- Email: [email protected]
COMPLETE TRANSPOSITION OF THE GREAT VESSELS: A SUCCESSFUL COMPLETE CORRECTION
COMPLETE TRANSPOSITION OF THE GREAT VESSELS: A SUCCESSFUL COMPLETE
CORRECTION
C. N. Barnard, M.D., M.Med, (Cape Town), V. Schrire, M.B., Ph.D. (Cape Town), W. Beck, M.Sc,
M.Med.
Cape Town, South
M.S., Ph.D.
M.R.C.P. (Lond.),
(Cape Town),
M.R.C.P.
(Minnesota), F.R.C.P.E., and
(Lond.),
Africa
C
transposition of the great vessels may be denned as a congenital malformation in which the aorta arises exclusively from the anterior or systemic venous ventricle, the pulmonary trunk from the posterior or pulmonary venous ventricle, and the two ventricles function as separate chambers. The right atrium receives blood from the two venae cavae and coronary sinus and communicates through the tricuspid valve with the anterior ventricle. The left atrium communicates with the pulmonary veins and, through the mitral valve, empties its blood into the posterior ventricle. The aorta, with its origin from the anterior ventricle, therefore carries venous blood, whereas the pulmonary artery, arising from the posterior ventricle, carries oxygenated blood. Survival after birth is only possible if some sort of communication exists between the two sides of the heart, or great vessels, allowing mixing of the two circulations. The three most common means of communication are through defects in the atrial or ventricular septa, or a patent ductus arteriosus. One, two, or all of these may be present in a given case. Since the prognosis for pa tients born with complete transposition is very poor,1"4 many attempts have been made to correct this condition. The various operative procedures developed can be divided into two types, palliative and corrective. OMPLETE
PALLIATIVE PROCEDURES
Survival after birth is possible only because of associated defects which allow shunts between the systemic and pulmonary circuits. These must be balanced, lest one circuit be bled " d r y , " while the other becomes plethoric. Palliation can be achieved by operation if it increases mixing of the two circula tions, provided they remain balanced. 3 The early attempts were aimed at pro ducing extracardiac shunts or increasing intracardiac mixing. Five different types of extracardiac shunts, both arterial and venous, were discussed by Blalock and Hanlon, 3 but the results were uniformly bad. It apProm the Departments of Surgery and Medicine, University of Cape Town; Cardiac Clinic, Groote Schuur Hospital, and Council for Scientific and Industrial Research Cardiopulmonary Group, Cape Town, South Africa. Received for publication June 27, 1961.
768
Vol. 43, No. 6 June. 1962
COMPLETE TRANSPOSITION OF GREAT VESSELS
769 ' vv
peared that these extracardiac shunts function mainly in one direction, result ing in unbalanced circulations. Techniques for transposing the right pulmonary veins and inferior vena cava have been described by Lillehei and Varco, 4 Murphy and associates,5 and Baffes.6 These procedures allow intracardiac mixing of the blood from the inferior vena cava and left pulmonary veins in the left atrium and blood from the superior vena cava and right pulmonary veins in the right atrium. Since the two circulations remained balanced, the palliation obtained was good.7 Blalock and Hanlon 3 described a technique of creating an atrial defect to promote mixing between the two atria. Cooley8 favors this operation and claims fair results. Various combinations of the above techniques have been suggested. 3 ' 9 Blalock and Hanlon 3 claimed that their best results were obtained when atrial defects were created in combination with an anastomosis between the subclavian and pulmonary arteries. It was disappointing to find that there was only moderate improvement among the survivors and that the arterial oxygen satura tion generally remained below 75 per cent. CORRECTIVE PROCEDURES
Complete correction of blood flow in complete transposition can be obtained either by redirecting the systemic and pulmonary venous connections to the heart, thus producing a "corrected transposition," or by re-arrangement of the aorta and pulmonary arteries. As the systemic and pulmonary venous return is normal and the abnormal ity involves the origins of the aorta and pulmonary artery, the obvious approach would be to correct the anomaly at this point. Several authors10"14 have described various techniques with this in mind but no survivors have been reported. Morbid anatomic studies have shown that since the coronary arteries arise from the aorta, a mere switch-over of the major trunks results in the heart receiving desaturated blood. 4 ' 13 Furthermore, the right ventricle functions as the systemic or high pressure pump. The left ventricle in the absence of a large ventricular septal defect or pulmonary stenosis functions as a pulmonary or low pressure pump. Switching the major arteries alters the functional requirements of each ventricle. Hypotension and pulmonary edema may immediately follow. The procedure most likely to succeed is one in which the venous returns are transposed to correct the arterial transposition. With this in mind, one-stage intracardiac procedures have been devised.14"18 Only 4 successful cases have been reported. 14 ' 19 The purpose of this report is to describe a successful one-stage correction by intra-atrial venous transposition, using a plastic graft between the openings of the pulmonary veins and the tricuspid valve. CASE REPORT J . K., a 16-year-old Coloured boy, was admitted to Gioote Schuur Hospital in January, 1961, with severe disability. Cyanosis and dyspnea had been present for as long as he could remember, he had never thrived, development had been retarded, and all activities were ex tremely limited.
770
BARNARD, SCHRIRE, BECK
J. Thoracic and Cardiovas. Surg.
On examination he looked like a child of 7 years of age, being 44 inches tall and weighing 50 pounds. Moderate cyanosis (grade 2 of 4 grades) and clubbing (grade 2 of 4 grades) were equally present in fingers and toes. A striking " a " wave was visible in the jugular venous pulse (Fig. 1) which was elevated about 10 cm. above the sternal angle, and presystolic pulsation of the liver could be felt. The peripheral pulses were small, with a blood pressure of 130/110 mm. H g in the arms and a higher pressure in the legs. The clinical signs associated with Eisenmenger complex were present. Thus there was cardiomegaly, mainly right venticular in type, with a palpable second sound in the second left intercostal space. A loud ejection click was audible a t all areas, maximal in the second left intercostal space. The second sound was loud and single with an early diastolic murmur (grade 2 of 4 grades) between the second and fourth intercostal spaces (Fig. 1 ) . The electro cardiogram (Fig. 2) showed severe right atrial and right ventricular hypertrophy. The radio-
Fig. 1.—Phonocardiographic record showing a striking "a" wave (A) in the jugular ve nous pulse tracing (JUG). At the second left intercostal space (PA), the mitral area (MA), and the fourth left intercostal space (l,LS), there is a loud ejection click (X) followed by a short systolic murmur. The second heart sound is loud and single. A long early diastolic murmur is shown a t all areas except at the second right intercostal space (AA). The bottom two tracings have been mounted below the top two, but have not been synchronously recorded.
