Complete transposition of the great arteries and coarctation of the aorta

CONGENITAL HEART DISEASE

Complete Transposition of the Great Arteries and Coarctation of the Aorta

MICHAEL VOGEL, MD, ROBERT M. FREEDOM, MD, JEFFREY F. SMALLHORN, MB, ChB,

WILLIAM G. WILLIAMS, MD, GEORGE A. TRUSLER, MD, and RICHARD D. ROWE, MD

Thirty-two patients with complete transposition of the great arteries (TGA) and coarctation of the aorta (C of A) were seen at The Hospital for Sick Children, Toronto, Canada, between 1963 and 1963. Three patients had only mild C of A and have not required coarctectomy (Group I); 29 had a severe form of C of A (Group II). Two patients in Group I and 21 in Group II had a ventricular septal defect. Subaortic obstruction was present in 5 patients in Group II. The mechanisms included anterior deviation of the infundibular ventricular septum, anomalous right ventricular muscle bundles, and abnormal ventric-

uloinfundibular fold. Five patients in Group II had a hypoplastic right ventricle. Coarctectomy was performed in 25 patients, and 5 dii (20% mortaltty rate). Sixteen patients had repair for TGA (13 Mustard, 2 Jatene, 1 Rastelli), and 2 died (12% mortality rate). Life-table analysis shows that only 66 % of the patients with TGA and C of A survived the first month of life. The 5-year survival in this group was 57 %. In the same period, 94 % of patients with uncomplicated TGA survived the first month of life and the S-year survival rate was 89%.

(Am J Cardiol 1984;53:1627-1632)

Obstructive anomalies of the aortic arch tend to reflect the severity of those intracardiac disturbances that favor pulmonary blood flow at the expense of aortic blood flow.‘m3 Many reports have been devoted to the anatomy and surgical implications of the abnormal left ventricular outflow tract in patients with obstructive anomalies of the aortic arch and concordant atrioven- tricular (AV) and ventriculoarterial connections.1,3-8 Less information is available about the right ventricle and its outflow tract in patients with coarctation of the aorta (C! of A) and complete transposition of the great arteries (TGA).gm*l This report focuses on the morphologic features of the right ventricle in 32 patients with combined complete TGA and C of A.

Methods

Patients: Thirty-two patients with complete TGA and C of A were identified from the Cardiac Records of The Hospital for Sick Children in Toronto between 1963 and 1983. Patients with univentricular heart, AV valve atresia and double outlet ventricle were excluded. We also excluded from the study 3

From the Divisions of Cardiology and Cardiovascular Surgery, De- partments of Paediatrics and Surgery, University of Toronto Faculty of Medicine and Departments of Paediatrics and Surgery, The Hospital for Sick Children, Toronto, Ontario, Canada. Manuscript received September 2, 1983; revised manuscript received February 7, 1984, accepted February 8, 1984.

Address for reprints: Robert M. Freedom, MD, The Hospital for Sick Children, 555 University Avenue, Toronto, Ontario, Canada M5G 1X8.

patients with TGA and interruption of the aortic arch who did not survive the neonatal period. All patients had levocardia with atria1 situs solitus, concordant AV and discordant ventriculoarterial connections and 2 AV valves. The internal or- ganization of the morphologic right ventricle conformed to a “right-hand” pattern in all cases.12 Clinical data, chest ra- diographs and electrocardiograms were reviewed.

Noninvasive tests: Blood pressure was measured at the initial examination in 30 patients using appropriate cuffs and the Doppler flow technique13 with the transducer applied to the radial and tibialis posterior or dorsahs pedis artery. Measurements were usually repeated before cardiac catheterization.

Cross-sectional echocardiography: Cross-sectional echocardiography was performed in 7 patients seen after January 1980 (before cardiac catheterization). Routinely, precordial and subcostal4-chamber views were obtained.14 The transducer was angled anteriorly in the subcostal 4- chamber view to determine the ventriculoarterial connec- tion.15 The suprasternal view was used to assess the aortic arch’s and the modified suprasternal view to visualize an associated ductus arteriosus.17

Invasive tests: Thirty patients underwent cardiac catheterization and balloon septostomy. Twelve patients had 1 catheterization and 13 had 2 catheterizations before repair of TGA, 14 patients underwent cardiac catheterization after the C of A repair, and in 13 of these a pressure pullback was performed from the ascending to the descending aorta. Nine patients, including 2 who had an arterial switch (Jatene),la underwent postoperative catheterization.

