- Email: [email protected]
The case for anatomic correction of transposition of the great arteries
The case for anatomic correction of transposition of the great arteries Magdi H. Yacoub, F.R.C.S.,* London, England
Although inflow "correction" of complete transposition of the great arteries (TGA) by the Mustard I or Senning operation": :l has given good early and medium-term results in selected patients,~-6 these procedures are not correcti ve. Concern about the long-term results continues because of the relatively high incidence of complications, which include obstruction of the pulmonary or systemic venous return." H serious arrhythmias.": 10 and tricuspid regurgitation.": 11 Technical modifications have lowered the incidence of the first two complications. but the basic problem of the right ventricle and tricuspid valve serving the systemic circulation cannot be altered. On theoretical grounds, these two structures are not anatomically suitable to sustain the high pressure of the systemic circulation for a long time. Unlike the left ventricle, the right ventricle has a muscular inlet and outlet with the myocardium arranged as a tube wrapped around the left ventricle. 12 In contrast. the left ventricle is flask shaped with both outlet and inlet orifices situated in its base, so that the myocardium is enabled to deliver a bolus of blood against high resistance with less difficulty. These theoretical considerations are supported by the fact that, in the absence of TGA, pulmonary hypertension to near systemic levels produces right ventricular failure and tricuspid regurgitation in a relatively short period. Furthermore, patients with anatomically corrected or incomplete transposition can develop severe leftsided (tricuspid) atrioventricular (A V) valve regurgitation and right ventricular failure in early adulthood, despite the absence of anatomic defects of the tricuspid valve. Late right ventricular failure, after inflow "correction," has also been reported. l:l Hemodynamic studies have shown that, after inflow "correction," most patients have varying degrees of impairment of right ventricular function and a significant number have tricuspid regurgitation, which in some cases was not suspected clinically.": 6. I~ Abnormal function of the 'Consultant Cardiac Surgeon. Harefield Hospital, Middlesex, and National Heart Hospital, London, W. I, England.
mitral val ve and left ventricular outflow, evidenced by echocardiographic findings of systolic anterior movement and coarse diastolic fluttering of the mitral valve, is not uncommon after the Mustard operation. 1;;.16 This abnormal function probably is due to the abnormal shape and bulge of the interventricular septum into the left ventricular outflow tract. This bulge probably also is responsible for the common finding of gradients across the pulmonary outflow tract in these patients. 16.17 Partial or complete loss of the reservoir and contractile function of the atria may also impair cardiac performance, as suggested by the echocardiographic findings of fluttering of the mitral valve and by the marked change in amplitude of mitral valve excursion and in left ventricular end-diastolic dimension with respiration, which is particularly prominent during deep respiratory effort. Ifi Abnormal distribution of pulmonary blood flow with preferential flow to the right lung occurs in approximately 50 percent of patients with TGA. I H. I!I This preferential flow leads to progressive hypoplastic changes in the left pulmonary vascular bed. These changes tend to progress or develop after inflow "correction, "IH. 20 because the abnormalities responsible for this hemodynamic defect (the abnormal direction of the main pulmonary artery and the tendency to subpulmonary stenosis) are left uncorrected. All of these hemodynamic abnormalities probably are accentuated by exercise and may limit the functional capacity of the children. Exercise stress tests late after inflow correction have shown less than normal values in all patients tested.F' The progress of these abnormalities is unknown, but they could have serious implications in the future. Because of these theoretical considerations as well as the clinical and hemodynamic findings, the need for an alternative, more direct method of treatment, as has been previously stressed.F is still valid. Recently, techniques for anatomic correction of TGA at the arterial level were independently developed and applied by several groups.v" " Review of the available knowledge including analysis of a personal experience with 30
0022-5223/79/070003+04$00.40/0 © 1979 The C. V. Mosby Co.