Vol. 43, No. 6 June, 1962
COMPLETE T R A N S P O S I T I O N O F GREAT VESSELS
logic appearances gave the clue to the anatomic diagnosis (Fig. 3, A), being present with a narrow pedicle and pulmonary plethora.
771
an egg-shaped heart
Cardiac catheterization was performed from the right median basilic vein, the catheter entering the superior vena cava and right atrium in the usual way. I t could be advanced into a high pressure ventricle, identified as the systemic ventricle by the identical femoral arterial and ventricular systolic pressures, the identical oxygen saturations, and the dilution curve recorded at the femoral artery following injection into this ventricle (Fig. 4, A). The catheter could also be advanced through an atrial septal defect into a low pressure ventricle (40 mm. H g ) with a high oxygen saturation (93 per cent). From this ventricle the catheter entered the pulmonary artery which had similar systolic pressures and oxygen saturations. Dilution curves following injection into this low pressure ventricle and into the pulmonary artery showed identical curves quite different from those obtained from the systemic ventricle (Fig. 4, A). X-ray studies of the catheter in the pulmonary artery showed this vessel to be placed well posterior and medial to its normal position. As the aorta could not be entered with the
Pig. 2.—Before operation, the electrocardiogram shows marked right axis deviation and severe right atrial and right ventricular hypertrophy. The postoperative tracing shows a striking change in the P wave.
Fig. 3.—Before operation (A<, tin1 :interoposterior roentgenogram shows an "egg-shaped" heart with a narrow vascular pedicle, a prominent superior vena cava, and pulmonary plethora. During convalescence after operation, bilateral pulmonary edema has developed '(B). "x By the time of discharge (C), 2 months after operation, the lung fields are clear and pulmonary plethora has diminished.
S:^
td H o W
I—(
w w w a
a
w
I
>
>
CO
Vol. 43, No. 6 June, 1962
COMPLETE TRANSPOSITION OF GREAT VESSELS
773
venous catheter, retrograde catheterization through the right brachial artery was performed. X-ray studies now showed the ascending aorta to be anterior and lateral to the pulmonary artery, establishing the presence of transposition of the great vessels. An interatrial communication with a bidirectional shunt was demonstrated by saturation data (Table I ) . Dilution curves recorded in the pulmonary artery following injection into the ascending aorta showed no early appearing dye (Fig. 4, B), excluding an aorticopulmonary communication. When dye was injected into the systemic ventricle (via the catheter passed DYE CURVES RECORDED IN RIGHT FEMORAL ARTERY GREEN
Fig. 4.—A, Dilution curves recorded at the femoral artery show that the right ventricle is the systemic ventricle, whereas the left ventricle is the pulmonary ventricle. B, Dye injected into the systemic ventricle (right ventricle) shows a minute amount of early ap pearing dye in the pulmonary artery, indicating either a small ventricular septal defect or tricuspid incompetence with a right-to-left shunt In the atria, whereas injection into the ascending aorta shows no early appearing dye, excluding an aorticopulmonary communication. retrogradely through the aortic valve), a minute amount of early appearing dye was detected in the pulmonary artery (Fig. 4, B). This suggested either a small ventricular septal defect or tricuspid valve incompetence with the shunt occurring at atrial level. The former appeared unlikely in the absence of a ventricular septal defect murmur, with a large pressure differen tial between the two ventricles. The preoperative diagnosis was, therefore, complete transposition of the great vessels with normal pulmonary resistance, pulmonary plethora and a bidirectional shunt at atrial level, tricuspid and aortic valve incompetence. A patent ductus arteriosus or ventricular septal defect was excluded. From the hemodynamic point of view the patient appeared suit able for surgical correction.
BARNARD, SCHRIRE, BECK
774
J. Thoracic and Cardiovas. Surg.
On Feb. 13, 1961, under general anesthesia (Muothane, nitrous oxide and oxygen), profound hypothermia and extracorporeal circulation with the DeWall-Lillehei bubble oxygenator, 20 the operation was performed. The chest was entered through a median sternotomy and the pericardium was opened in the midline from the roots of the great vessels down to the dome of the diaphragm. The aorta was observed to arise from the anterior ventricle, both coronary vessels from the aorta, and the pulmonary artery from the posterior ventricle. The root of the aorta and the superior and inferior venae cavae were encircled with cotton tapes. The ductus arteriosus was obliterated. Digital exploration of the interior of the heart through the right atrial appendage revealed the presence of an atrial septal defect and tricuspid incompetence, but no ventricular septal defect.
Fig. 5.—A, T-shaped incision of the anterior wall of the right atrium; B, the atrial septum has been widely excised to expose the four pulmonary veins. After systemic heparinization, a single venous catheter was inserted into the right atrium through the atrial appendage and connected to the venous line of the oxygenator. ( I n the presence of an interatrial communication, a single catheter in the right atrium will drain the venous blood and, in addition, decompresses the left heart during cooling and rewarming.) The right common femoral artery was catheterized and used for the return of oxygenated blood from the oxygenator. Bypass and cooling was commenced and continued until the midesophageal temperature was lowered to 15° C. Bypass was discontinued and the venous TABLE
I
PREOPERATIVE SITE
Superior vena cava Right atrium Inferior vena cava Left atrium Right pulmonary vein Left ventricle Pulmonary artery Right ventricle Aorta Right femoral artery
|
PRESSURE
15/7, mean 10 8/3, mean 7
POSTOPERATIVE | %
SAT.
65 79.5 69.5 88
40/2-3 35/15 125/5 125/75
99 93 93 79 79
140/85
79
Estimated 0 2 uptake, 130 c.c./min. Surface area, 0.74 M 2 , hemoglobin 20.2 Om. % Pulmonary flow, 12 L. min. Systemic flow, 4 L. min. Pulmonary vascular resistance = 1.4 units
SITE
|
PRESSURE
| %
Superior vena cava | 24/16, Right atrium i mean 20 Inferior vena cava J Left atrium (func tioning right atrium) 20/4 Left ventricle (func tioning right ven tricle ) 55/6 Right brachial artery 135/90 Withdrawal from anatomic LV-LA- 55/6 - 20/4 RA 24/16 0 2 uptake, 153 c.c./min. Surface area, 0.85 M 2 , hemoglobin 12.7 Gm. % Systemic flow, 6.6 L. min.
SAT.
