Anatomic correction of atrioventricular discordance

Anatomic correction of atrioventricular discordance Between June 1989 and September 1991, 11 patients underwent anatomic correction of atrioventricular discordance. Their ages at operation ranged from 1 to 11 years (mean 6.7 years) and their weights ranged from 7.1 to 31.8 kg (mean 19.1 kg). Atrial situs was solitus in nine and inversus in two patients. Ventriculoarterial connection was discordant in five and was double-outlet right ventricle in six patients. Associated congenital heart defects were seen in all patients, including 10 with ventricular septal defect, eight with atrial septal defect, nine with pulmonary stenosis or pulmonary atresia, seven with tricuspid regurgitation, and four with mitral regurgitation. Five patients had prior Blalock-Taussig shunts. One patient with an intact ventricular septum had repeated pulmonary banding. Anatomic correction consisted of the Senning and Rastelli procedures in three, the Mustard and Rastelli procedures in five, the Senning and arterial switch operations in two, and the Mustard and arterial switch operations in one patient. In addition, mitral valvuloplasty or valvular annuloplasty was performed in three patients. We did not encounter kinking or torsion of the translocated coronary arteries in our three patients with the arterial switch operation. There was one surgical death. The other patients pursued satisfactory postoperative courses (mean follow-up period of 12.6 months). We recommend that anatomic correction for atrioventricular discordance should be indicated, especially in patients with any sign of systemic right ventricular dysfunction. (J THORAC CARDIOVASC SURG 1993; 105:1067-76)

Masaaki Yamagishi, MD, Yasuharu Imai, MD, Shuichi Hoshino, MD, Kazuaki Ishihara, MD, Yongsong Koh, MD, Masayoshi Nagatsu, MD, Toshiharu Shinoka, MD, and Masaaki Koide, MD, Tokyo, Japan

h e morphologic right ventricle remains as the systemic chamber in typical surgical repair of intracardiac anomalies of atrioventricular discordance. Although excellent early results of typical surgical repair have been reported.' the issue of long-term function of the systemic right ventricle persists as a matter for debate.U Several late postoperative studies of isolated congenitally corrected transposition showed right ventricular dysfunction, and systemic right ventricular ejection fraction failed to increase with exercise. 1-3.6 Similar results were reported in patients with complete transposition of the great arteries after the Senning or Mustard procedure. 7- 12 It will be clear from these examples that patients with atriovenFrom the Department ofPediatric Cardiovascular Surgery. The Heart Institute ofJapan. Tokyo Women's Medical College. Tokyo,Japan. Received for publication Jan 2, 1992. Accepted for publication July 1, 1992. Address for reprints: Masaaki Yarnagishi, MD, Department of Cardiovascular Surgery. Jikei University School of Medicine, 3-25-8 Nishishinhashi. Minato-ku, Tokyo 105, Japan. Copyright : 1993 by Mosby-Year Book, Inc. 0022-5223/93 $\.00+ .10

12/1/40777

tricular discordance are always exposed to the danger of systemic right ventricular failure. Concern about longterm ventricular function isof increasing significance with the advent of such alternative operations.P because the left ventricle must function against systemic pressure. This report reviews our experience with II patients with anatomic correction of atrioventricular discordance. Patients and methods

Between June 1989 and September 1991, II patients ranging in age from I to II years (mean 6.7 years) underwent anatomic correction of congenitally corrected transposition of the great arteries, with double-outlet right ventricle with atrioventricular discordance. These patients weighed 7.1 to 31.8 kg (mean 19.1 kg). There werefive boys and sixgirls. Table I lists theobserved associated anomalies. The position of the heart was levocardia in three, mesocardia in three, and dextrocardia in five. Atrial situs was solitus in nine and inversus in two. The ventriculoarterial connection was discordant in five and was double-outlet right ventricle in six. Associated congenital heart defects were seen in all patients, including 10 with ventricular septaldefect (eight with perimembranous defect and two with subarterialmuscular defect),eightwithatrial septaldefect,four withpulmonary stenosis, five withpulmonary atresia,seven with tricuspid regurgitation, and four with mitral regurgitation 1067

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Table I. Clinical data Ages at operation (yr}

Patient No.