3
The Journal of
4
Yacoub
patients undergoing anatomic correction during the past 7 years has served to identify several problems and provide some answers concerning this procedure. The first problem relates to the necessity of transposing the coronary arteries to the posterior vessel at a very young age without tension, torsion, or kinking. As the mode of origin and early course of the coronary arteries vary considerably in TGA,:IO-:l2 it was envisaged that only a minority of patients will be suited for anatomic correction.P" However, following a detailed anatomic study, methods were evolved for transfer of the different types of coronary arteries.F Currently, we believe that all anatomic types are suitable for transfer. The second problem relates to the ability of the left ventricle to support the systemic circulation immediately after operation. This poses no difficulty in patients with additional lesions that maintain a high left ventricular systolic pressure, such as large ventricular septal defects, patent ductus arteriosus, or subpulmonary stenosis.t"?" However, in patients with TGA and intact interventricular septum (which constitutes the majority), rapid diminution in left ventricular mass occurs shortly after birth because of the normal fall in left ventricular pressure associated with the drop in pulmonary vascular resistance.Vi :" With few exceptions,:ln.:17 the left ventricle is rendered incapable of supporting the systemic circulation, as shown by our early experience with three patients operated upon between 1972 and 1975, who developed fatal pulmonary edema several hours after operation, because of progressive failure of a thin-walled left ventricle. Similar experience has since been reported.P': :IH In these patients it is possible to redevelop the left ventricle by banding of the pulmonary artery with or without an aortopulmonary shunt proximal to the band. :I!l* Our more recent experience has shown that the shunt is unnecessary. To date, 10 patients in our series have undergone anatomic correction following prior banding. There were three early and no late deaths during a period of follow-up varying from 2 months to 2 1/ 2 years. Two of the deaths were due to the wrong position of the band, which was too high in one (producing severe pulmonary arterial branch stenosis) and too low in the other (producing significant semilunar valve regurgitation). We believe that the ideal age for the first-stage procedure is during the first few weeks of life to prevent the left ventricle from becoming too thin prior to banding and to have the biggest impact on the natural history of the disease. However, in our small series two children who under*Yacoub MH. Bernhard A, Radley-Smith. R. Stephan E. Lange P. Heintzen PH: Anatomical correction of transposition of the great arteries with intact interventricular septum. Unpublished data.
Thoracic and Cardiovascular Surgery
went banding at the age of 2 1/ 2 years were subsequently able to have successful anatomic correction. The third problem relates to the need for bridging the gap between the proximal end of the transected aorta and the distal pulmonary artery. Although direct anastomosis is possible.i": :17 undue tension may lead to pulmonary arterial stenosis or pressure on one of the coronary arteries. The gap can be bridged by a Dacron or homologous dura tube.:" The latter offers the possibility of using a sufficiently large tube in young infants to last through adult life. However, the long-term behavior of these nonvalved conduits is not known, and it is possible that they may require replacement at a later date. The fourth problem relates to the ability of the coronary and aortic anastomoses to grow. Repeat cardiac catheterization was performed I year or more after operation on five occasions in four patients.* This examination showed no signs of narrowing of either anastomosis despite considerable growth during these periods. The longest period was in a child investigated 2 1/ 2 years after anatomic correction at the age of 8 weeks. However, longer periods of follow-up are necessary to determi ne the fate of these anastomoses. The fifth problem relates to the ability of the new aortic valve and sinuses of Valsalva to function normally without progressive dilatation and incompetence. The marked discrepancy in size between the pulmonary arterial root and the ascending aorta, which is encountered only in older children, produces an abnormal angiographic shape similar to aneurysm of the aortic root. This abnormality in shape, combined with the thin arterial wall of the pulmonary artery, may lead to progressive dilatation later in life. However, progression has never been documented. Although significant postoperative aortic regurgitation was reported in one patient;" this could have been present since operation. Among 12 patients reinvestigated 3 to 30 months after operation, minimal aortic regurgitation was observed in II. * Any abnormality of the pulmonary valve encountered at the time of operation is considered to be a contraindication to arterial switch. The sixth problem relates to the ability of the left ventricle to maintain long-term normal function after correction. Analysis of echocardiographic and angiographic findings after anatomic correction in 12 patients in our series showed that, after an initial period of depressed left ventricular function for 2 to 3 weeks, the left ventricle continued to function normally. Although there are still unanswered questions about the long-term results of anatomic correction, the avail*Radley-Smith R. Yacoub M: Unpublished data.