66 72 70
— 70 85
Vol. 43, N o . 6
June, 1962
COMPLETE T R A N S P O S I T I O N OF GREAT VESSELS
775.
catheter removed. The right atrium was widely opened with a T-shaped incision, the top of the T running about one inch from, and parallel to, the atrioventricular groove from the base of the appendage to a point one half inch above the entrance of the inferior vena cava (Fig. 5, A). The shaft of the T extended from the midpoint of the above incision in a slightly caudad direction to end a t the interatrial groove, below the entrance of the right pulmonary veins (Fig. 5, A). The atrial septum was now excised as widely as possible, avoiding damage to the coronary sinus and the conducting system of the heart (Fig. 5, B).
Fig. 6.—A, The construction of the pouch around the tricuspid valve orifice. B, Teflon graft in position. C, Reconstruction of the right atrium. Two venous catheters were placed through the atrial incision in the superior and inferior venae eavae and connected to the venous line of the oxygenator. The caval tapes were tight ened and bypass and cooling restarted, maintaining about a third of the flow required at normal body temperature and with a mid-esophageal temperature between 15° and 20° C. A fair degree of aortic incompetence was present so that the aorta was cross-clamped to prevent the influx of blood into the heart through the incompetent valve. The aim of the operation is to divert the pulmonary venous blood from the posterior atrium to the anterior ventricle, by means of a suitably sized graft. This graft must pass through the enlarged interatrial septal defect without obstructing flow of venous blood around it, from the anterior atrium to the posterior ventricle. Since the graft in use is made of inelastic plastic material with little storage capacity it is important that it should not merely extend between the pulmonary veins and the tricuspid orifice. An atrial chamber should be constructed from the atrial wall. Even if this is not large at the time of operation it has the potentiality of developing and enlarging as time goes by.
776
BARNARD, SCHRIRE, BECK
J. Thoracic and Cardiovas. Surg.
For this reason a pouch was constructed from the remaining right atrial wall between the atrioventricular groove and the first atrial incision. The top and bottom were stitched around the cephalad, caudal, and posterior portion of the tricuspid valve ring until an opening 1.5 cm. in diameter remained (Fig. 6, A). Care was taken to exclude the coronary sinus from this chamber. This opening now formed the entrance to the newly constructed ' ' l e f t ' ' atrium. A graft of woven Teflon, 1.5 cm. in diameter, was now fashioned to fit between
Fig1. 7.—I-ateral angiogram from the superior vena cava which shows the pulmonary artery arising posteriorly from the left ventricle (A), whereas the aorta arises anteriorly from the right ventricle (B). In B, the aorta is outlined anterior to the pulmonary artery, behind which can be seen the remnant of the left atrium joining the pulmonary veins to the prosthesis. The prosthesis is not outlined.
Pig. 8.—Anterior angiogram from the superior vena cava showing the superior vena cava draining into the right atrium. The dye flows around the prosthesis, which appears as a filling defect, into the left atrium, left ventricle, and pulmonary artery. the opening and the entrance of the four pulmonary veins (Fig. 6, B). One end was at tached by continuous 4-0 silk suture to the atrial wall in such a way that the entire pulmonary venous drainage entered the graft. The other end of the graft was anastomosed to the opening left in the newly formed ' ' left a t r i u m " in a similar manner, leaving a small open ing through which the left side of the heart could be decompressed during rewarming, until an effective heartbeat was re-established. The two venous catheters were now positioned in the atrial appendage and rewarming commenced. The " r i g h t a t r i u m " was reconstructed by direct suture (Fig. 6, C). Had there
Vol. 43, No. 6 June, 1962
COMPLETE T R A N S P O S I T I O N O F GREAT VESSELS
777 ' ' '
been insufficient atrial wall, a plastic roof would have been inserted. If obstruction to flow of systemic venous blood through the interatrial defect to the posterior ventricle had been noted, the atrial incision could have been continued across the atrial groove into the posterior atrium. A plastic roof could then have been extended across to increase the interatrial opening. After rewarming, the heart was defibrillated with an electric shock. All air was then aspirated from the left atrium and anterior ventricle and the suture of the graft com pleted. On release of the venae caval tapes the heart took over with a good beat. Bypass was discontinued and the venae caval catheters removed. After giving Polybrene to neutralize the heparin, the femoral arterial catheter was removed and the femoral arteriotomy repaired with a continuous 6-0 silk suture. The following pressures were recorded at this stage: arterial, 120/60 mm. H g ; pulmonary artery, 25/12 mm. H g ; inferior vena cava, 15/10 mm. H g ; superior vena cava, 12/8 mm. H g ; right pulmonary venous pressure, 20/15 mm. H g ; arterial saturation was 96 per cent. After careful hemostasis, the pericardium was loosely approx imated. Bypass lasted 2 hours. The pericardial sac and right pleural cavities were drained and the wound closed in the usual manner. The immediate postoperative period was uneventful, but on the tenth postoperative day, with increasing activity, recurrent episodes of acute pulmonary edema developed and recurred when he was allowed out of bed (see F i g . 3, B). Intensive therapy with diuretics and digitalis and prolonged bed rest was required before improvement was noted. Two months after opera tion the patient was discharged almost acyanotic, ambulant, and free of symptoms, although still on digitalis. Signs of marked " t r i c u s p i d " incompetence were present, with pulsating jugular veins and hepatomegaly. The heart was enlarged (see Fig. 3, C) and the auscultatory findings were unchanged. The hemoglobin had dropped from 20.2 to 12.7 Gm. per cent. Repeat investigation indicated complete transposition of the great vessels with functional correction as a result of surgical transposition of the venous connections of the atria (Fig. 7 ) . There was still a small bidirectional shunt at atrial level both from dye and saturation data (Table I ) , presumably due to a small leak between the "common a t r i u m " and the prosthesis. In addition, obstruction to flow between the right atrium and that part of the left atrium that connected the mitral valve to the venous left ventricle was demonstrated by pressure data and angiocardiography (Fig. 8 and Table I ) . This was thought to be at the site where the prosthesis, carrying the pulmonary venous blood to the tricuspid valve, partially obstructed the atrial defect which allowed blood to flow from the right atrium to the mitral valve. The aortic and tricuspid valve incompetence were not regarded as of sufficient hemodynamic importance to merit surgical correction.
