Options for surgical repair in hearts with univentricular atrioventricular connection and subaortic stenosis

J

THORAC CARDIOVASC SURG

1990;100:672-81

Options for surgical repair in hearts with univentricular atrioventricular connection and subaortic stenosis Thirteen patients bave undergone surgical treatment because of subaortic obstruction in hearts with a univentricuJar atrioventricular connection. Nine patients underwent surgical enlargement of the ventricular septal defect and four patients bad construction of an aortopulmonary anastomosis and closure of the pulmonary trunk (the Damus-Kaye-Stansel procedure). Two patients undergoing enlargement of the septal defect and two having the Damus-Kaye-Stansel procedure also bad a modified Fontan procedure•. One patient had complete atrioventricular dissociation after direct enlargement of the ventricular septal defect, which necessitated insertion of an epicardial pacemaker. One patient died within 30 days of the operation after enlargement of the defect and two patients after the Damus-Kaye-Stansel procedure. There was one late death, occurring in a patient who underwent enlargement of the ventricular septal defect Ten patients bave subsequently undergone conventional cardiac catheterization and angiography or transcutaneous Doppler flow studies to assess the relief of the subaortic obstruction. The result has been satisfactory in aU. Because of this experience, we now recommend direct surgical enlargement of the restrictive ventricualr septal defect for direct relief of subaortic stenosis occurring with a univentricular atrioventricular connection to a dominant left ventricle, inasmuch as it appears to be hemodynamically effective with a low operative mortality and morbidity The Damus-Kaye-Stansel procedure can also bave a role in relieving subaortic stenosis when the atria are connected to a dominant right ventricle.

Henry C. Cheung, FRCS, Christopher Lincoln, FRCS, Robert H. Anderson, BSC, MD, FRCPath, Siew Yen Ho, BSc, PhD, Elliot A. Shinebourne, MD, FRCP, Simos Pallides, MD, and Michael L. Rigby, MD, FRCP, London, England

In patients with a univentricular atrioventricular (AV) connection to a dominant left ventricle in whom the ventriculoarterial (VA) connection is discordant, the ventricular septal defect may be restrictive and there may be muscular subaortic obstruction within the rudimentary right ventricle, so that there are two potential sites for subaortic obstruction. These may be part of the malforFrom the National Heart and Lung Institute and Hospitals, London, England. R.H.A. and S.Y.H. are supported by the British Heart Foundation together with the Joesph Levy Foundation. Received for publication April25, 1989. Accepted for publication Dec. I, 1989 Address for reprints: Christopher Lincoln, Brompton Hospital, Fulham Road, London, SW3 6HP, England.

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mation itself or may develop after banding of the pulmonary trunk, when the latter is performed at an early age to protect the pulmonary vasculature. 1•3 The resultant hypertrophy and functional impairment of the dominant ventricle have been said to impart a prohibitively high risk on subsequent corrective operations. 4• 5 Subaortic stenosis can also be a problem when there is double inlet to a dominant right ventricle and a concordant VA connection. Surgical options for the patients with a dominant left ventricle include either a direct approach at the site of obstruction, with enlargement of the restrictive ventricular septal defect, or a bypass of the obstruction by transection of the pulmonary truck and anastomosis of its proximal end to the aorta (Damus-Kaye-Stansel procedure). The Damus-Kaye-Stansel procedure is the only option when there is subaortic stenosis with double-inlet right ventricle and a concordant VA connection. We

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Subaortic stenosis in univentricular A V connection 6 7 3

Left

Right sided rudimentary ventricle

Fig. 1. Diagrammatic representation of the anatomy as seen by the surgeon through the opened rudimentary and incomplete right ventricle in hearts with dominant left ventricle. The inset shows the terms used for description of the margins of the ventricular septal defect. The dotted lines show the anticipated course of the A V conduction axis, which descends on the dominant ventricular aspect of the septum.

report here our operative results on patients with such anatomic anomalies in whom either direct resection or a bypass procedure was performed to relieve the subaortic stenosis.