Volume 78
Correction of TGA
Number 1
5
July. 1979
able evidence suggests that this procedure should playa major role in the future management of patients with TGA.
16
REFERENCES
:2 3
4
5
6
7
8
9
10
II
12
13
14
15
Mustard WT, Chute AL, Keith JD, Sirek A. Rowe RD, Vlad PA; Surgical approach to transposition of the great vessels with extracorporcal circuit. Surgery 36:39, 1954. Senning A: Surgical correction of transposition of the great vessels. Surgery 45;966. 1959 Quacgebeur JM, Rohmer J, Brom AG: Revival of the Senning operation in the treatment of transposition of the great arteries. Preliminary report on recent experience. Thorax 32:517. 1977 Stark J, de Leval M, Waterston OJ, Graham GR, Bonham-Carter RE: Corrective surgery of transposition of the great arteries in the first year of life. Results in 63 infants. J THoRAc CARDIOVASC SURG 67:673. 1974 Clarkson PM, Neutze JM. Barratt-Boyes BG, Brandt PW: Late postoperative hemodynamic results and cineangiocardiographic findings after Mustard atrial baffle repair for transposition of the great arteries. Circulation 53:525, 1976 Hagler OJ, Ritter DG. Mair DO. Davis GO. McGoon DC: Clinical. angiographic and hemodynamic assessment of late results after Mustard operation. Circulation 57:1214, 1978 Stark J. Silove ED, Taylor JFN, Graham GR: Obstruction to systemic venous return following the Mustard operation for transposition of the great arteries. J THORAC CARDIOVASC SURG 68:742, 1974 Berman MA, Talner NS, Stansel HC Jr: Experience with Mustard's operation in infants less than one year of age. Emphasis on late complications including patch stenosis. Surgery 73: 133, 1973 EI Said G. Rosenberg HS, Mullins CEo Hallman GL, Cooley DA. McNamara DG: Dysrhythmias after Mustard's operation for transposition of the great arteries. Am J Cardiol 30:526, 1972 Clarkson PM. Barrett-Boyes RG. Neutze JM: Late dysrhythmias and disturbances of conduction following Mustard operation for complete transposition of the great arteries. Circulation 53:519. 1976 Tynan M, Aberdeen E, Stark J: Tricuspid incompetence after the Mustard operation for transposition of the great arteries. Circulation 45:Suppl I: III. 1972 Zimmerman J, Bailey CP: The surgical significance of the fibrous skeleton of the heart J THORAC CARDIOVASC SURG 44:701. 1962 Buja LM. Miller WW: Nixon JV. Atkins JM. Curry Late right ventricular failure after Mustard operation for transposition of the great arteries. Cathet Cardiovasc Diagn 4:175.1978 Mair DO. Hagler OJ: Late results of the Mustard operation for transposition of the great arteries. Proceedings of the Eighth World Congress of Cardiology. Tokyo. 1978 Hagler OJ. Tajik AJ, Ritter DG: Fluttering of atrioven-
oc.