SUMMARY AND CONCLUSIONS
1. A case of complete transposition of the great vessels with aortic and tricuspid incompetence, severe disability, and cyanosis is presented. Surgical correction of the transposition was successfully achieved. 2. A precise preoperative diagnosis is essential since it is important for the surgeon to be aware of the number and position of the communications between the pulmonary and systemic circuits, the pulmonary resistance, and the presence of additional abnormalities, such as pulmonary stenosis or other deformities. The value of left- and right-heart catheterization, of dye dilution curves, and of angiocardiography in establishing the precise pre- and postoperative hemodynamics is demonstrated. 3. Functional correction of the transposition was achieved by excising the atrial septum and inserting a prosthesis inside the atrial cavity. The prosthesis was so designed that the pulmonary venous return drained through it, to the
778
BARNARD, SCHRIRE, BECK
J. Thoracic and Cardiovas. Surg.
anatomic right but functional left ventricle, while the systemic venous blood flowed around it to enter the anatomic left but functional right ventricle. 4. The importance of providing a prosthesis which will allow a normal flow of blood during diastole without an undue rise in pulmonary venous pressure is emphasized. If one assumes that Poiseuille's law applies to flow through such a prosthesis, one can calculate its dimensions by substituting average normal values for the other variables. Thus, F =
P x 8
T
x - x r n 1
Where F = diastolic flow in c.c./sec. P = the mean pressure differential be tween the pulmonary vein and end-diastolic pressures in the left ventricle in millimeters of mercury.—5—= the "numerical" factor, n = the viscosity of o
blood in poise units, r 4 = the fourth power of the radius in centimeters. 1 = length of the tube in centimeters. Assuming a diastolic filling period of 0.5 of a second, at a heart rate of 80 per minute, and a cardiac output of 6 L. per minute, diastolic flow will amount to 150 c.c. per second. Assuming that a pressure differential of 5 mm. Hg at rest can safely be allowed and that the viscosity of blood at body temperature and with a normal hematocrit is 0.03 poise units, if the length of the prosthesis is 1, 2, or 3 cm., then the diameter of the tube should be 2.5, 3, and 3.25 cm., respectively. Surgical correction must include the fashioning of a left atrial muscular chamber which is anastomosed to the inelastic prosthesis. In the course of time, adequate adaptation of this chamber may develop, restoring the reservoir func tion. Ideally, the "inner t u b e " formed by the prosthesis should be constructed of atrial muscle to promote this adaptation. 5. The communication between left and right atria was not sufficiently enlarged so that the '' inner tube,'' formed by the prosthesis, partially obstructed free flow of venous blood around it, producing a "supravalvular stenosis." This resulted in systemic venous hypertension. Obstruction can be avoided by completely excising the atrial septum and, if necessary, enlarging the atrium by inserting a plastic roof. 6. Complete correction of complete transposition of the great vessels can be achieved. We wish to thank Professor J . H. Louw of the Department of Surgery, University of Cape Town, for his encouraging support of our work and the technical staff of the Marais Laboratory and the Cardiac Clinic for their assistance. We are grateful to the Medical Super intendents of the Groote Schuur Hospital and Red Cross Hospital, Drs. J . G. Burger and J . F . Mostert, respectively, for permission to report details of this case. Thanks are also due to the Council for Scientific and Industrial Research and the City Council of Cape Town, and to the C. L. Herman and Eourcade Research grants for financial support. ADDENDUM One year after operation, this patient is doing very well.
Vol. 43, No. 6 June. 1962
COMPLETE TRANSPOSITION OF GREAT VESSELS
77Q •' J
REFERENCES
1. Taussig, H. B . : Congenital Malformations of the Heart, New York, 1947, The Common wealth Fund, p. 199. 2. Hanlon, C. R., and Blaloek, A.: Complete Transposition of the Aorta and Pulmonary Arteries. Experimental Observations on Venous Shunts as Corrective Procedures, Ann. Surg. 127: 385. 1948. 3. Blaloek, A., and Hanlon, C. R.: The Surgical Treatment of Complete Transposition of the Aorta and the Pulmonary Artery, Surg. Gynec. & Obst. 90: 1, 1950. 4. Lillehei, C. W., and Varco, R. L . : Certain Physiologic, Pathologic, and Surgical Features of Complete Transposition of the Great Vessels. Surgerv 34: 376, 1953. 5. Murphy, T. O., Gott, V., Lillehei, C. W., and Varco, R. L . : The Results of Surgical Pallia tion in 32 Patients With Transposition of the Great Vessels, Surg. Gynec. & Obst. 101: 541, 1955. 6. Baffes, T. G.: A New Method for Surgical Correction of Transposition of the Aorta and Pulmonary Artery, Surg. Gynec. & Obst. 102: 227, 1956. 7. Baffes, T. G., and Potts, W. J . : Surgical Correction of Transposition of the Aorta and the Pulmonary Artery, Prog. Cardiovas. Dis. 1: 102, 1958. 8. Cooley, D . : Discussion of Toole et al. 9 9. Toole, A. L., Glenn, W. W. L., Fisher, W. H., Whittemore, R., Ordway, N . K., and Vidone, R. A.: Operative Approach to Transposition of the Great Vessels, Surgery 48: 43, 1960. 10. Bailey, C. P., Cookson, B. A., Downing, D. F . , and Neptune, W. B . : Cardiac Surgery Under Hypothermia, J . THORACIC SURG. 27: 73, 1954.
11. Bjork, V. O., and Bouckaert, L . : Complete Transposition of the Aorta and the Pulmonary Artery: An Experimental Study of Surgical Possibilities for I t s Treatment, J . THORACIC SURG. 2 8 : 632, 1954.
12. Kay, E . B., and Cross, F . S.: Surgical Treatment of Transposition of the Great Vessels, Surgery 38: 712, 1955. 13. Mustard, W. T., Chute, A. L., Keith, M. D., Sirek, A., Rowe, R. D., and Vlad, P . A . : A Surgical Approach to Transposition of the Great Vessels With Extracorporeal Circuit, Surgery 36: 39, 1954. 14. Senning, A.: Surgical Correction of Transposition of the Great Vessels, Surgery 45: 966, 1959. 15. Albert, H. M.: Surgical Correction of Transposition of the Great Vessels, Surgical Forum, 1954, American College Surgeons, Philadelphia, 1955, W. B . Saunders Com pany, p. 74. 16. Meredino, K. A., Jesseph, J . E., Herron, P . W., Thomas, G. I., and Vetto, R. R.: Interatrial Venous Transposition: A One-Stage Intracardiac Operation for the Conver sion of Complete Transposition of the Aorta and Pulmonary Artery to Corrected Transposition, Surgery 42: 898, 1957. 17. Creech, O., Jr., Mahaffey, D. E., Sayegh, S. F., and Sailors, E. L . : Complete Transposi tion of the Great Vessels: A Technique for Intracardiac Correction, Surgery 4 3 : 349, 1958. 18. Glotzer, P., Bloomberg, A. E., and Hurwitt, E . S.: An Experimental Procedure for Correction of Transposition of the Great Vessels, A. M. A. Arch. Surg. 80: 12, 1960. 19. Kirklin, J . W.: Personal communication, 1961. 20. Barnard, C. N., Terblanche, J., and Ozinsky, J . : Profound Hypothermia and the Helix Reservoir Bubble Oxygenator, South African M. J . 35: 107, 1961.