Atrial situs

Ventriculoarterial connection

Position of the heart

8

Solitus

DORV

Dextrocardia

2

8

Solitus

Discordant

Levocardia

3

6 7 8 II

Solitus Solitus Solitus

DORV DORV DORV DORV Discordant DORV Discordant Discordant Discordant

Dextrocardia Dextrocardia Dextrocardia Mesocardia Mesocardia Mesocardia Dextrocardia Levocardia Levocardia

4 5 6 7 8

9 10 II

9

Inversus Inversus

8 6 I 2

Solitus Solitus Solitus Solitus

Associated anomalies

VSD (subarterial muscular), PA, ASD, PDA, PLSVC VSD (subarterial muscular), PA, ASD, PLSVC, PAPVC VSD (perimembranous), PS, ASD, WPW VSD (perimembranous), PA, ASD VSD (perimembranous), PA, ASD, PLSVC VSD (perimembranous), PA, ASD, PDA VSD (perimembranous), PS, ASD, PRSVC VSD (perimembranous), PS, ASD, PDA VSD (perimembranous), PLSVC, LVOTO VSD (perimembranous), PLSVC, WPW Congenital AVB

TR

1\ '/4 %

MR

31. cleft( +) 1\ cleft( +) '/, 1\ cleftt +)

'I.

'"

DORV. Double-outlet right ventricle; VSD, ventricular septal defect; PA, pulmonary atresia; PS, pulmonary stenosis; ASD. atrial septal defect; PDA, patent ductus arteriosus; PLSVC. persistent left superior vena cava; PRSVC. persistent right superior vena cava; PAPVR, partial anomalous pulmonary venous return; LVOTO, leftventricular outflow tractobstruction; WPW, Wolff-Parkinson- White syndrome; A VB, atrioventricular block; TR, tricuspid regurgitation; M R, mitral regurgitation.

Table II. Previous operation, operative procedure, and results Patient No. I

2 3 4

5 6 7 8 9

10 II

Procedure

Results

Mustard + Rastelli (26 mm Xenomedica conduit) Mustard + Rastelli (22 mm Xenomedica conduit) Mustard + Rastelli (22 mm Xenomedica conduit), Sealy Mustard + Rastelli (26 mm Xenomedica conduit) Mustard + Rastelli (26 mm Xenomedica conduit) Senning + Rastelli (26 mm Xenomedica conduit), MVP Senning + Rastelli (26 mm Xenomedica conduit), MVP + MAP Senning + Rastelli (22 mm Xenomedica conduit) Mustard + arterial switch, VSD closure, MVP + MAP, MVR Senning + arterial switch, VSD closure, Sealy Senning + arterial switch, pacemaker implantation

Alive Alive Alive Alive Alive Alive Alive Alive

Previous operation

L-BT R-BT, L-BT R-BT R-BT, L-BT R-BT, L-BT, central shunt

PABs

L-BT. Left Blalock-Taussig shunt; R-BT, ty: MVR, mitral valve replacement; HD.

HD

Alive Alive

right Blalock-Taussig shunt; PABs. pulmonary artery bandings: MVP, mitral valvuloplasty; MAP, mitral annuloplashospital death; other abbreviations as in Table I.