17
18
19
20
21
22 23
24 25
26
27
28
29
30
31
tricular valves in patients with d-transposition of the great arteries after Mustard operation. Mayo Clinic Proc 50:69, 1975 Neches WC, Zuberbuhler JR, Mathews RA. Park Lenox Cc, Fricker F: Echocardiographic and hemodynamic correlation in transposition of the great arteries. Circulation 57:291, 1978 Fisher EA, Muster AJ, Lev M, et al; Angiographic and anatomic findings in transposition of the great arteries with left ventricular outflow tract gradients (abstr). Am J Cardiol 25:95, 1970 Vidne BA, Duszynski 0, and Subramanian S: PUlmonary flow distribution in transposition of the great arteries (abstr). Am J Cardiol 37:178, 1976 Muster AJ, Paul MH, van Grondelle A. Conway JJ: Asymmetrical distribution of pulmonary blood flow between the right and left lungs in D-transposition of the great arteries. Am J Cardiol 38:352, 1976 Morgan JR, Miller BL, Daicoff GR, Andrews EJ: Hemodynamic and angiocardiographic evaluation after Mustard procedure for transposition of the great arteries. J THoRAc CARDIOVASC SURG 64:878, 1972 Weller Ph, Haworth SG, Taylor JFN, Macartney FJ, de Leval M, Stark J: Working capacities of children with TGA after Mustard repair (abstr). Br Heart J 48: 1066P, 1978 McGoon DC: Surgery for transposition of the great arteries. Circulation 45:1147, 1972 Anagnostopoulos CE, Athanasuleas CL, Arcilla RA: Toward a rational operation for transposition of the great arteries. Ann Thorac Surg 16:458, 1973 Stansel HC: A new operation for 0 loop transposition of the great vessels. Ann Thorac Surg 19:565, 1975 Jatene AD, Fontes VF, Paulista PP, Souza LCB, Neger F, Galantier M, Sousa JEMR: Successful anatomic correction of transposition of the great vessels. A preliminary report Arq Bras Cardiol 28:461, 1975 Yacoub MH, Radley-Smith R, Hilton CJ: Anatomical correction of complete transposition of the great arteries and ventricular septal defect in infancy. Br Med J I: 1112, 1976 Ross 0, Rickards A, Sommerville J: Transposition of the great arteries. Logical anatomical arterial correction. Br Heart J 1:1101,1976 Starr A: Discussion of Jatene AD, Fontes VF, Paulista PP, Souza LCB, Neger F, Galantier M, Sousa JEMR: Anatomic correction of transposition of the great vessels. J THORAC CARDIOVASC SURG 72:364, 1976 Aubert J, Pannetier A, Couvelly JP, Unal 0, Rouault F, Delarue A: Transposition of the great arteries. New technique for anatomical correction. Br Heart J 40:204, 1978 Elliot LP, Amplatz K, Edwards JE: Coronary arterial patterns in complete transposition complexes. Anatomic and angiographic studies. J Cardiol 17:362, 1966 Shaher RM, Puddis GC: The coronary arterial anatomy in complete transposition of the great vessels. Am J Cardiol 17:355, 1966
sc.
The Journal of
6
Yacoub
Thoracic and Cardiovascular Surgery
32 Yacoub MH, Radley-Smith R: Anatomy of the coronary arteries in transposition of the great arteries and methods for their transfer in anatomical correction. Thorax
33:418, 1978 33 Hvass U: Coronary arteries in 0 transposition. A necropsy study of reimplantation. Br Heart J 39: 1234, 1977 34 Tynan M: Transposition of the great arteries. Changes in circulation after birth. Circulation 46:809, 1972 35 Editorial: Br Med J 1: 1104, 1976 36 Mauck HP Jr. Robertson LW, Parr EJ, Lower RR: Anatomic correction of transposition of the great arteries without significant ventricular septal defect or patent due-
tus arteriosus. J THORAC CARDIOVASC SURG 74:631, 1977 37 Abe T, Kuribayashi R, Sato M, Nieda S, Takahashi M, Okubo T: Successful Jatene operation for transposition of the great arteries with intact ventricular septum. A case report. J THoRAc CARDIOVASC SURG 75:64, 1978 38 Major WK Jr. Matsuda H, Subramanian S: Failure of the Jatene procedure in a patient with D-transposition and intact ventricular septum. Ann Thorac Surg 22:386, 1976 39 Yacoub MH, Radley-Smith R, Maclaurin R: Two-stage operation for anatomical correction of transposition of the great arteries with intact interventricular septum. Lancet 1:1275, 1977
Information for authors Most of the provisions of the Copyright Act of 1976 became effective on January I, 1978. Therefore, all manuscripts must be accompanied by the following written statement, signed by one author: "The undersigned author transfers all copyright ownership of the manuscriptItitle of article) to The C. V. Mosby Company in the event the work is published. The undersigned author warrants that the article is original, is not under consideration by another journal, and has not been previously published. I sign for and accept responsibility for releasing this material on behalf of any and all co-authors." Authors will be consulted, when possible, regarding republication of their material.