CORRECTION
C. N. Barnard, M.D., M.Med, (Cape Town), V. Schrire, M.B., Ph.D. (Cape Town), W. Beck, M.Sc,
M.Med.
Cape Town, South
M.S., Ph.D.
M.R.C.P. (Lond.),
(Cape Town),
M.R.C.P.
(Minnesota), F.R.C.P.E., and
(Lond.),
Africa
C
transposition of the great vessels may be denned as a congenital malformation in which the aorta arises exclusively from the anterior or systemic venous ventricle, the pulmonary trunk from the posterior or pulmonary venous ventricle, and the two ventricles function as separate chambers. The right atrium receives blood from the two venae cavae and coronary sinus and communicates through the tricuspid valve with the anterior ventricle. The left atrium communicates with the pulmonary veins and, through the mitral valve, empties its blood into the posterior ventricle. The aorta, with its origin from the anterior ventricle, therefore carries venous blood, whereas the pulmonary artery, arising from the posterior ventricle, carries oxygenated blood. Survival after birth is only possible if some sort of communication exists between the two sides of the heart, or great vessels, allowing mixing of the two circulations. The three most common means of communication are through defects in the atrial or ventricular septa, or a patent ductus arteriosus. One, two, or all of these may be present in a given case. Since the prognosis for pa tients born with complete transposition is very poor,1"4 many attempts have been made to correct this condition. The various operative procedures developed can be divided into two types, palliative and corrective. OMPLETE
PALLIATIVE PROCEDURES
Survival after birth is possible only because of associated defects which allow shunts between the systemic and pulmonary circuits. These must be balanced, lest one circuit be bled " d r y , " while the other becomes plethoric. Palliation can be achieved by operation if it increases mixing of the two circula tions, provided they remain balanced. 3 The early attempts were aimed at pro ducing extracardiac shunts or increasing intracardiac mixing. Five different types of extracardiac shunts, both arterial and venous, were discussed by Blalock and Hanlon, 3 but the results were uniformly bad. It apProm the Departments of Surgery and Medicine, University of Cape Town; Cardiac Clinic, Groote Schuur Hospital, and Council for Scientific and Industrial Research Cardiopulmonary Group, Cape Town, South Africa. Received for publication June 27, 1961.
768
Vol. 43, No. 6 June. 1962
COMPLETE TRANSPOSITION OF GREAT VESSELS
769 ' vv
peared that these extracardiac shunts function mainly in one direction, result ing in unbalanced circulations. Techniques for transposing the right pulmonary veins and inferior vena cava have been described by Lillehei and Varco, 4 Murphy and associates,5 and Baffes.6 These procedures allow intracardiac mixing of the blood from the inferior vena cava and left pulmonary veins in the left atrium and blood from the superior vena cava and right pulmonary veins in the right atrium. Since the two circulations remained balanced, the palliation obtained was good.7 Blalock and Hanlon 3 described a technique of creating an atrial defect to promote mixing between the two atria. Cooley8 favors this operation and claims fair results. Various combinations of the above techniques have been suggested. 3 ' 9 Blalock and Hanlon 3 claimed that their best results were obtained when atrial defects were created in combination with an anastomosis between the subclavian and pulmonary arteries. It was disappointing to find that there was only moderate improvement among the survivors and that the arterial oxygen satura tion generally remained below 75 per cent. CORRECTIVE PROCEDURES
Complete correction of blood flow in complete transposition can be obtained either by redirecting the systemic and pulmonary venous connections to the heart, thus producing a "corrected transposition," or by re-arrangement of the aorta and pulmonary arteries. As the systemic and pulmonary venous return is normal and the abnormal ity involves the origins of the aorta and pulmonary artery, the obvious approach would be to correct the anomaly at this point. Several authors10"14 have described various techniques with this in mind but no survivors have been reported. Morbid anatomic studies have shown that since the coronary arteries arise from the aorta, a mere switch-over of the major trunks results in the heart receiving desaturated blood. 4 ' 13 Furthermore, the right ventricle functions as the systemic or high pressure pump. The left ventricle in the absence of a large ventricular septal defect or pulmonary stenosis functions as a pulmonary or low pressure pump. Switching the major arteries alters the functional requirements of each ventricle. Hypotension and pulmonary edema may immediately follow. The procedure most likely to succeed is one in which the venous returns are transposed to correct the arterial transposition. With this in mind, one-stage intracardiac procedures have been devised.14"18 Only 4 successful cases have been reported. 14 ' 19 The purpose of this report is to describe a successful one-stage correction by intra-atrial venous transposition, using a plastic graft between the openings of the pulmonary veins and the tricuspid valve. CASE REPORT J . K., a 16-year-old Coloured boy, was admitted to Gioote Schuur Hospital in January, 1961, with severe disability. Cyanosis and dyspnea had been present for as long as he could remember, he had never thrived, development had been retarded, and all activities were ex tremely limited.
770
BARNARD, SCHRIRE, BECK
J. Thoracic and Cardiovas. Surg.
On examination he looked like a child of 7 years of age, being 44 inches tall and weighing 50 pounds. Moderate cyanosis (grade 2 of 4 grades) and clubbing (grade 2 of 4 grades) were equally present in fingers and toes. A striking " a " wave was visible in the jugular venous pulse (Fig. 1) which was elevated about 10 cm. above the sternal angle, and presystolic pulsation of the liver could be felt. The peripheral pulses were small, with a blood pressure of 130/110 mm. H g in the arms and a higher pressure in the legs. The clinical signs associated with Eisenmenger complex were present. Thus there was cardiomegaly, mainly right venticular in type, with a palpable second sound in the second left intercostal space. A loud ejection click was audible a t all areas, maximal in the second left intercostal space. The second sound was loud and single with an early diastolic murmur (grade 2 of 4 grades) between the second and fourth intercostal spaces (Fig. 1 ) . The electro cardiogram (Fig. 2) showed severe right atrial and right ventricular hypertrophy. The radio-
Fig. 1.—Phonocardiographic record showing a striking "a" wave (A) in the jugular ve nous pulse tracing (JUG). At the second left intercostal space (PA), the mitral area (MA), and the fourth left intercostal space (l,LS), there is a loud ejection click (X) followed by a short systolic murmur. The second heart sound is loud and single. A long early diastolic murmur is shown a t all areas except at the second right intercostal space (AA). The bottom two tracings have been mounted below the top two, but have not been synchronously recorded.