(mitral cleft was observed in three patients). Five patients had prior Blalock-Taussig shunts, one of whom subsequently had an additional central shunt (Table II). A 2-year-old boy (patient No. II) who had moderate systemic tricuspid regurgitation with an intact ventricular septum had repeated pulmonary banding for the purpose of training the left ventricle 7 months before anatomic correction. At the first pulmonary artery banding, the pulmonary artery was banded to elevate the left ventricular pressure as well as 80% of the systemic arterial pressure. A few days after the pulmonary artery banding, Doppler echocardiography indicated that the left ventricular pressure had declined to 60% of the systemic arterial pressure and that the pressure gradient at the site of the banding also had declined to 25 mm Hg. Therefore, 12 days after the first banding, the pulmonary artery banding was tightened to elevate the left ventricular pressure so that it was equal to the systemic arterial pressure. Right and left ventricular pressures were equal in all patients at anatomic correction. Nine patients had at least one risk factor in the right ventricle to support the systemic circulation

(Table III). Preoperative systemic right ventricular end-diastolic volume (RVEDV) and pulmonary left ventricular end-diastolic volume (L VEDV) ranged from 62% to 241% of normal (126.9 ± 56.5% of normal), and 91% to 269% of normal (148.3 ± 53.0% of normal), respectively (Fig. I). In two patients (Nos. 2 and 5), RVEDV was rather small, less than 80% of normal (Fig. I). Systemic right ventricular ejection fraction (RVEF), ranging from 0.41 to 0,77 (mean 0.57 ± 0.11), was obviously reduced in three patients. Pulmonary left ventricular ejection fraction (L VEF) ranged from 0.51 to 0,75 (mean 0.63 ± 0.08) (Fig. I). In this report, we have used the morphologic nomenclature. For example, "the right ventricle" denotes "the morphological right ventricle." Left ventricular volumes were determined by the area-length method and Simpson's rule was applied to calculate right ventricular volumes.' End-diastolic volume (EDV) is expressed as a percentage of the expected normal values for the respective ventricle.l" Values are presented as the mean ± I SD.

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'to of normal

1 069

a

250

• •

200

0.8

a a

0.7

a

0.6

100

I

• • ••

•• •

50

•

a

••

00

80

a

••

00 150

•

I

0.5

•

t

§

80 a

a a

I

0.4

1

f RVEDV LVEDV (systemic) (pulmonary)

LVEF RVEF (systemic) (pulmonary)

Fig. 1. Preoperative systemic right and pulmonary left ventricular characteristics. Left, Ventricular end-diastolic volume as a function of the percentage of predicted normal. Right, Ventricular ejection fractions. RVEDV, Right ventricular end-diastolic volume; LVEDV, left ventricular end-diastolic volume; RVEF, right ventricular ejection fraction; LVEF, left ventricular ejection fraction. Operative techniques. All patients underwent repair with cardiopulmonary bypass under moderate systemic hypothermia (25° to 27° C). After median sternotomy in patients undergoing the arterial switch procedure, the ascending aorta and pulmonary trunk were separated, the ductus arteriosus was controlled, and both the right and left pulmonary arteries were dissected free to their point of branching. Cardiopulmonary bypass was established with an ascending aortic cannula and right-angled venous cannulas inserted directly into the superior and inferior vanae cavae for intraatrial rearrangement of the venous return. In patients with persistent left superior vena cava to coronary sinus, persistent left superior vena cava was also cannulated directly. Anatomic correction mainly consisted of two different procedures, as follows (Table II): Mustard and Rastelli procedure (five patients); Senning and Rastelli procedure (three patients); Mustard and arterial switch operation (one patient); and Senning and arterial switch operation (two patients). lntraatrial switch. The right atrium was opened vertically, anterior and parallel to the terminal crest. In patients No. I, 3 to 5, and 9, the right atrium was small in volume because of dextroversion and an overhanging left ventricle. Therefore the atrial septal defect was enlarged by septectomy and a systemic venous channel was created using a Xenomedica baffle (Xenomedica AG, Lucerne, Switzerland) as the Mustard maneuver (Fig. 2). The coronary sinus was positioned at the systemic venous channel. The pulmonary venous channel as well as the systemic atrium were deliberately enlarged with a Xenomedica patch by cutting into the confluence of the right pulmonary veins. Persistent left superior vena cava, partial anomalous pulmonary venous connection, and right upper pulmonary vein connected to the superior vena cava were also present in patient No.2, Therefore the right superior vena cava was ligated at the distal site of the connection of the partial anomalous pulmonary