Standard fluid-filled catheters were used. Complete right- and left-sided cardiac catheterization was performed in all 30

1626 TRANSPOSITION OF THE GREAT ARTERIES AND COARCTATION OF THE AORTA

patients. All underwent right ventricular angiography. The pulmonary artery was entered at the initial study in 14 patients. Surgery was performed by 3 surgeons in 29 patients. Fourteen patients died and autopsy data are available in 11. Life-table analysis was done using the method of Fleiss et all9 and compared with the life-table analysis in patients with uncomplicated TGA.

Results

The 32 patients were divided into 2 groups according to the severity of the C of A. Three patients had mild C of A, with a maximal gradient of 20 mm Hg between the ascending and descending aorta, and have not required surgery for the C of A after a mean follow-up of 6.3 years (Group I). Twenty-nine patients had significant C of A, 7 with hypoplasia of the transverse arch or isthmic hypoplasia (Fig. 1 to 3), and 25 of the 29 had surgery for the arch anomaly (Group II).

Clinical presentation: The male to female ratio was 5.3:1. The mean age of presentation in all patients was 8 days (range 12 hours to 45 days). The mean follow-up was 3.3 years (range 1 day to 19 years). All patients were cyanotic and 19 patients had signs of congestive heart failure at the initial presentation. Six patients received prostaglandin E at the time of presentation.

Electrocardiogram: All patients had right-axis deviation (mean QRS axis 122.7”). Four had right ventricular hypertrophy and 7 had left ventricular hypertrophy. Five patients had ST-segment depression or abnormal T waves in the right precordial leads and 13 had ST-segment abnormalities in the left precordial leads.

Chest radiograph: In Group 1, the heart was only moderately enlarged, with a mean cardiothoracic ratio of 56%. In Group II the mean cardiothoracic ratio was 60%. The lung vascularity was increased in all patients.

Blood pressure: In Group I, the blood pressure gradient between leg and arm on cuff measurements was 0 at a mean age of 14 days despite angiocardiographic evidence of mild C of A. At a subsequent catheterization (mean age 1.6 years), a mean gradient of 15.3 mm Hg

(range 10 to 20) between ascending and descending aorta was found. Cuff measurements were obtained in 26 of 29 patients in Group II. The mean gradient between arm and leg was 19 mm Hg (range 0 to 90); 7 patients had no gradient by cuff measurement. At the initial examination, all 7 of these patients had a ductus arteriosus. A gradient between ascending and descending aorta was obtained in 10 patients and the mean was 16 mm Hg (range 0 to 45).

Cross-sectional echocardiogram: In the 9 patients who underwent cross-sectional echocardiography, the TGA could be prospectively identified. In 2 patients from Group I, the aortic arch and isthmus were con- sidered to be normal.

Hemodynamics: In Group I the first catheterization was performed during the first day of life in 2 patients and at age 2 months in 1 patient. The mean initial systemic oxygen saturation was 57% (range 45 to 71). None of these patients had a gradient across the right ventricular outflow tract. One patient underwent a catheterization 7 months and one 29 months after the Mus- tard repair. Both patients had good right ventricular contractility as assessed angiographically and normal right ventricular end-diastolic pressures (3 and 5 mm Hg, respectively).

In the 29 patients with severe C of A and TGA, catheterization was performed initially in 25; 2 had initially undergone catheterization elsewhere and 2 died before catheterization could be performed. In those 25 the initial oxygen saturation was 73% (range 44 to 91). The mean age at initial catheterization was 10 days (range 1 to 24). Thirteen patients underwent repeat catheterization after a mean of 13 months (range 10 days to 5 years) after the C of A repair and 12 had no residual gradient across the C of A site. One patient underwent reoperation because of significant recoarc- tation. Five patients in Group II who had a Mustard repair at a relatively late mean age of 2 years underwent repeat catheterization a mean of 1 year (range 2 months to 2.5 years) after TGA repair. The first patient who had

FIGURE 1. A coarctation of the aorta in a neonate with transposition of the great arteries, an intact ventricular septum, a normal-sized right ventricle, and a patent ductus arteriosus. Left, frontal right ventricule gram showing a normal-size right ventricle (RV) and transposed aorta (AO). Right, lateral aottogram showing a coarctation of aorta (arrow) and small ductus arteriosus (atierlsk).