Vol. 43, No. 6 June, 1962
COMPLETE T R A N S P O S I T I O N O F GREAT VESSELS
logic appearances gave the clue to the anatomic diagnosis (Fig. 3, A), being present with a narrow pedicle and pulmonary plethora.
771
an egg-shaped heart
Cardiac catheterization was performed from the right median basilic vein, the catheter entering the superior vena cava and right atrium in the usual way. I t could be advanced into a high pressure ventricle, identified as the systemic ventricle by the identical femoral arterial and ventricular systolic pressures, the identical oxygen saturations, and the dilution curve recorded at the femoral artery following injection into this ventricle (Fig. 4, A). The catheter could also be advanced through an atrial septal defect into a low pressure ventricle (40 mm. H g ) with a high oxygen saturation (93 per cent). From this ventricle the catheter entered the pulmonary artery which had similar systolic pressures and oxygen saturations. Dilution curves following injection into this low pressure ventricle and into the pulmonary artery showed identical curves quite different from those obtained from the systemic ventricle (Fig. 4, A). X-ray studies of the catheter in the pulmonary artery showed this vessel to be placed well posterior and medial to its normal position. As the aorta could not be entered with the
Pig. 2.—Before operation, the electrocardiogram shows marked right axis deviation and severe right atrial and right ventricular hypertrophy. The postoperative tracing shows a striking change in the P wave.
Fig. 3.—Before operation (A<, tin1 :interoposterior roentgenogram shows an "egg-shaped" heart with a narrow vascular pedicle, a prominent superior vena cava, and pulmonary plethora. During convalescence after operation, bilateral pulmonary edema has developed '(B). "x By the time of discharge (C), 2 months after operation, the lung fields are clear and pulmonary plethora has diminished.
S:^
td H o W
I—(
w w w a
a
w
I
>
>
CO
Vol. 43, No. 6 June, 1962
COMPLETE TRANSPOSITION OF GREAT VESSELS
773
venous catheter, retrograde catheterization through the right brachial artery was performed. X-ray studies now showed the ascending aorta to be anterior and lateral to the pulmonary artery, establishing the presence of transposition of the great vessels. An interatrial communication with a bidirectional shunt was demonstrated by saturation data (Table I ) . Dilution curves recorded in the pulmonary artery following injection into the ascending aorta showed no early appearing dye (Fig. 4, B), excluding an aorticopulmonary communication. When dye was injected into the systemic ventricle (via the catheter passed DYE CURVES RECORDED IN RIGHT FEMORAL ARTERY GREEN
Fig. 4.—A, Dilution curves recorded at the femoral artery show that the right ventricle is the systemic ventricle, whereas the left ventricle is the pulmonary ventricle. B, Dye injected into the systemic ventricle (right ventricle) shows a minute amount of early ap pearing dye in the pulmonary artery, indicating either a small ventricular septal defect or tricuspid incompetence with a right-to-left shunt In the atria, whereas injection into the ascending aorta shows no early appearing dye, excluding an aorticopulmonary communication. retrogradely through the aortic valve), a minute amount of early appearing dye was detected in the pulmonary artery (Fig. 4, B). This suggested either a small ventricular septal defect or tricuspid valve incompetence with the shunt occurring at atrial level. The former appeared unlikely in the absence of a ventricular septal defect murmur, with a large pressure differen tial between the two ventricles. The preoperative diagnosis was, therefore, complete transposition of the great vessels with normal pulmonary resistance, pulmonary plethora and a bidirectional shunt at atrial level, tricuspid and aortic valve incompetence. A patent ductus arteriosus or ventricular septal defect was excluded. From the hemodynamic point of view the patient appeared suit able for surgical correction.
BARNARD, SCHRIRE, BECK
774
J. Thoracic and Cardiovas. Surg.
On Feb. 13, 1961, under general anesthesia (Muothane, nitrous oxide and oxygen), profound hypothermia and extracorporeal circulation with the DeWall-Lillehei bubble oxygenator, 20 the operation was performed. The chest was entered through a median sternotomy and the pericardium was opened in the midline from the roots of the great vessels down to the dome of the diaphragm. The aorta was observed to arise from the anterior ventricle, both coronary vessels from the aorta, and the pulmonary artery from the posterior ventricle. The root of the aorta and the superior and inferior venae cavae were encircled with cotton tapes. The ductus arteriosus was obliterated. Digital exploration of the interior of the heart through the right atrial appendage revealed the presence of an atrial septal defect and tricuspid incompetence, but no ventricular septal defect.
Fig. 5.—A, T-shaped incision of the anterior wall of the right atrium; B, the atrial septum has been widely excised to expose the four pulmonary veins. After systemic heparinization, a single venous catheter was inserted into the right atrium through the atrial appendage and connected to the venous line of the oxygenator. ( I n the presence of an interatrial communication, a single catheter in the right atrium will drain the venous blood and, in addition, decompresses the left heart during cooling and rewarming.) The right common femoral artery was catheterized and used for the return of oxygenated blood from the oxygenator. Bypass and cooling was commenced and continued until the midesophageal temperature was lowered to 15° C. Bypass was discontinued and the venous TABLE
I
PREOPERATIVE SITE
Superior vena cava Right atrium Inferior vena cava Left atrium Right pulmonary vein Left ventricle Pulmonary artery Right ventricle Aorta Right femoral artery
|
PRESSURE
15/7, mean 10 8/3, mean 7
POSTOPERATIVE | %
SAT.
65 79.5 69.5 88
40/2-3 35/15 125/5 125/75
99 93 93 79 79
140/85
79
Estimated 0 2 uptake, 130 c.c./min. Surface area, 0.74 M 2 , hemoglobin 20.2 Om. % Pulmonary flow, 12 L. min. Systemic flow, 4 L. min. Pulmonary vascular resistance = 1.4 units
SITE
|
PRESSURE
| %
Superior vena cava | 24/16, Right atrium i mean 20 Inferior vena cava J Left atrium (func tioning right atrium) 20/4 Left ventricle (func tioning right ven tricle ) 55/6 Right brachial artery 135/90 Withdrawal from anatomic LV-LA- 55/6 - 20/4 RA 24/16 0 2 uptake, 153 c.c./min. Surface area, 0.85 M 2 , hemoglobin 12.7 Gm. % Systemic flow, 6.6 L. min.
SAT.
66 72 70
— 70 85
Vol. 43, N o . 6
June, 1962
COMPLETE T R A N S P O S I T I O N OF GREAT VESSELS
775.
catheter removed. The right atrium was widely opened with a T-shaped incision, the top of the T running about one inch from, and parallel to, the atrioventricular groove from the base of the appendage to a point one half inch above the entrance of the inferior vena cava (Fig. 5, A). The shaft of the T extended from the midpoint of the above incision in a slightly caudad direction to end a t the interatrial groove, below the entrance of the right pulmonary veins (Fig. 5, A). The atrial septum was now excised as widely as possible, avoiding damage to the coronary sinus and the conducting system of the heart (Fig. 5, B).