Table III. Risk factors for systemic right ventricular function Patient No. I 3 4 6 7

8 9 10

II

Risk factors for systemic right ventricular function

TR (1f4) TR ('14) Reduced RVEF (0.42) Older age (II yr) TR Cl4) TR ('14), Reduced RVEF (0.48) TR ('14), Reduced RVEF (0.41) TR (!4) TR('!4)

RV, Right ventricle; RVEF, right ventricular ejection fraction; other abbreviations as in Table I.

venous connection so as to lead the pulmonary venous blood from the right upper pulmonary vein into the atrium via the right superior vena cava. The atrium was parted by a Xenomedica baffle to lead the systemic venous blood from the inferior vena cava and into the tricuspid valve (Fig. 3). Since the right atrium in the other patients had an adequate volume (patients No.6 to 8, 10, and II), an atrial septal flap was developed by cutting around the fossa ovalis after closing the atrial septal defect; then an intraatrial switch operation was performed according to the Senning maneuver. Repair of the mitral valve. In patients No.6, 7, and 9, the mitral valve had a complete cleft in the anterior leaflet, which was closed with interrupted sutures using autologous pericardial tapes as reinforcement. Reed's annuloplasty was added to the lateral commissure in patients No.7 and 9. In patient No.9, however, several chordae of the anterior leaflet, which inserted onto the interventricular septum near the ventricular septal

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was detoured left to the aorta in situs solitus to avoid compression by the sternum. Arterial switch operation. In patients No.9 and 10, the ventricular septal defect was closed by de Leval's maneuver!" through the right atrium. Thereafter the atrial systemic venous channel was completed. After cardioplegia was induced, the aorta and pulmonary artery were transsected. Both coronary arteries, which were the mirror images of normal in all three patients, were removed as teardrop-shaped or buttonlike cuffs and were translocated into the facing pulmonary wall above the pulmonary sinus, using running sutures. The distal aorta was brought down under the distal pulmonary artery and was anastomosed with the pulmonary stump. Coronary defects were patched up usinga Xenomedica patch and the pulmonary artery was reconstructed anterior to the new aorta. Other associated procedures. Epicardial mapping revealed the Kent bundle on the posterior (patient No.3) and lateral (patient No. 10) aspects of the left atrium; thus a Sealy procedure was performed in these patients. In patient No. II a permanent pacemaker was implanted for congenital atrioventricular block.

Results

Fig. 2. Schematic representation of combined Mustard and Rastelli procedure. S ve, Superior vena cava; IVe, inferior vena cava; es, coronary sinus; L V, left ventricle; RV, right ventricle; PA, pulmonary artery; AD, aorta; intraventricular tunnel; *extracardiac conduit.

*

defect, caused left ventricular outflow obstruction. For this reason the mitral valve was resected, which was followed by mitral valve replacement in this patient. Intraventricular rerouting followed by Rastelli procedure (Fig. 2). External cardiac conduit repair with intraventricular rerouting was utilized in patients No. I through 8 because of pulmonary stenosis or atresia. A Xenomedica rolled conduit, 22 or 26 mm in diameter equipped with a trileaflet pulmonary valve,15 was used for the external conduit. The pulmonary trunk was transsected at the site of the bifurcation and its stump was oversewn. The distal opening of the pulmonary artery was enlarged and was anastomosed with the distal end of the Xenomedica conduit. After cardioplegia was induced, the right ventricle was entered through an oval hole in its outflow tract. The infundibular septum was absent in patients No. I and 2. The ventricular septal defect was large enough to lead blood flow through it in all patients with intraventricular rerouting; consequently, an intraventricular conduit was created with a two-ply Xenomedica patch to lead systemic blood flow from the left ventricle into the aorta. All sutures in the anterior and inferior margin of the ventricular septal defect were placed at the right ventricular aspect. The right ventriculotomy was covered with the proximal skirt of the conduit. The Xenomedica conduit

