prevent such fatal outcomes [5–8]. Their rationales are (1) better long-term function of the LV in its "natural" systemic position, and (2) in case of TI, avoidance of tricuspid valve replacement by repositioning in the low-pressure subpulmonary position [7, 23, 24]. Such anatomic corrections are technically demanding because they associate either atrial and arterial switches in case of unrestrictive isolated VSD, or atrial switch, LV-to-aorta blood rerouting, and RV–PA tube when an LVOTO is present.
Our retrospective study calls attention to morphologic situations that could have made anatomic repair impossible in 6 of 52 patients: (1) 4 patients had a severe mitral anomaly (also previously reported by others in CCTGA [25]) and (2) 2 patients treated by additional cavopulmonary shunts had hypoplastic LV. Furthermore, anatomic repair would have been difficult in other unfavorable morphologic situations: 20 patients with LVOTO had heart malposition (mesocardia), which could hinder RV–PA tube placement, 1 patient had a criss-cross heart, and 1 patient had mitral straddling. Other circumstances may also be detrimental. A developed subaortic conus can make the LV-to-aorta rerouting via the VSD difficult [26], and restrictive VSD (observed exclusively when no LVOTO is present in our experience) necessitates preparatory PA banding [27]. Only 10 of 19 patients (52%) reported by the Osaka group underwent anatomic repair, probably because such unfavorable situations may have been encountered in 9 cases [8].
Both early and late results of the classic repair of corrected transposition are less than satisfactory. Therefore, this study does not argue against anatomic complete repairs, which may demonstrate a real surgical advancement in future years, especially for early correction of severe TI in CCTGA without LVOTO [24]. However, we think that indications for anatomic corrections have to be determined very precisely with exhaustive preoperative morphologic data.
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M. Imamura, J. J. Drummond-Webb, D. J. Murphy Jr, L. R. Prieto, L. A. Latson, S. D. Flamm, and R. B.B. Mee Results of the double switch operation in the current era Ann. Thorac. Surg., July 1, 2000; 70(1): 100 - 105. [Abstract] [Full Text] [PDF]
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T. Yeh Jr, M. S. Connelly, J. G. Coles, G. D. Webb, P. R. McLaughlin, R. M. Freedom, P. B. Cerrito, and W. G. Williams ATRIOVENTRICULAR DISCORDANCE: RESULTS OF REPAIR IN 127 PATIENTS J. Thorac. Cardiovasc. Surg., June 1, 1999; 117(6): 1190 - 1211. [Abstract] [Full Text] [PDF]
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 C Alva, E Horowitz, S Y Ho, M L Rigby, and R H Anderson The feasibility of complete anatomical correction in the setting of discordant atrioventricular connections Heart, May 1, 1999; 81(5): 539 - 545. [Abstract] [Full Text]
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R. Sharma, A. Bhan, R. Juneja, S. Sunder Kothari, A. Saxena, and P. Venugopal Double switch for congenitally corrected transposition of the great arteries Eur J Cardiothorac Surg, March 1, 1999; 15(3): 276 - 282. [Abstract] [Full Text] [PDF]
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O STUMPER and W J BRAWN Anatomic repair of double discordant hearts Heart, November 1, 1998; 80(5): 424 - 425. [Full Text]
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M. H. Helvind, J. F. McCarthy, M. Imamura, L. Prieto, G. E. Sarris, J. J. Drummond-Webb, and R. B. B. Mee Ventriculo-arterial discordance: switching the morphologically left ventricle into the systemic circulation after 3 months of age Eur J Cardiothorac Surg, August 1, 1998; 14(2): 173 - 178. [Abstract] [Full Text] [PDF]
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D. Metras, B. Kreitmann, A. Fraisse, A. Riberi, F. Wernert, C. Nassi, C. Cestino, and M. Voisin Anatomic repair of corrected transposition or atrio-ventricular discordance: Report of 8 cases Eur J Cardiothorac Surg, February 1, 1998; 13(2): 117 - 123. [Abstract] [Full Text] [PDF]
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T. R. Karl, R. G. Weintraub, C. P. Brizard, A. D. Cochrane, and R. B. B. Mee Senning Plus Arterial Switch Operation for Discordant (Congenitally Corrected) Transposition Ann. Thorac. Surg., August 1, 1997; 64(2): 495 - 502. [Abstract] [Full Text]
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