Fig. 6.—A, The construction of the pouch around the tricuspid valve orifice. B, Teflon graft in position. C, Reconstruction of the right atrium. Two venous catheters were placed through the atrial incision in the superior and inferior venae eavae and connected to the venous line of the oxygenator. The caval tapes were tight ened and bypass and cooling restarted, maintaining about a third of the flow required at normal body temperature and with a mid-esophageal temperature between 15° and 20° C. A fair degree of aortic incompetence was present so that the aorta was cross-clamped to prevent the influx of blood into the heart through the incompetent valve. The aim of the operation is to divert the pulmonary venous blood from the posterior atrium to the anterior ventricle, by means of a suitably sized graft. This graft must pass through the enlarged interatrial septal defect without obstructing flow of venous blood around it, from the anterior atrium to the posterior ventricle. Since the graft in use is made of inelastic plastic material with little storage capacity it is important that it should not merely extend between the pulmonary veins and the tricuspid orifice. An atrial chamber should be constructed from the atrial wall. Even if this is not large at the time of operation it has the potentiality of developing and enlarging as time goes by.
776
BARNARD, SCHRIRE, BECK
J. Thoracic and Cardiovas. Surg.
For this reason a pouch was constructed from the remaining right atrial wall between the atrioventricular groove and the first atrial incision. The top and bottom were stitched around the cephalad, caudal, and posterior portion of the tricuspid valve ring until an opening 1.5 cm. in diameter remained (Fig. 6, A). Care was taken to exclude the coronary sinus from this chamber. This opening now formed the entrance to the newly constructed ' ' l e f t ' ' atrium. A graft of woven Teflon, 1.5 cm. in diameter, was now fashioned to fit between
Fig1. 7.—I-ateral angiogram from the superior vena cava which shows the pulmonary artery arising posteriorly from the left ventricle (A), whereas the aorta arises anteriorly from the right ventricle (B). In B, the aorta is outlined anterior to the pulmonary artery, behind which can be seen the remnant of the left atrium joining the pulmonary veins to the prosthesis. The prosthesis is not outlined.
Pig. 8.—Anterior angiogram from the superior vena cava showing the superior vena cava draining into the right atrium. The dye flows around the prosthesis, which appears as a filling defect, into the left atrium, left ventricle, and pulmonary artery. the opening and the entrance of the four pulmonary veins (Fig. 6, B). One end was at tached by continuous 4-0 silk suture to the atrial wall in such a way that the entire pulmonary venous drainage entered the graft. The other end of the graft was anastomosed to the opening left in the newly formed ' ' left a t r i u m " in a similar manner, leaving a small open ing through which the left side of the heart could be decompressed during rewarming, until an effective heartbeat was re-established. The two venous catheters were now positioned in the atrial appendage and rewarming commenced. The " r i g h t a t r i u m " was reconstructed by direct suture (Fig. 6, C). Had there
Vol. 43, No. 6 June, 1962
COMPLETE T R A N S P O S I T I O N O F GREAT VESSELS
777 ' ' '
been insufficient atrial wall, a plastic roof would have been inserted. If obstruction to flow of systemic venous blood through the interatrial defect to the posterior ventricle had been noted, the atrial incision could have been continued across the atrial groove into the posterior atrium. A plastic roof could then have been extended across to increase the interatrial opening. After rewarming, the heart was defibrillated with an electric shock. All air was then aspirated from the left atrium and anterior ventricle and the suture of the graft com pleted. On release of the venae caval tapes the heart took over with a good beat. Bypass was discontinued and the venae caval catheters removed. After giving Polybrene to neutralize the heparin, the femoral arterial catheter was removed and the femoral arteriotomy repaired with a continuous 6-0 silk suture. The following pressures were recorded at this stage: arterial, 120/60 mm. H g ; pulmonary artery, 25/12 mm. H g ; inferior vena cava, 15/10 mm. H g ; superior vena cava, 12/8 mm. H g ; right pulmonary venous pressure, 20/15 mm. H g ; arterial saturation was 96 per cent. After careful hemostasis, the pericardium was loosely approx imated. Bypass lasted 2 hours. The pericardial sac and right pleural cavities were drained and the wound closed in the usual manner. The immediate postoperative period was uneventful, but on the tenth postoperative day, with increasing activity, recurrent episodes of acute pulmonary edema developed and recurred when he was allowed out of bed (see F i g . 3, B). Intensive therapy with diuretics and digitalis and prolonged bed rest was required before improvement was noted. Two months after opera tion the patient was discharged almost acyanotic, ambulant, and free of symptoms, although still on digitalis. Signs of marked " t r i c u s p i d " incompetence were present, with pulsating jugular veins and hepatomegaly. The heart was enlarged (see Fig. 3, C) and the auscultatory findings were unchanged. The hemoglobin had dropped from 20.2 to 12.7 Gm. per cent. Repeat investigation indicated complete transposition of the great vessels with functional correction as a result of surgical transposition of the venous connections of the atria (Fig. 7 ) . There was still a small bidirectional shunt at atrial level both from dye and saturation data (Table I ) , presumably due to a small leak between the "common a t r i u m " and the prosthesis. In addition, obstruction to flow between the right atrium and that part of the left atrium that connected the mitral valve to the venous left ventricle was demonstrated by pressure data and angiocardiography (Fig. 8 and Table I ) . This was thought to be at the site where the prosthesis, carrying the pulmonary venous blood to the tricuspid valve, partially obstructed the atrial defect which allowed blood to flow from the right atrium to the mitral valve. The aortic and tricuspid valve incompetence were not regarded as of sufficient hemodynamic importance to merit surgical correction.