There was one hospital death resulting from residual left ventricular outflow obstruction because of the abnormal attachment of mitral chordae onto the interventricular septum. All other patients followed satisfactory postoperative courses and were in New York Heart Association functional class 1. The period of follow-up ranged from I to 28 months (mean 12.6 months). The electrocardiogram revealed normal sinus rhythm in nine patients and pacemaker rhythm in one patient (patient No. 11). There were no instances of life-threatening arrhythmias. Postoperative angiograms and two-dimensional echocardiograms showed no significant stenosis at the site of both systemic and pulmonary venous atrial channels. In all patients who underwent the Rastelli procedure, the angiogram showed a wide left ventricular outflow tract, and catheterization data revealed no significant pressure gradient across the left ventricular outflow tract. The tricuspid valve of the Xenomedica conduit functioned very well, as was to be expected, and neither regurgitation nor a significant pressure gradient was observed. Preoperative mitral regurgitation of grade 3 in patient No.6 and of grade 2 in patient No.7 disappeared as a result of mitral valvuloplasty and valvular annuloplasty, respectively. Significant tricuspid regurgitation disappeared in four patients, persisted apparently unchanged in two patients, and newly appeared in two patients after the operation. Systolic right ventricular pressure was significantly reduced to 40.2 ± 9.6 mm Hg. Angiograms showed normal left ventricular contraction patterns in all patients with L VEF, ranging from 0.42 to 0.60 (mean 0.53 ± 0.08). Two-dimensional echocardiograms also showed normal left ventricular wall motion in

The Journal of Thoracic and Cardiovascular Surgery Volume 105, Number 6

fractional shortening in all patients. Pulmonary R VEF ranged from 0.48 to 0.65 (mean 0.59 ± 0.07). Cardiac index ranged from 2.02 to 4.38 L/min/m 2 (mean 3.04 ± 0.68 Lyrnin/rn") (Fig. 4). An ll-year-old girl (patient No.6) who underwent a combined Mustard and Rastelli procedure was reexamined 1 year after the operation by gated equilibrium radionuclide ventriculography at rest and with exercise. The following results were obtained. Left ventricular wall motion was normal; resting LVEF of 0.42 1 month after the operation had recovered to 0.55 at the time of examination; and LVEF during supine bicycle exercise was reduced to 0.46 but immediately recovered to 0.58 after exercise (Fig. 5).

Yamagishi et ai.

RSVC

107 1

LSVC

~

RUPV

Discussion Whether the right ventricle can support the systemic circulation over a normal lifetime has been the subject of much controversy. A prevalence of systemic right ventricular dysfunction and abnormal ejection fraction response to exercise has been pointed out in patients with congenitally corrected transposition and with Mustard repair of D-transposition of the great arteries. 6-!2 Graham and associates/ and Peterson and co-workers- also reported systemic ventricular dysfunction after adolescence and the inability of the right ventricle to function as the systemic ventricle in most patients with isolated corrected transposition of the great arteries. The older patients had a lower ejection fraction than did younger patients.-' Furthermore, the risk of right ventricular dysfunction appeared to be enhanced by associated intracardiac malformations. Tricuspid regurgitation, systemic atrioventricular valve regurgitation in corrected transposition of the great arteries, is one of the most serious risk factors for systemic right ventricular function. Once tricuspid regurgitation is accompanied by corrected transposition, systemic right ventricular function is easily exacerbated by serious volume overload. Tricuspid regurgitation also develops in some patients immediately after the usual type of operation.' Tricuspid valve replacement should be required in such patients, but this valvular reoperation still has a high mortality rate.' On the other hand, the procedures for tricuspid regurgitation were not combined with anatomic correction in our four patients who had tricuspid regurgitation of grade 2 or more preoperatively. No significant tricuspid regurgitation persisted after anatomic correction. Although in some patients early postoperative LVEF was reduced to the lower limits of the normal range, it is likely that this reduction of LVEF is transient, as shown in patient No.6, and the left ventricle can function against systemic pressure over a normal lifetime. It