Although inflow "correction" of complete transposition of the great arteries (TGA) by the Mustard I or Senning operation": :l has given good early and medium-term results in selected patients,~-6 these procedures are not correcti ve. Concern about the long-term results continues because of the relatively high incidence of complications, which include obstruction of the pulmonary or systemic venous return." H serious arrhythmias.": 10 and tricuspid regurgitation.": 11 Technical modifications have lowered the incidence of the first two complications. but the basic problem of the right ventricle and tricuspid valve serving the systemic circulation cannot be altered. On theoretical grounds, these two structures are not anatomically suitable to sustain the high pressure of the systemic circulation for a long time. Unlike the left ventricle, the right ventricle has a muscular inlet and outlet with the myocardium arranged as a tube wrapped around the left ventricle. 12 In contrast. the left ventricle is flask shaped with both outlet and inlet orifices situated in its base, so that the myocardium is enabled to deliver a bolus of blood against high resistance with less difficulty. These theoretical considerations are supported by the fact that, in the absence of TGA, pulmonary hypertension to near systemic levels produces right ventricular failure and tricuspid regurgitation in a relatively short period. Furthermore, patients with anatomically corrected or incomplete transposition can develop severe leftsided (tricuspid) atrioventricular (A V) valve regurgitation and right ventricular failure in early adulthood, despite the absence of anatomic defects of the tricuspid valve. Late right ventricular failure, after inflow "correction," has also been reported. l:l Hemodynamic studies have shown that, after inflow "correction," most patients have varying degrees of impairment of right ventricular function and a significant number have tricuspid regurgitation, which in some cases was not suspected clinically.": 6. I~ Abnormal function of the 'Consultant Cardiac Surgeon. Harefield Hospital, Middlesex, and National Heart Hospital, London, W. I, England.
mitral val ve and left ventricular outflow, evidenced by echocardiographic findings of systolic anterior movement and coarse diastolic fluttering of the mitral valve, is not uncommon after the Mustard operation. 1;;.16 This abnormal function probably is due to the abnormal shape and bulge of the interventricular septum into the left ventricular outflow tract. This bulge probably also is responsible for the common finding of gradients across the pulmonary outflow tract in these patients. 16.17 Partial or complete loss of the reservoir and contractile function of the atria may also impair cardiac performance, as suggested by the echocardiographic findings of fluttering of the mitral valve and by the marked change in amplitude of mitral valve excursion and in left ventricular end-diastolic dimension with respiration, which is particularly prominent during deep respiratory effort. Ifi Abnormal distribution of pulmonary blood flow with preferential flow to the right lung occurs in approximately 50 percent of patients with TGA. I H. I!I This preferential flow leads to progressive hypoplastic changes in the left pulmonary vascular bed. These changes tend to progress or develop after inflow "correction, "IH. 20 because the abnormalities responsible for this hemodynamic defect (the abnormal direction of the main pulmonary artery and the tendency to subpulmonary stenosis) are left uncorrected. All of these hemodynamic abnormalities probably are accentuated by exercise and may limit the functional capacity of the children. Exercise stress tests late after inflow correction have shown less than normal values in all patients tested.F' The progress of these abnormalities is unknown, but they could have serious implications in the future. Because of these theoretical considerations as well as the clinical and hemodynamic findings, the need for an alternative, more direct method of treatment, as has been previously stressed.F is still valid. Recently, techniques for anatomic correction of TGA at the arterial level were independently developed and applied by several groups.v" " Review of the available knowledge including analysis of a personal experience with 30
0022-5223/79/070003+04$00.40/0 © 1979 The C. V. Mosby Co.