Patients and methods Between January 1985 and December 1988, 13 patients required operation, 12 having a univentricular A V connection to a dominant left ventricle and a discordant VA connection with restriction of the ventricular septal defect. The other patient had double inlet to a dominant right ventricle with a rudimentary left ventricle and a concordant VA connection. The clinical data are summarized in Table I. All patients had been brought for treatment in the first year of life. Twelve had undergone palliative operations by banding of the pulmonary trunk, and one also required a modified Blalock-Taussig shunt 4 years afterward. A systemic-pulmonary shunt had been constructed to provide initial palliation in the remaining patient (patient !). Four patients required concurrent repair of aortic coarctation during the banding procedure and one underwent correction of an interruped aortic arch. Subaortic obstruction was demonstrated in seven patients at the initial catheterization. In the remaining six, it was detected

at subsequent catheterization I to 10 years (mean 5.0 ± 0.6 years) after the initial banding procedure. The gradient between the aorta and the morphologically left ventricle before relief of obstruction was between 15 and 105 mm Hg (mean 39.6 ± 8.7 mm Hg). No gradient could be demonstrated in two patients, even though the ventricular defect appeared convincingly restrictive at both echocardiography and angiography. All had significant ventricular hypertrophy. This was so severe in one patient (patient 6) that cavity obliteration was demonstrated. Surgical anatomy. In all the patients with a dominant left ventricle, the ventricular septal defect was bounded superiorly by the outlet septum (the muscular mass separating the su baortic outflow tract of the rudimentary and incomplete right ventricle from the subpulmonary outflow tract of the dominant ventricle). Its apical border was the crest of the apical muscular septum. The other boundaries of the defect were also muscular, joining the roof and floor, and when viewed from the rudimentary ventricle (Fig. 1), could be designated as the right and left borders according to whether they were closest to the acute or obtuse margins of the ventricular mass. This arrangement and description of the borders of the defect held good irrespective of whether the rudimentary right ventricle was located on the right or left shoulder of the ventricular mass or was directly anterior (Fig. 1). The most significant relation of the defect was to the

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Table I Patient No.

2 3 4 5 6

7 8

9 10 11

12 13

Diagnosis RA VV A, VA discordance, restrictive VSD DIL V, VA discordance, restrictive VSD D IL V, VA discordance, restrictive VSD, IAA RA VV A, VA discordance, restrictive VSD, coarctation DILV, VA discordance, restrictive VSD, coarctation DILV, VA discordance, restrictive VSD DILV, VA discordance, restrictive VSD, coarctation DIRV, VA concordance

DILV, VA discordance, restrictive VSD RA VV A, VA discordance, restrictive VSD LA VV A, VA discordance, restrictive VSD, restrictive ASD DILV, VA discordance, restrictive VSD, coarctation DILV, VA discordance, restrictive VSD

First palliative operation (age)

Operation for SAO relief

Age SAO detected/relieved

RBTS ( 1.8 yr)

60 days/8 yr

Enlarge VSD

PAB (147 days)

85 days/3.3 yr

Enlarge VSD (failed DKS)

40 days/0.35 yr 0.6 yr 59 days/ 1.5 yr

Enlarge VSD Reenlarge VSD, patch RVOT Enlarge VSD, patch R VOT

6 days/4 yr

Enlarge VSD, patch R VOT

3.5 yr /3.5 yr

Enlarge VSD, patch RVOT

PAB, correction of coarctation (85 days) RBTS (4.5 yr) PAB (7 days)

8yr/8yr

DKS

!Oyrj!Oyr

DKS

PAB (300 days)

4 yr/4 yr

DKS

PAB (90 days)

I yr/1.3 yr

DKS

PAB (60 days)

60 days/0.75 yr

Enlarge VSD, patch RVOT

PAB, correction of coarctation ( 13 days) PAB (!50 days), reband PA (240 days)

7 days/ 1.6 yr

Enlarge VSD, patch RVPT

6yrj6yr

Enlarge VSD

PAB, correction of coarctation (50 days) PAB, correction of coarctation (6 days) PAB (49 days)

SAO, Subaortic obstruction; RAY VA, right atrioventricular valve atresia; VA, ventriculoarterial, VSD, ventricular septal defect; DIL V, double-inlet left ventricle; IAA, interrupted aortic arch; LA VV A, left atrioventricular valve atresia; ASD, atrial septal defect; RBTS, right Blalock-Taussig shunt: PAB, pulmonary artery banding; PA, pulmonary artery; DKS, Damus-Kaye-Stansel; RVOT, right ventricular outflow tract; AscAo, descending aorta; RPA, rig~t pulmonary artery; RAVV, right atrioventricular valve; LA VV, left atrioventricular valve; R-L, right-to-left.