FIGURE 2. Very severe isthmic hypoplasia in a neonate with transposition of the great arteries and intact ventricular septum. Left, lateral right ventriculogram showing the anteriorly positioned aorta (AO), the normally expanded subaortic infundibulum (asterisk). and an intact ventricular septum. Right, aortogram showing a severe isthmic hypoplasia (asterisk). a constricted ductus arteriosus (arrow), and a dilated pulmonary artery (PA). RV = right ventricle.

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TABLE I Associated Defects in Patients with Complete Transposition of Ihe Great Arteries and Obstructive Anomalfes of the Aortic Arch _

Group I Group II (n = 3) (n = 29)

PDA 1(33%) 28 (97%) VSD 2 Hypoplastic right ventricle 0 2; $7;

Subaortic stenosis 0 5 (17;)

PDA = patent ductus arteriosus; VSD = ventricular septal defect.

a large ventricular septaI defect (VSD) and had previ- ously undergone pulmonary trunk banding was in congestive heart failure 2 months after the Mustard repair, and underwent an early repeat catheterization. He had decreased right ventricular contractility and pulmonary hypertension (pulmonary artery pressure 50/20 mm Hg [mean 301). The other 4 patients had good hemodynamic and angiographic results. The mean right ventricular end-diastolic pressure was 5 mm Hg (range 3 to 6). No patient had tricuspid regurgitation. The 2 patients who had a Jatene procedure had good angiocardiographic and hemodynamic results after repair, with normal end-diastolic left ventricular pressures. Seven patients, including the 2 who had a Jatene procedure, underwent catheterization after the TGA repair, with good hemodynamic results.

Associated defects (Table I): Of the 3 patients with minor C of A (Group I), 2 had small VSDs, both of which closed spontaneously, and 1 patient had an intact ventricular septum. At the time of the initial cardiac catheterization, the ductus arteriosus was patent in 1 patient. The right ventricle was angiographically normal in these 3 patients. Of the 29 patients with severe C of A (Group II), 16 had a large VSD, 5 had a small VSD that later closed and 8 had an intact ventricular septum. At the initial cardiac catheterization, 25 had a patent ductus arteriosus. The coarctation was preductal in 21 patients, juxtaductal in 3 and postductal in 1 patient.

Five patients had a hypoplastic right ventricle, 2 of whom had obvjous tricuspid stenosis (Fig. 4). Four patients had subaortic stenosis; its causes were anterior deviation of the infundibular septum in 2 patients in association with an abnormal ventriculoinfundibular fold, and anomalous right ventricular muscle bundles in 1 patient. (Fig. 5 and 6); 1 patient had hemodynamic and angiographic evidence of aortic stenosis (Fig. 7). Two patients had left juxtaposition of the right atria1 appendages and 1 patient each had a cleft mitral valve, subpulmonary stenosis and right aortic arch (Fig. 8).

Ventricular septal defect: Twenty-three of the 32 patients in the study (72%) had a VSD. Ten of those had a perimembranous defect, 4 had a perimembranous defect excavating into the infundibular septum, 7 an infundibular or subarterial defect, and 1 patient each a muscular defect and small multiple muscular defects near the apex. The VSD was 68% (range 23 to 100) of the size of the aortic root as assessed angiographically or at autopsy.

Surgery: No patient in Group I has required surgery for C of A. One patient had a Blalock-Hanlon procedure at age 7 days. All 3 patients had a Mustard procedure at a mean age of 9 months (range 3 to 12), with no deaths. Of the 29 patients in Group II, 25 had surgery for the C of A at a mean age of 4.2 months (range 2 days to 5 years); 14 had a coarctectomy and 11 a left subclavian flap procedure. One patient required repair of a residual C of A 1 year and 2 months after the initial C of A repair. In 10 of the patients with a large VSD, pulmonary artery banding was performed at the same time as the coarctation repair. Palliative treatment for TGA in this group consisted of 13 Blalock-Hanlon and I Starling-Edwards procedures. The corrective surgery for TGA was done at a mean of 2 years (range 60 days to 3 years) after the C of A repair. Ten Mustard procedures, 2 Jatene procedures and 1 Rastelli procedure were done. Two patients died after Mustard repair, VSD closure and pulmonary trunk debanding, 1 of these

FIGURE 3. Severe coarctation of the aorta in a neonate with transposition of the great arteries and an infundibutar ventricular septal defect. Left, lateral ao&gram Sh0WS a hypoplastic tm~%VefSe aOrtiC arch (x)

and a duct&z, arteriosus (arrow) that is continuous with the descending thoracic aorta. Right, long axial oblique left ventriculogram shows the subpulmonary ventricular septal defect (arrow) and the dilated pulmonary artery (PA), which was surgically confirmed. LV = left ventricle.