Fig. 3. Schematicrepresentation of modified Mustard procedure in patientNo.2 withpartialanomalous pulmonary venous return intothe right superior venacava. RSVC, Right superior vena cava; LSVC, left superior vena cava; INN. V, innominate vein; RUPV, right upper pulmonary vein; CS, coronarysinus; LV, left ventricle; RV, right ventricle.

follows therefore that anatomic correction is indicated in patients with right ventricular dysfunction resulting from aging or tricuspid regurgitation in whom the right ventricle cannot support the systemic circulation. Mitral valve anomalies were uncommon in corrected transposition, and furthermore, significant regurgitation occurred in only a few patients.' Gerlis and colleagues'? reported, however, that abnormalities of the mitral valve were found in 55% of hearts with corrected transposition. Significant mitral regurgitation was observed in 4 of 11 patients in our series, and three of them had a cleft in the anterior leaflet of the mitral valve. In a 6-year-old girl (patient No.9), the anterior leaflet had a cleft down to the valve anulus and direct insertion of the chordae onto the interventricular septum near the ventricular septal defect, which caused left ventricular outflow obstruction. Thus we must draw attention to anomalies of the mitral valve during anatomic correction of atrioventricular discordance. The mitral valve, however, can withstand the systemic circulation in consequence of valvuloplasty or valvular annuloplasty. The extracardiac conduit and intraventricular tunnel across the ventricular septal defect are required in patients with both ventricular septal defect and pulmonary stenosis or atresia. When the ventricular septal

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•

l l min t m/

0.7 o

I. 0.6

o

I

••

3.5

o o

o

0.5

4.0

I

2.5

.

2.0

•

3.0

o o

••

o o

0.4

RVEF LVEF (pulmonary) (systemic)

Cardiac index

Fig. 4. Postoperative ventricular ejection fraction and cardiac index. Left, Systemic left and pulmonary right ventricular ejection fraction. LVEF, Left ventricular ejection fraction; RVEF, right ventricular ejection fraction. Right, Cardiac index.

LVEF 0.6

•

after exercise rest

0.5 ., during exe rcise

0.4

1

12

months after operation

Fig. 5. Patient No.6. Early and medium-term postoperative systemic left ventricular ejection fraction response at rest, during exercise, and after exercise. LVEF, Left ventricular ejection fraction.

defect is situated in the perimembranous and subpulmonary position and extends anteriorly, the infundibular septum is much shorter and only a little tissue separates the aortic and pulmonary valves.!" Accordingly, intra-

ventricular rerouting may be easy. Also, in patients with subarterial muscular outlet ventricular septal defect, 19 the infundibular septum is absent so that intraventricular rerouting can be performed with great ease. Whichever

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Pre op.

I 073

Post op,

Fig. 6. Right and left ventriculograms in patient No.3 with ventricular septal defect and pulmonary stenosis. This patient underwent a combined Mustard and Rastelli procedure (22 mm Xenomedica conduit) with intraventricular rerouting. Left, Preoperative ventriculograms. The aorta arises from the right ventricle and the pulmonary artery arises from the left ventricle. Right, Postoperative ventriculograms. Xenomedica conduit is interposed between the right ventricle and the pulmonary artery. R V, Right ventricle; LV, left ventricle; PA, pulmonary artery; AD, aorta.

situation the ventricular septal defect is located in, excellent exposure of the ventricular septal defect is provided through right ventriculotomy I 3 and the ventriculotomy is covered with the proximal side of the extracardiac conduit. In our patients who underwent a combined Senning or Mustard and Rastelli procedure, the ventricular septal defect was large enough to lead blood flow from the left ventricle into the aorta. The ventricular septal defect, however, should be enlarged in these patients, such as those with partial occlusion ofthe ventricular septal defect by fibrous tissue.i" In most cases with situs solitus, the nonbranching atrioventricular bundle encircles the anterolateral quadrants of the pulmonary outflow tract and courses down at the anterior margin of the ventricular