A V conduction axis. In all patients, again irrespective of the position of the rudimentary ventricle, the axis was carried on the left ventricular aspect of the apical septum closest to the right border of the defect. The safe areas for surgical enlargement, therefore, were either the roof of the defect (the outlet septum) or else the segment of apical septum closest to the obtuse margin of the heart (the left border of the defect, Fig. 2). In the patient with a dominant right ventricle, the lesion represented, in essence, the extreme form of an A V septal defect with right ventricular dominance. The subaortic outflow tract arising from the rudimentary left ventricle was tightly sandwiched between the scooped-out septum and the bound-down superior bridging component of the A V valve. Because direct relief of this extensive area of obstruction was impossible, the only surgical option was a Damus-Kaye-Stansel procedure. Surgery. Relief of subaortic obstruction was performed between4.5monthsand !Oyearsofage(mean4.0 ± 0.7years), 6 months to 10 years (mean 4.7 ± 0.6 years) after the initial banding procedure. Surgical relief of obstruction together with correction of interrupted aortic arch and banding of the pulmonary trunk was attempted in only one patient (patient 3) at the age of 4.5 months. The obstruction recurred in this child and he required a second operation 2 months later. Nine patients underwent direct enlargement of the ventricular septal defect. A transventricular approach was used, involv-

ing a vertical incision in the pariental wall of the rudimentary and incomplete right ventricle. The incision was directly in line with the long axis of the first part of the ascending aorta, the location of the rudimentary ventricle usually being evident because of the major coronary arteries at its right and left lateral borders (Fig. I). A generous myotomy made in the border of the defect closest to the obtuse margin of the ventricular mass, cutting toward the ventricular apex, enlarged it dramatically, allowing free communication between the ventricles. In six patients the thickness of the parietal wall of the rudimentary right ventricle was noted to be an additional limiting factor, and in these cases an Impra gusset (Impra, Inc., Tempe, Ariz.) was used to enlarge the "roof' of the oufiow tract (Fig. 3 ). A modified Fontan procedure constructed according to the method of Kreutzer and his colleagues6 was performed at the same operation in two patients of this group. A Damus-Kaye-Stansel operation 7· 10 combined with a modified Fontan operation was performed in four patients, including the one with a dominant right ventricle. This operation was also attempted in a fifth patient (patient 2) but was abandoned subsequently because of gross pulmonary incompetence caused by valvular distortion, itself induced by the previously placed band that had migrated proximally on the pulmonary trunk. The anastomosis, therefore, had to be revised. The transected proximal end of the pulmonary trunk was closed and the

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Concurrent (subsequent) operation

Subaortic stenosis in univentricular A V connection 6 7 5

Aortic gradient (mm Hg)

Duration of follow-up

Preop.

Postop.

Modified Fontan

17

5 (recath)

3 yr

Alive and well

RBTS, close PA

60

0 (recath)

1.6 yr

Alive and well

Repair IAA, PAB

6 40 15

0 (recath) 0 (echo)

0.75 yr

Alive and well Died 9 mo postop

57

16 (echo)

1.5 yr

Alive and well

AscAo-RPA shunt, pacemaker insertion Modified Fontan

105

0 (recath)

0.35

Alive and well

0 (recath)

3.5 yr

Alive and well

Modified Fontan (reclose RAVV, LA VV annuloplasty 6 days postop.) Modified Fontan

50

0 (recath)

3 yr

Alive, cyanotic (small R-L shunt)

Modified Fontan (reclose ASD) 3 days postop.

30 0.5 yr

Operative death (3 days) Operative death (3 days) Alive and well

I mo

Operative death (suddenly 8 days) Alive and well

15

30

0 (recath)

17 Modified Fontan

0

pulmonary artery was detached. The pulmonary arterial circulation was maintained by construction of an aortopulmonary anastomosis with a 6 mm segment of Impra polytetraftuoroethylene graft. The ventricular septal defect was then enlarged directly.