FIGURE 4. Fim venbkuku hypoplasii of moderate degee in a neonate with complete transposition of the great arteries, mitd anterior displacement of the infundibuiar septum (is), ventricular septal defect and coarctation of aorta. Left, frontal right ventricuiogram shows the small right ventricle (IV), the normal ascending aorta (ao), and tubular hypoplasia of the aortic isthmus (asterisk). Right, diastolic frame showing the mild anterior displacement of the IS, which narrows the subaortic infundibulum (asterlsk).


when the artery that supplied the AV node was acci- dentally cut.

Deaths and life-table analysis: All patients in Group I are alive. In Group II, 14 of the 29 patients with severe coarctation died (7 treated medically and 7 surgically). Two patients had cardiac arrest and died after cardiac catheterization (before the use of prostaglandin E) and 1 died from severe heart failure. Two patients died of sepsis, 1 of endocarditis and 1 had pericarditis 21 days after repair of C of A. Two patients died after Mustard repair, VSD closure and pulmonary artery debanding. Thus, 14 of the 32 patients died. The probability of survival of the neonatal period (the first month of life) in our group of patients with TGA and complicating obstructive anomalies of the aortic arch is only 68%. The probability of surviving the first year of life is 64%, and the 5-year survival rate is 57% (Fig. 9). The

FfGURE 6. Posterior transposition with mild subaortic narrowing sec- ondary to anterior right ventricular wall muscle bands (asterisk). A0 = aorta; RV = right ventricle.

FIGURE 5. Various angiographic ap- pearances of subaortic stenosis in transposition of the great arteries and obstructive anomalies of the aortic arch. Left, hypertrophy of infundibular septum (IS) in a neonate with modsrate hypoplasia of morphologic right ventricle (RV!, with preferential opacification of a dilated pulmonary artery (PA). Middle, patient with a large ventricular septal defect (asterisks). pre- viously banded PA, and anterior displacement of IS. Rfght, subaortic stenosis @O-mm Hg gradient) in this patient results from “wedging” of the subaortic outflow tract (x) between the ventriculoinfundibular fold and the IS. This right ventriculogram is filmed in a shallow right long axial oblique projection. The ventricular septal defect (arrow) is not ideally profiled by this projection. These features were confirmed at the time of an unsuccessful Damus-Kaye-Stansel procedure.

probability of survival of patients with uncomplicated TGA was 10% in the first month and 89% for the first 5 years of life (Fig. 9).

Discussion

Data from The Hospital for Sick Children indicate that 5% of patients with complete TGA and a biventricular heart have an associated C of A, which is usually severe. That the presence of such an aortic arch anomaly adversely affects survival is not at all surprising. The life-table analysis generated from our data shows that much of the mortality is early, with a 5-year survival rate of only 49%. Such survival statistics in this particular group of patients are less favorable than for patients with TGA in isolation or with a small VSD. The increased cumulative early and late mortality rate reflects both the adverse hemodynamic effects of significant impedance to systemic blood flow in an already hypoxic

FIGURE 7. Aortic stenosis in a neonate with transposftion of the great arteries, ventricular septal defect and coarctation of aorta. This lateral right ventriculogram shows a dilated ascending aorta (AO) and an ec- centric jet of opacified blood (x). RV = right ventricle.

June 1, 1984 THE AMERICAN JOURNAL OF CARDIOLOGY Volume 53 1631

patientz0121 as well as the presence of associated intracardiac defects.22 In reports of patients with TGA and C of A,20-23 abnormalities of the right AV junction (in the patient with atria1 situs solitus and concordant AV connections),24 hypoplasia of the morphologic right ventricle l1 VSD l”,ll and abnormalities of the subaortic infundidulum resulting in subaortic stenosisgJO are often mentioned. Our data indicate that about half of all patients with complete TGA and an obstructive anomaly of the aortic arch will have at least 1 such complicating feature.