septal defect. 21 Thus anterior enlargement of the ventricular septal defect causes serious damage to the atrioventricular conduction bundle. The infundibular septum, the superior margin of the ventricular septal defect, can only be enlarged by carefully avoiding injury to the aortic valve. The anterior site of the ventricular septal defect can be enlarged by resection of muscular interventricular septa in cases with situs inversusv" 23 and in exceptional cases with the posterior atrioventricular node and bundle. 24 Residual left ventricular outflow obstruction should be noticed after the arterial switch operation in anatomic correction, mainly because corrected transposition carries the oblique left ventricular outflow tract as a result of the

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Pre op.

Post op.

Fig. 7. Right and left ventriculograms in patient No. II without ventricular septal defect. This patient underwent combined Senning and arterial switch procedure after pulmonary artery banding. Left, Preoperative ventriculograms. Right, Postoperative ventriculograms. See legend to Fig. 6.

deeply wedged pulmonary artery between the inverted mitral and tricuspid valves.P In patients with an accompanying constrictive ventricular septal defect and pulmonary stenosis or atresia, the arterial switch operation and intraventricular rerouting are impossible, so that typical surgical repair for corrected transposition has to be chosen. Application of left ventricular outflow reconstruction and pulmonary valvular replacement 26• 27 for anatomic correction, however, remains to be proved in these patients. Atrial volume has an effect on the selection of the intraatrial switch procedure. The Mustard operation must be chosen in patients with situs solitus with mesocardia or dextrocardia on the basis that the right atrium,

located behind the ventricles, is diminished in volume. The Senning procedure can be performed in situs solitus with levocardia, which has an adequate atrial volume. In cases of situs solitus, the coronary sinus can be positioned at the systemic venous channel of the intraatrial baffle, because the atrioventricular node locates anteriorly.i! away from the coronary sinus and the suture lines of the atrial baffle. Supraventricular arrhythmias and the intraatrial baffle obstruction, which sometimes occur after the atrial switch operation in Dvtransposition.V must be taken into consideration. Supraventricular arrhythmias are mainly caused by atrial overload resulting from right ventricular dysfunction and tricuspid regurgitation in the case of

The Journal of Thoracic and Cardiovascular Surgery Volume 105, Number 6

D-transposition. Atrial overloads, however, are avoided after anatomic correction of atrioventricular discordance, so the risk of supraventricular arrhythmias may be decreased. Careful observation of the baffle obstruction is still required with longer follow-up. The coronary arteries in situs solitus demonstrate the anatomy appropriate to their ventricles; that is, the anterior descending and circumflex arteries usually arise from a common stem from the right posterior aortic sinus and the right coronary artery has its ostium in the left posterior aortic sinus.!? With this pattern, it is not difficult to translocate the coronary arteries. Although the left coronary artery in corrected transposition has a short main trunk.i" we did not encounter kinking or torsion of the translocated coronary arteries in our three patients with the arterial switch operation. In addition, the new pulmonary trunk, constructed with the modification reported by Lecompte and coworkers.l" did not compress the left coronary artery. In conclusion, systemic ventricular failure can be avoided for a long time by anatomic correction of atrioventricular discordance, establishing the left ventricle as the systemic chamber. We believe that anatomic correction is indicated, especially in the types of patients listed below, who are in danger of heart failure: (I) postadolescent patients; (2) those with evidence of systemic right ventricular dysfunction; and (3) those with moderate or severe tricuspid regurgitation. We thank Dr. Hiromi Kurosawa, Chairman and Professor of the Department of Cardiovascular Surgery, Jikei University Schoolof Medicine, Tokyo, Japan, for many helpful discussions. REFERENCES I. McGrath LB, Kirklin JW, Blackstone EH, Pacifico AD, Kirklin JK, Bargeron LM Jr. Death and other events after cardiac repair in discordant atrioventricular connection. J THORAC CARDIOVASC SURG 1985;90:711-28. 2, Graham TP Jr, Parrish MD, Boucek RJ Jr, et a\. Assessment of ventricular size and function in congenitally corrected transposition of the great arteries. Am J Cardio\. 1983;51:244-51.