Results One of the nine patients (patient 12) who underwent direct enlargement of the ventricular septal defect died unexpectedly on the eighth day after a smooth postoperative course, for a hospital mortality rate of 11%. At autopsy the ventricular septal defect was found to be large and nonrestrictive (Fig. 4) and the resection was judged to be well clear of the A V conduction axis. Complete heart block did develop postoperatively in one patient (patient 6), however. She was found to have severe ventricular hypertrophy with a gradient of 105 mm Hg between the ventricles. Extensive muscular resection had been necessary to relieve the obstruction, and a shunt was constructed from the ascending aorta to the right pulmonary artery to improve the pulmonary blood flow. She required ventricular pacing postoperatively and had a protracted postoperative course. Despite this stormy course she now remains free of symptoms 4 months after the operation. The other patients who had enlargement of ventricular

0 (echo)

Outcome and status

septal defect alone enjoyed a smooth recovery with an average stay in the intensive care unit of 3 days. Both patients survived who had a Fontan repair concomitant with enlargement of the septal defect, although they required a much longer hospital stay. The follow-up periods of the surviving eight patients are between 1 month and 3 years (mean 1.1 ± 0.5 years). There was one late death (patient 4), which occurred 9 months after surgical enlargment of the restrictive defect. Autopsy again showed a good-sized venticular septal defect and preservation of the A V conduction axis. Recurrent obstruction necessitating a second operation developed in one patient. This patient had undergone banding of the pulmonary trunk, correction of an interrupted aortic arch, and initial enlargement of the ventricular septal defect at the age of 4.5 months as a combined primary procedure. After the second operation, which was done at the age of 7.2 months, there was no further recurrence of obstruction. Five patients who had undergone enlargement of the defect underwent cardiac catheterization and angiography. The ventricular septal defect was shown to be widely patent in all (Fig. 5). No gradient was found either across the aorta or between the ventricles in four of them. The fifth, who also had a Fontan procedure, had a

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Outlet

Right border & conduction axis Fig. 2. Upper panel, Left-sided rudimentary and incomplete right ventricle from a heart wlith double-inlet left ventricle orientated as it might be seen by the surgeon in the operating room. Lower panel, Terms used for description of the borders of the ventricular septal defect (see Fig. I). Note the site of the wedge of septal tissue which, according to our experience, can safely be reviewed at operation. The heart is from the Cardiopathological Museum of Children's Hospital of Pittsburgh and is photographed and reproduced by kind permission of Dr. J. R. Zuberbuhler.

gradient of 5 mm Hg. Despite this, she remains free of symptoms. One patient who refused recatheterization had Doppler echocardiographic studies that demonstrated a gradient of 16 mm Hg. She is well with good exercise tolerance. The remaining patient, who underwent operation just 1 month ago, had no demonstrable gradients on Doppler studies. Excluding the patient in whom the procedure was abandoned (patient 2), four patients underwent a DamusKaye-Stansel procedure concomitant with a modified Fontan operation. Two died on the third postoperative

day because of persistent low cardiac output. Of these, one was found to have a right-to-left shunt across a leak in the patch closing the atrial septum (patient 10). He underwent reoperation but could not be revived. A third patient (patient 8), who had a dominant right ventricle and obstruction of the subaortic outlet from the rudimentary left ventricle, was found to have a leak in the patch used to close the right A V valve, this being sufficiently large to result in arterial desaturation. He underwent reexplr mtion on the sixth postoperative day and the site of leakage was closed. An annuloplasty was also per-

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Subaortic stenosis in univentricular A V connection 6 7 7

Fig. 3. Sequence of surgical procedures, culminating in insertion of a gusset to enlarge the subaortic infundibulum. Compare with Figs. I and 2.