SUMMARY AND CONCLUSIONS
1. A case of complete transposition of the great vessels with aortic and tricuspid incompetence, severe disability, and cyanosis is presented. Surgical correction of the transposition was successfully achieved. 2. A precise preoperative diagnosis is essential since it is important for the surgeon to be aware of the number and position of the communications between the pulmonary and systemic circuits, the pulmonary resistance, and the presence of additional abnormalities, such as pulmonary stenosis or other deformities. The value of left- and right-heart catheterization, of dye dilution curves, and of angiocardiography in establishing the precise pre- and postoperative hemodynamics is demonstrated. 3. Functional correction of the transposition was achieved by excising the atrial septum and inserting a prosthesis inside the atrial cavity. The prosthesis was so designed that the pulmonary venous return drained through it, to the
778
BARNARD, SCHRIRE, BECK
J. Thoracic and Cardiovas. Surg.
anatomic right but functional left ventricle, while the systemic venous blood flowed around it to enter the anatomic left but functional right ventricle. 4. The importance of providing a prosthesis which will allow a normal flow of blood during diastole without an undue rise in pulmonary venous pressure is emphasized. If one assumes that Poiseuille's law applies to flow through such a prosthesis, one can calculate its dimensions by substituting average normal values for the other variables. Thus, F =
P x 8
T
x - x r n 1
Where F = diastolic flow in c.c./sec. P = the mean pressure differential be tween the pulmonary vein and end-diastolic pressures in the left ventricle in millimeters of mercury.—5—= the "numerical" factor, n = the viscosity of o
blood in poise units, r 4 = the fourth power of the radius in centimeters. 1 = length of the tube in centimeters. Assuming a diastolic filling period of 0.5 of a second, at a heart rate of 80 per minute, and a cardiac output of 6 L. per minute, diastolic flow will amount to 150 c.c. per second. Assuming that a pressure differential of 5 mm. Hg at rest can safely be allowed and that the viscosity of blood at body temperature and with a normal hematocrit is 0.03 poise units, if the length of the prosthesis is 1, 2, or 3 cm., then the diameter of the tube should be 2.5, 3, and 3.25 cm., respectively. Surgical correction must include the fashioning of a left atrial muscular chamber which is anastomosed to the inelastic prosthesis. In the course of time, adequate adaptation of this chamber may develop, restoring the reservoir func tion. Ideally, the "inner t u b e " formed by the prosthesis should be constructed of atrial muscle to promote this adaptation. 5. The communication between left and right atria was not sufficiently enlarged so that the '' inner tube,'' formed by the prosthesis, partially obstructed free flow of venous blood around it, producing a "supravalvular stenosis." This resulted in systemic venous hypertension. Obstruction can be avoided by completely excising the atrial septum and, if necessary, enlarging the atrium by inserting a plastic roof. 6. Complete correction of complete transposition of the great vessels can be achieved. We wish to thank Professor J . H. Louw of the Department of Surgery, University of Cape Town, for his encouraging support of our work and the technical staff of the Marais Laboratory and the Cardiac Clinic for their assistance. We are grateful to the Medical Super intendents of the Groote Schuur Hospital and Red Cross Hospital, Drs. J . G. Burger and J . F . Mostert, respectively, for permission to report details of this case. Thanks are also due to the Council for Scientific and Industrial Research and the City Council of Cape Town, and to the C. L. Herman and Eourcade Research grants for financial support. ADDENDUM One year after operation, this patient is doing very well.
Vol. 43, No. 6 June. 1962
COMPLETE TRANSPOSITION OF GREAT VESSELS
77Q •' J
REFERENCES
1. Taussig, H. B . : Congenital Malformations of the Heart, New York, 1947, The Common wealth Fund, p. 199. 2. Hanlon, C. R., and Blaloek, A.: Complete Transposition of the Aorta and Pulmonary Arteries. Experimental Observations on Venous Shunts as Corrective Procedures, Ann. Surg. 127: 385. 1948. 3. Blaloek, A., and Hanlon, C. R.: The Surgical Treatment of Complete Transposition of the Aorta and the Pulmonary Artery, Surg. Gynec. & Obst. 90: 1, 1950. 4. Lillehei, C. W., and Varco, R. L . : Certain Physiologic, Pathologic, and Surgical Features of Complete Transposition of the Great Vessels. Surgerv 34: 376, 1953. 5. Murphy, T. O., Gott, V., Lillehei, C. W., and Varco, R. L . : The Results of Surgical Pallia tion in 32 Patients With Transposition of the Great Vessels, Surg. Gynec. & Obst. 101: 541, 1955. 6. Baffes, T. G.: A New Method for Surgical Correction of Transposition of the Aorta and Pulmonary Artery, Surg. Gynec. & Obst. 102: 227, 1956. 7. Baffes, T. G., and Potts, W. J . : Surgical Correction of Transposition of the Aorta and the Pulmonary Artery, Prog. Cardiovas. Dis. 1: 102, 1958. 8. Cooley, D . : Discussion of Toole et al. 9 9. Toole, A. L., Glenn, W. W. L., Fisher, W. H., Whittemore, R., Ordway, N . K., and Vidone, R. A.: Operative Approach to Transposition of the Great Vessels, Surgery 48: 43, 1960. 10. Bailey, C. P., Cookson, B. A., Downing, D. F . , and Neptune, W. B . : Cardiac Surgery Under Hypothermia, J . THORACIC SURG. 27: 73, 1954.
11. Bjork, V. O., and Bouckaert, L . : Complete Transposition of the Aorta and the Pulmonary Artery: An Experimental Study of Surgical Possibilities for I t s Treatment, J . THORACIC SURG. 2 8 : 632, 1954.
12. Kay, E . B., and Cross, F . S.: Surgical Treatment of Transposition of the Great Vessels, Surgery 38: 712, 1955. 13. Mustard, W. T., Chute, A. L., Keith, M. D., Sirek, A., Rowe, R. D., and Vlad, P . A . : A Surgical Approach to Transposition of the Great Vessels With Extracorporeal Circuit, Surgery 36: 39, 1954. 14. Senning, A.: Surgical Correction of Transposition of the Great Vessels, Surgery 45: 966, 1959. 15. Albert, H. M.: Surgical Correction of Transposition of the Great Vessels, Surgical Forum, 1954, American College Surgeons, Philadelphia, 1955, W. B . Saunders Com pany, p. 74. 16. Meredino, K. A., Jesseph, J . E., Herron, P . W., Thomas, G. I., and Vetto, R. R.: Interatrial Venous Transposition: A One-Stage Intracardiac Operation for the Conver sion of Complete Transposition of the Aorta and Pulmonary Artery to Corrected Transposition, Surgery 42: 898, 1957. 17. Creech, O., Jr., Mahaffey, D. E., Sayegh, S. F., and Sailors, E. L . : Complete Transposi tion of the Great Vessels: A Technique for Intracardiac Correction, Surgery 4 3 : 349, 1958. 18. Glotzer, P., Bloomberg, A. E., and Hurwitt, E . S.: An Experimental Procedure for Correction of Transposition of the Great Vessels, A. M. A. Arch. Surg. 80: 12, 1960. 19. Kirklin, J . W.: Personal communication, 1961. 20. Barnard, C. N., Terblanche, J., and Ozinsky, J . : Profound Hypothermia and the Helix Reservoir Bubble Oxygenator, South African M. J . 35: 107, 1961.