3
The Journal of
4
Yacoub
patients undergoing anatomic correction during the past 7 years has served to identify several problems and provide some answers concerning this procedure. The first problem relates to the necessity of transposing the coronary arteries to the posterior vessel at a very young age without tension, torsion, or kinking. As the mode of origin and early course of the coronary arteries vary considerably in TGA,:IO-:l2 it was envisaged that only a minority of patients will be suited for anatomic correction.P" However, following a detailed anatomic study, methods were evolved for transfer of the different types of coronary arteries.F Currently, we believe that all anatomic types are suitable for transfer. The second problem relates to the ability of the left ventricle to support the systemic circulation immediately after operation. This poses no difficulty in patients with additional lesions that maintain a high left ventricular systolic pressure, such as large ventricular septal defects, patent ductus arteriosus, or subpulmonary stenosis.t"?" However, in patients with TGA and intact interventricular septum (which constitutes the majority), rapid diminution in left ventricular mass occurs shortly after birth because of the normal fall in left ventricular pressure associated with the drop in pulmonary vascular resistance.Vi :" With few exceptions,:ln.:17 the left ventricle is rendered incapable of supporting the systemic circulation, as shown by our early experience with three patients operated upon between 1972 and 1975, who developed fatal pulmonary edema several hours after operation, because of progressive failure of a thin-walled left ventricle. Similar experience has since been reported.P': :IH In these patients it is possible to redevelop the left ventricle by banding of the pulmonary artery with or without an aortopulmonary shunt proximal to the band. :I!l* Our more recent experience has shown that the shunt is unnecessary. To date, 10 patients in our series have undergone anatomic correction following prior banding. There were three early and no late deaths during a period of follow-up varying from 2 months to 2 1/ 2 years. Two of the deaths were due to the wrong position of the band, which was too high in one (producing severe pulmonary arterial branch stenosis) and too low in the other (producing significant semilunar valve regurgitation). We believe that the ideal age for the first-stage procedure is during the first few weeks of life to prevent the left ventricle from becoming too thin prior to banding and to have the biggest impact on the natural history of the disease. However, in our small series two children who under*Yacoub MH. Bernhard A, Radley-Smith. R. Stephan E. Lange P. Heintzen PH: Anatomical correction of transposition of the great arteries with intact interventricular septum. Unpublished data.
Thoracic and Cardiovascular Surgery
went banding at the age of 2 1/ 2 years were subsequently able to have successful anatomic correction. The third problem relates to the need for bridging the gap between the proximal end of the transected aorta and the distal pulmonary artery. Although direct anastomosis is possible.i": :17 undue tension may lead to pulmonary arterial stenosis or pressure on one of the coronary arteries. The gap can be bridged by a Dacron or homologous dura tube.:" The latter offers the possibility of using a sufficiently large tube in young infants to last through adult life. However, the long-term behavior of these nonvalved conduits is not known, and it is possible that they may require replacement at a later date. The fourth problem relates to the ability of the coronary and aortic anastomoses to grow. Repeat cardiac catheterization was performed I year or more after operation on five occasions in four patients.* This examination showed no signs of narrowing of either anastomosis despite considerable growth during these periods. The longest period was in a child investigated 2 1/ 2 years after anatomic correction at the age of 8 weeks. However, longer periods of follow-up are necessary to determi ne the fate of these anastomoses. The fifth problem relates to the ability of the new aortic valve and sinuses of Valsalva to function normally without progressive dilatation and incompetence. The marked discrepancy in size between the pulmonary arterial root and the ascending aorta, which is encountered only in older children, produces an abnormal angiographic shape similar to aneurysm of the aortic root. This abnormality in shape, combined with the thin arterial wall of the pulmonary artery, may lead to progressive dilatation later in life. However, progression has never been documented. Although significant postoperative aortic regurgitation was reported in one patient;" this could have been present since operation. Among 12 patients reinvestigated 3 to 30 months after operation, minimal aortic regurgitation was observed in II. * Any abnormality of the pulmonary valve encountered at the time of operation is considered to be a contraindication to arterial switch. The sixth problem relates to the ability of the left ventricle to maintain long-term normal function after correction. Analysis of echocardiographic and angiographic findings after anatomic correction in 12 patients in our series showed that, after an initial period of depressed left ventricular function for 2 to 3 weeks, the left ventricle continued to function normally. Although there are still unanswered questions about the long-term results of anatomic correction, the avail*Radley-Smith R. Yacoub M: Unpublished data.