formed in the left AV valve because of significnt regurgitation across it. He survived after a protracted postoperative course. On follow-up after 3 years he was mildy cyanotic on exertion but could participate in normal activities (including swimming). Cardiac catheterization showed a small residual right-to-left shunt. No gradient could be demonstrated between the ventricles and the aorta. The other surviving patient in this group who had double-inlet left ventricle is well and free of symptoms. He was restudied 3.5 years after the operation. An angiogram showed the pers~tently small ventricular septal defect and the widely patent aortopulmonary anastomosis (Fig. 6). There was no gradient between the aorta and the ventricles. Discussion The univentricular AV connection is now a well-established entity among congenital cardiac malformations, the treatment of which remains a challenge to both physicians and surgeons. The current policy for "correction" adopted by most centers involves a Fontan procedure or, more rarely, a ventricular septation in suitably selected cases. Either procedure is usually performed during mid or late childhood.4• 6• II-! 4 In most cases, this deliberate

delay in the corrective operation necessitates protection of the pulmonary vasculature by means of banding of the pulmonary truck in infancy or early childhood. This procedure itself, when the atria are connected to a dominant left ventricle, has been shown to precipitate ventricular hypertrophy and subaortic obstruction because of restriction at the ventricular septal defect. 1• 3 When (and if) it occurs, this complication must be relieved promptly because its presence substantially increases the hazards of a subsequent "corrective" operation.4 • 5 The simplest and most logical way of relieving the subaortic obstruction when there is univentricular connection to a dominant left ventricle (double inlet or tricuspid atresia) is to enlarge the site of restriction, which is usually the ventricular septal defect. Early attempts at this procedure met with an extremely high mortality. One of the most important reasons for failure was the prevalence of complete heart block, this being the direct result of damage to the AV conduction axis, which is intimately related to the borders of the ventrictilar septal defect. 14 With sound knowledge on the disposition of this conduction axis, this highly fatal complication can be avoided. There is apparently still some uncertainty (albeit unjustified) regarding the location of these vital tissues. 15 It is

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Fig. 4. Morphologic features of the rudimentary right ventricle in patient 12, who died 8 days after enlargement of the ventricular septal defect. The communication produced is widely patent and the tissue resected is well clear of the conduction axis (dotted line).

Fig. 5. Preoperative (A) and postoperative (B) angiograms in one of the patients with a dominant left ventricle (LV) and a rudimentary right ventricle (RV) who underwent enlargement of the ventricular septal defect (asterisks). The arrowhead indicates the band on the pulmonary trunk (PA). The aorta (Ao) arises from the right ventricle.

a fact that the course of the axis is uniform in hearts with a univentricular A V connection to a dominant left ventricle, irrespective of the location of the incomplete and rudimentary right ventricle. 16 The reason is that, when there is usual atrial arrangement (situs solitus), the A V

node is always found anterolaterally within the right A V junction (beneath the mouth of the right atrial appendage). The ventricular conduction tissues are always carried on the left ventricular aspect of the apical muscular septum. The long non branching bundle joining these two

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Subaortic stenosis in univentricu/ar A V connection 6 7 9

Fig. 6. Postoperative angiograms from the surviving patient with double-inlet left ventricle treated with the Damus-Kaye-Stansel procedure. The ventriculogram shown in lateral projeqion (A) shows the restrictive ventricular septal qefect (asterisk) and the aorta (Ao), filled mostly through the proximal segment of the pulmonary trunk (PA), the anastomosis being widely patent (small asterisks). The right atrial (RAJ injection, profiled in frontal projection (B), shows the direct anastomosis to the distal segment of the pulmonary truck (M PA), which then fills the pulmonary arteries (RPA, LPA). Other abbreviations as in Fig. 5.

segments always runs down the right margin of the defect (that closest to the acute margin of the ventricular mass, see Figs. 1 and 2). When viewed from the rudimentary right ventricle, therefore, it is always the posteroinferior margin of the defect that is most "at risk." The safe areas for excision of muscular tissue are either the outlet septum (the "roof') or else the segment of apical septum closest to the obtuse margin of the ventricular mass (demarcated by the "anterior descending" delimiting artery). Because autopsy of hearts 14 had shown that the outlet septum was often deficient, during this experience we chose to excise a wedge-shaped segment of apical septum, judging this to be the most reliable means of consistently enlarging the defect. The transventricular approach that we used, in which the incision is placed in the parietal wall of the rudimentary right ventricle, is safe and offers excellent exposure of the relevant anatomy. The exposure from an aortotomy 17 is much more limited. We believed it would have restricted markedly our surgical maneuverability around the ventricular septal defect to be enlarged. Our experience also militates against the contention that a transventricular approach prolongs the time of cardiopulmonary bypass. 18 Futhermore, because the thickness