3, Peterson RJ, Franch RH, Fajman WA, Jones RH. Comparison of cardiac function in surgically corrected and congenitally corrected transposition of the great arteries. J THORAC CARDIOVASC SURG 1988;96:227-36. 4. Dimas AP, Moodie DS, Sterba R, Gill Cc. Long-term function of the morphologic right ventricle in adult patients with corrected transposition of the great arteries. AM HEART J 1989;118:526-30. 5. Benson LN, Burns R, Schwaiger M, et a\. Radionuclide angiographic evaluation of ventricular function in isolated congenitally corrected transposition of the great arteries. Am J Cardiol 1986;58:319-24.

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6. Parrish MD, Graham TP Jr, Bender HW, Jones JP, Patton J, Partain CL. Radionuclide angiographic evaluation of right and left ventricular function during exercise after repair of transposition of the great arteries. Comparison with normal subjects and patient with congenitally corrected transposition. Circulation 1983;67: 178-83. 7. Trusler GA. The Mustard procedure: still a valid approach. In: Moulton AL, ed. Congenital heart surgery. Current technique and controversies. Pasadena: Appleton Davies, 1984:3-11.

8, Graham TP Jr, Atwood GF, Boucek RJ Jr, Beoerth RC, Bender HW Jr. Abnormalities of right ventricular function following Mustard's operation for transposition of the great arteries. Circulation 1975;52:678-84. 9. Godman MJ, Friedli B, Pasternac A, Kidd BSL, Trusler GA, Mustard WT. Hemodynamic studies in children four to ten years after the Mustard operation for transposition of the great arteries. Circulation 1976;53:532-8. 10. Hagler DJ, Ritter DG, Mair DD, et a\. Right and left ventricular function after the Mustard procedure in transposition of the great arteries. Am J Cardiol 1979;44:27683.

II. Benson LN, Bonet J, McLaughlin P, et a\. Assessment of right ventricular function during supine bicycle exercise after Mustard's operation. Circulation 1982;65:1052-9. 12. Ramsay JM, VenablesAW, Kelly MJ, KalffV. Right and left ventricular function at rest and with exercise after the Mustard operation for transposition of the great arteries. Br Heart J 1984;51:364-70. 13. Ilbawi MN, DeLeon SY, Backer CL, et a\. An alternative approach to the surgical management of physiologically corrected transposition with ventricular septal defect and pulmonary stenosis or atresia. J THORAC CARDIOVASC SURG 1990;100:410-5. 14. Nakazawa M, Marks PA, Isabel-Jones J, Jarmakani JM. Right and left ventricular volume characteristics in children with pulmonary stenosis and intact ventricular septum. Circulation 1976;53:884-9. 15. Harada Y, Kawada M, Ishihara K, Higashidate M, Kurosawa H, Imai Y. A new valved conduit with commissures using a glutaraldehyde preserved equine pericardium. Kyobu Geka 1989;42:457-9. 16. de Leval MR, Bastos P, Stark JS, Taylor JFN, MaCartney FJ, Anderson RH. Surgical technique to reduce the risks of heart block followingclosure of ventricular septal defect in atrioventricular discordance. J THORAC CARDIOVASC SURG 1979;78:515-26. 17. Gerlis LM, Wilson N, Dickson DF. Abnormalities of the mitral valve in congenitally corrected transposition (discordant atrioventricular and ventriculoarterial connections). Br Heart J 1986;55:475-9, 18. Losekoot TG, Anderson RH, Becker AE, Danielson GK, Soto B. Congenitally corrected transposition. New York: Churchill Livingstone, 1983:107-21. 19. Okamura K, Konno S. Two types of ventricular septal defect in corrected transposition of the great arteries: reference to surgical approaches. Am Heart J 1973;85:483-90.

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