Volume 78
Correction of TGA
Number 1
5
July. 1979
able evidence suggests that this procedure should playa major role in the future management of patients with TGA.
16
REFERENCES
:2 3
4
5
6
7
8
9
10
II
12
13
14
15
Mustard WT, Chute AL, Keith JD, Sirek A. Rowe RD, Vlad PA; Surgical approach to transposition of the great vessels with extracorporcal circuit. Surgery 36:39, 1954. Senning A: Surgical correction of transposition of the great vessels. Surgery 45;966. 1959 Quacgebeur JM, Rohmer J, Brom AG: Revival of the Senning operation in the treatment of transposition of the great arteries. Preliminary report on recent experience. Thorax 32:517. 1977 Stark J, de Leval M, Waterston OJ, Graham GR, Bonham-Carter RE: Corrective surgery of transposition of the great arteries in the first year of life. Results in 63 infants. J THoRAc CARDIOVASC SURG 67:673. 1974 Clarkson PM, Neutze JM. Barratt-Boyes BG, Brandt PW: Late postoperative hemodynamic results and cineangiocardiographic findings after Mustard atrial baffle repair for transposition of the great arteries. Circulation 53:525, 1976 Hagler OJ, Ritter DG. Mair DO. Davis GO. McGoon DC: Clinical. angiographic and hemodynamic assessment of late results after Mustard operation. Circulation 57:1214, 1978 Stark J. Silove ED, Taylor JFN, Graham GR: Obstruction to systemic venous return following the Mustard operation for transposition of the great arteries. J THORAC CARDIOVASC SURG 68:742, 1974 Berman MA, Talner NS, Stansel HC Jr: Experience with Mustard's operation in infants less than one year of age. Emphasis on late complications including patch stenosis. Surgery 73: 133, 1973 EI Said G. Rosenberg HS, Mullins CEo Hallman GL, Cooley DA. McNamara DG: Dysrhythmias after Mustard's operation for transposition of the great arteries. Am J Cardiol 30:526, 1972 Clarkson PM. Barrett-Boyes RG. Neutze JM: Late dysrhythmias and disturbances of conduction following Mustard operation for complete transposition of the great arteries. Circulation 53:519. 1976 Tynan M, Aberdeen E, Stark J: Tricuspid incompetence after the Mustard operation for transposition of the great arteries. Circulation 45:Suppl I: III. 1972 Zimmerman J, Bailey CP: The surgical significance of the fibrous skeleton of the heart J THORAC CARDIOVASC SURG 44:701. 1962 Buja LM. Miller WW: Nixon JV. Atkins JM. Curry Late right ventricular failure after Mustard operation for transposition of the great arteries. Cathet Cardiovasc Diagn 4:175.1978 Mair DO. Hagler OJ: Late results of the Mustard operation for transposition of the great arteries. Proceedings of the Eighth World Congress of Cardiology. Tokyo. 1978 Hagler OJ. Tajik AJ, Ritter DG: Fluttering of atrioven-
oc.