of the parietal wall of the rudimentary right ventricle may also be a limiting factor, use of a ventriculotomy permits a gusset to be placed so as to enlarge the subaortic outflow tract. This was necessary in six of our nine patients undergoing enlargement of the ventricular septal defect. All obtained satisfactory relief of the obstruction. Our experience has shown that even a generous myotomy in the anterior and leftward border of the ventricular septal defect will avoid cutting into the conduction tissues, thereby avoiding the much dreaded complication of complete heart block. Extensive muscle resection is rarely necessary if the operation is timed to occur before the development of extreme ventricular hypertrophy. Major resection was, nevertheless, required in one of our patients. This patient was referred to us late, the ventricular hypertropy being so severe that the cavity of the rudimentary right ventricle was obliterated during systole. Perhaps not unexpectedly, in view of the extent of resection needed to relieve the obstruction, complete heart block did develop in his patient and necessitated permanent pacing postoperatively. The other eight patients remained in sinus rhythm after enlargement of the ventricular septal defect, including the two patients who died after 8 days and 9 months. The two patients who also

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underwent concurrent construction of a modified Fontan operation both survived, which shows that enlargement of the defect in itself does not increase the risk of corrective surgery, which can be offered as a one-stage procedure to those with suitable anatomy. The single death occurring in the hospital after enlargement of the ventricular septal defect came unexpectedly on the eigth postoperative day in a patient whose early postoperative course had been smooth. Autopsy failed to reveal any definite cause of death and the ventricular septal defect was shown to be widely patent. The early recurrence of obstruction in one patient was due to technical error and could have been avoided with a more generous myotomy. All surviving patients have had good relief of symptons with a mean follow-up of 1.1 years. Angiographic and echocrdiographic studies have demonstrated persistently wide interventricular communications The Damus-Kaye-Stansel procedure, although effective in those who survive, 19• 21 is also known to carry a high mortality rate. 4• 5• 22 The procedure is complicated and, inasmuch as a Fontan procedure is usually performed concurrently, it is basically a form of subtotal "correction." Because of our experience, we suggest that, if the procedure is to be used, it would be safer first to relieve the obstruction at the ventricular septal defect. The more "corrective" operation can then be postponed to a later date when it can be performed under more optimal conditions. Our experience also suggests that previous banding of the pulmonary trunk may be a contraindication to the procedure because it distorted the pulmonary valve in one of our patients. This resulted in gross pulmonary incompetence when the pulmonary truck was anastomed to the side of the ascending aorta. Because of this problem, the modification recently suggested by Waldman and associates,22 in which a side-by-side anastomosis is created between the adjacent aortic and pulmonary trunks, is certainly worth considering. This produces a bivalved arterial conduit arising from the heart to which the distal ascending aorta is then resutured. It is significant that both arterial valves remained competent in all six of their patients. This success is the more noteworthy because the Damus-Kaye-Stansel procedure is likely to be the only surgical option when subaortic stenosis occurs in double-inlet right ventricle with a concordant VA connection. Surgical enlargement of the restrictive ventricular septal defect can now be recommended for relief of subaortic stenosis in patients with a univentricular A V connection to a dominant left ventricle and a discordant VA connection. The procedure is simple and effective and is