Considerable attention has been focused on the pathologic basis of anatomic obstruction of the right ventricular outflow tract in TGA.gJo Moene et al,1° in a recent necropsy review of 126 hearts, reported that only 2 of 71 patients with TGA and an intact ventricular septum had right ventricular outflow tract obstruction. However, among the 55 hearts with a VSD, 15 (27%) showed distinct anatomic obstruction of the right ventricular outflow tract. The VSD was perimembranous extending into the infundibular septum in 12 of these 15. Similarly, in 12 of the 15 patients, outflow tract obstruction resulted from anterior displacement or malalignment of the infundibular septum from the tra- becula septomarginahs and from contributions from the ventriculoinfundibular fold. The anterior displacement of the infundibular septum is analogous to the infundibular anatomy in the patient with tetralogy of Fallot (normal ventriculoarterial connections).25 Rarely, subaortic atresia can be found in the patient with TGA.2”

Our data and those of Moene et allo suggest some variability in the type of VSD in this group of patients. The consequence of anterior displacement or malalignment of the infundibular septum is clear. There is subaortic narrowing and the interventricular commu-

FIGURE 8. A neonate with right aortic arch, transposition of the great arteries, intact ventricular septum, and coarctation of the aorta. Left, frontal right ventriculogram with opacification of ascending aorta (AO), right aortic arch and coarctation of aorta (arrow). Right, lateral view (a slightly later frame) shows the posterior shelf (white asterisk) and the posterior pulmonary artery (PA). Note the appearance of the normally expanded subaortic infundibulum (black asterisk). Compare the appearance of the normal subaortic infundibulum of this neonate with the narrowed subaortic infundibulum (Fig. 4 and 5). RV = right ventricle.

nication is inferior to the displaced infundibular septum, usually extending into the membranous septum. But the defect may result from isolated deficiency of the infundibular septum (without malalignment), or the defect may be membranous or trabecular.6 In Oppen- heimer-Dekker’s review of interventricular communi- cation in TGA,27 there is little reference to VSDs resulting from anterior displacement of the infundibular septum.

The chance of surviving the neonatal period with TGA and obstructive anomalies of the aortic arch has improved because of the routine use of prostaglandin E and because of surgical expertise in dealing with obstructive anomalies of the aortic arch in the neonate and young infant.2s-30 For the patient who survives the neonatal period, the presence, number and the size of the VSD as well as the size of the systemic (right) ventricle will determine further management, morbidity, mortality and prognosis. The condition in patients with a hypoplastic right ventricle, TGA and C of A can be palliated by pulmonary artery banding and Blalock- Hanlon septectomy. 31 Pulmonary trunk banding carries the risk of potentiating subaortic obstruction in the patient with anterior displacement of the infundibular septum or right ventricular muscle bundles.32 De-

ACTUARIAL SURVIVAL OF 32 CHILDREN

WITH COMPLt3E TRANSPOSITION AND coARClAlloN OF THE AORTA

FIGURE 9. Top, life-table analysis of 32 patients with obstructive anomalies of the aortic arch and transposition of the great arteries. Most of the deaths occur in the first month of life. Bollom, life-table analysis of 394 patients with complete transposition of the great arteries and intact ventricular septum (excluding patients with associated obstructive anomalies of the aortic arch).


pending on the degree of hypoplasia of the right ventricle, the arterial switch procedure’s in isolation or combined with a Fontan”” type procedure, as in patients with tricuspid atresia and TGA,34 is an alternative to an intraatrial repair. The patient with TGA, C of A and an angiographically small VSD did not undergo pulmonary trunk banding. Those who survived coarctectomy later underwent intraatrial repair. Some infants with a moderate VSD also had an intraatrial repair combined with closure of the VSD. The infant with associated large VSD underwent pulmonary trunk banding plus repair of the C of A as the initial procedure, and then later debanding, closure of the VSD, and an intraatrial repair was carried out. For this last group of patients, we have developed a different surgical approach. Data from this institution suggest that the long-term outlook for the infant with TGA and large VSD (with or without previous pulmonary trunk banding) treated with VSD closure and Mustard repair is not good. Thus, we have taken the approach advo- cated by Jatene.la When the coronary artery anatomy is favorable, an arterial repair with coronary translo- cation is our procedure of choice, combined with closure of the VSD.35,36 If subaortic stenosis is present or if the coronary anatomy is unfavorable, a Damus-Kaye- Stansel procedure (anatomic repair without coronary artery relocation) is another surgical alternative.“?

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Complete transposition of the great arteries and coarctation of the aorta

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