17
18
19
20
21
22 23
24 25
26
27
28
29
30
31
tricular valves in patients with d-transposition of the great arteries after Mustard operation. Mayo Clinic Proc 50:69, 1975 Neches WC, Zuberbuhler JR, Mathews RA. Park Lenox Cc, Fricker F: Echocardiographic and hemodynamic correlation in transposition of the great arteries. Circulation 57:291, 1978 Fisher EA, Muster AJ, Lev M, et al; Angiographic and anatomic findings in transposition of the great arteries with left ventricular outflow tract gradients (abstr). Am J Cardiol 25:95, 1970 Vidne BA, Duszynski 0, and Subramanian S: PUlmonary flow distribution in transposition of the great arteries (abstr). Am J Cardiol 37:178, 1976 Muster AJ, Paul MH, van Grondelle A. Conway JJ: Asymmetrical distribution of pulmonary blood flow between the right and left lungs in D-transposition of the great arteries. Am J Cardiol 38:352, 1976 Morgan JR, Miller BL, Daicoff GR, Andrews EJ: Hemodynamic and angiocardiographic evaluation after Mustard procedure for transposition of the great arteries. J THoRAc CARDIOVASC SURG 64:878, 1972 Weller Ph, Haworth SG, Taylor JFN, Macartney FJ, de Leval M, Stark J: Working capacities of children with TGA after Mustard repair (abstr). Br Heart J 48: 1066P, 1978 McGoon DC: Surgery for transposition of the great arteries. Circulation 45:1147, 1972 Anagnostopoulos CE, Athanasuleas CL, Arcilla RA: Toward a rational operation for transposition of the great arteries. Ann Thorac Surg 16:458, 1973 Stansel HC: A new operation for 0 loop transposition of the great vessels. Ann Thorac Surg 19:565, 1975 Jatene AD, Fontes VF, Paulista PP, Souza LCB, Neger F, Galantier M, Sousa JEMR: Successful anatomic correction of transposition of the great vessels. A preliminary report Arq Bras Cardiol 28:461, 1975 Yacoub MH, Radley-Smith R, Hilton CJ: Anatomical correction of complete transposition of the great arteries and ventricular septal defect in infancy. Br Med J I: 1112, 1976 Ross 0, Rickards A, Sommerville J: Transposition of the great arteries. Logical anatomical arterial correction. Br Heart J 1:1101,1976 Starr A: Discussion of Jatene AD, Fontes VF, Paulista PP, Souza LCB, Neger F, Galantier M, Sousa JEMR: Anatomic correction of transposition of the great vessels. J THORAC CARDIOVASC SURG 72:364, 1976 Aubert J, Pannetier A, Couvelly JP, Unal 0, Rouault F, Delarue A: Transposition of the great arteries. New technique for anatomical correction. Br Heart J 40:204, 1978 Elliot LP, Amplatz K, Edwards JE: Coronary arterial patterns in complete transposition complexes. Anatomic and angiographic studies. J Cardiol 17:362, 1966 Shaher RM, Puddis GC: The coronary arterial anatomy in complete transposition of the great vessels. Am J Cardiol 17:355, 1966
sc.
The Journal of
6
Yacoub
Thoracic and Cardiovascular Surgery
32 Yacoub MH, Radley-Smith R: Anatomy of the coronary arteries in transposition of the great arteries and methods for their transfer in anatomical correction. Thorax
33:418, 1978 33 Hvass U: Coronary arteries in 0 transposition. A necropsy study of reimplantation. Br Heart J 39: 1234, 1977 34 Tynan M: Transposition of the great arteries. Changes in circulation after birth. Circulation 46:809, 1972 35 Editorial: Br Med J 1: 1104, 1976 36 Mauck HP Jr. Robertson LW, Parr EJ, Lower RR: Anatomic correction of transposition of the great arteries without significant ventricular septal defect or patent due-
tus arteriosus. J THORAC CARDIOVASC SURG 74:631, 1977 37 Abe T, Kuribayashi R, Sato M, Nieda S, Takahashi M, Okubo T: Successful Jatene operation for transposition of the great arteries with intact ventricular septum. A case report. J THoRAc CARDIOVASC SURG 75:64, 1978 38 Major WK Jr. Matsuda H, Subramanian S: Failure of the Jatene procedure in a patient with D-transposition and intact ventricular septum. Ann Thorac Surg 22:386, 1976 39 Yacoub MH, Radley-Smith R, Maclaurin R: Two-stage operation for anatomical correction of transposition of the great arteries with intact interventricular septum. Lancet 1:1275, 1977
Information for authors Most of the provisions of the Copyright Act of 1976 became effective on January I, 1978. Therefore, all manuscripts must be accompanied by the following written statement, signed by one author: "The undersigned author transfers all copyright ownership of the manuscriptItitle of article) to The C. V. Mosby Company in the event the work is published. The undersigned author warrants that the article is original, is not under consideration by another journal, and has not been previously published. I sign for and accept responsibility for releasing this material on behalf of any and all co-authors." Authors will be consulted, when possible, regarding republication of their material.