The Journal of Thoracic and Cardiovascular Surgery

associated with a low morbidity and mortality. It can safely be offered as the operation of choice in the interim period after initial presentation so as to optimize subsequent definitive "corrective" repair. We now reserve the Damus-Kaye-Stansel procedure for rarer cases, such as those involving double-inlet right ventricle and a concordant A V connection. We are indebted to Beverly Tyler and Susan Ley for preparation of the manuscript. REFERENCES 1. FreedomRM,Benson LN,SamallhornJF, Williams WG, Trusler GA, Rowe RD. Subaortic stenosis, the univentricular heart, and banding of the pulmonary artery: an analysis of the courses of 43 patients with univentricular heart palliated by pulmonary artery banding Circulation 1986; 73:758-64. 2. Freedom RM. The dinosaur and banding of the main pulmonary truck in the heart with functionally one ventricle and transposition of the great arteries: a saga of evolution and caution. JAm Coli Cardiol1987;10:427-9. 3. Freed MR, Rosenthal A, Plauth W Jr, Nadas AS. Development of subaortic stenosis after pulmonary artery banding. Circulation 1973;43(Pt 2):1146. 4. McKay R, Pacifico AD, Blackstone EH, Kirklin JW, Bargeron LM. Septation of the univentricular heart with left anterior subaortic outlet chamber. J THORAC CARDIOV ASC SuRG 1982;84:77-87. 5. Penkoske PA, Freedom RM, Williams WG, Trusler GA, Rowe RD, Surgical pallation of subaortic stenosis in the univentricular heart. J THORAC CARDIOVASC SURG 1984; 87:767-81. 6. Kreutzer GO, Vargas FJ, Schlichter AJ, eta!. Atriopulmonary anastomosis. 1 THORAC CARDIOVASC SURG 1982; 83:427-36. 7. Kaye MP. Anatomic correction of transpol?ition of great arteries Mayo Clin Proc 197 5;50:638-40. 8. Stansel HC. A new operation ford-loop transposition of the great arteries. Ann Thorac Surg 1975;19:565-7. 9. Damus P. Arterial repair without coronary relocation for complete transposition of the great vessels with ventricular septal defect: report of case. 1 THORAC CARDIOVASC SuRa 1982;83:316-8. 10. Daneilson GK, Tabry IF, Main DD, Fulton RE. Great vessel switch operation without coronary relocation for transposition of great arteries. Mayo Clin Proc 1978; 53:675-82. 11. Jonas RA, Castaneda AR, Lang P. Single ventricle (singleor double-inlet) complicated by subaortic stenosis: surgical options in infancy. Ann Thorac Surg 1985;39:361-6. 12. Fontan R, Deville C, Quaegebeur J, et al Repair of tricuspid atresia in 100 patients. J THORAC CARDIOVASC SURG 1983;85:647-60.

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13. Humes RA, Pater CJ, Mair DD, et a!. Intermediate followup and predicted survival after the modified Fontan procedure for tricusped atresia and double-inlet ventricle. Circulation 1987;76(Pt 2):III 67-71. 14. Anderson RH, Penkoske PA, Zuberbuhler JR. Variable morphology of ventricular septal defect in double outlet left ventricle. Am J Cardiol 1985;55:1560-5. 15. Smolinsky A, Castaneda AR, Van Praagh R. Infundibular septal resection: surgical anatomy of the superior approach. ] THORAC CARDIOVASC SURG 1988;95:486-94. 16. Anderson RH, Becker AE, Ho SY, Zuberbuhler JR, Wilkinson JL. Disposition of the conduction tissues in double inlet ventricle. In: Anderson RH, Crupi G, Parenzan L, eds. Tunbridge Wells: Castle House Press, 1987:72-97. 17. Newfeld EA, Nikaidoh H. Surgical management of subaortic stenosis in patinets with single ventricle and transposition of the great vessels. Circulation 1987;76(Pt 2):112933.

Subaortic stenosis in univentricular AV connection 6 8 1

18. Lin AE, Laks H, Barber G, Chin AJ, Williams RG. Subaortic obstruction in complex cangenital heart disease: management by proximal artery to ascending aorta endto-side anastomosis. JAm Coli Cardiol1986;7:617-24. 19. Park SC, Siewers RD, Neches WH, eta!. Surgical management of univentricular heart with subaortic obstruction. Ann Thorac Surg 1984;37 :417-21. 20. Ceitharnl EL, Puga FJ, Daneilson GK, McGoon DC, Ritter DG. Results of the Damus-Kaye-Stansel procedure for transpostion of the great arteries and for double-outlet right ventricle with subpulmonary ventricular septal defect. Ann Thorac Surg 1984;38:433-7. 21. Barber G, Hagler DJ, Edwards WD, eta!. Surgical repair of unventricular heart (double inlet left ventricle) with obstructed anterior subaortic outlet chamber. J Am Coli Cardiol 1984;4:771-8. 22. Waldman JD, Lamberti JJ, George L, eta!. Experience with Damus procedure. Circulation 1988;78 (Pt 2):III32-9.

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