Surgical closure of ventricular septal defect during the first twelve months of life

J

THORAC CARDIOVASC SURG

80:921-928, 1980

Surgical closure of ventricular septal defect during the first twelve months of life Fifty-two infants with a large ventricular septal defect (VSD) underwent primary surgical closure within the first 12 months of life. Operation was done because of medically intractable congestive heart failure in 39 patients (75%), failure to thrive in nine patients (17.3%), and increased pulmonary vascular resistance (PVR) (>8 unitslmi) in four patients (7.6%). Four patients (7.6%) died in the early postoperative period. Surgically induced heart block did not occur in any patient. Relief of heart failure and normalization of growth and weight gain was evident in all survivors. Late postoperative hemodynamic evaluation in 15 patients with preoperative elevation of PVR revealed normal pulmonary artery pressure and resistance in each instance. Residual VSD was found in only one patient (2%) with partial disruption of a muscular VSD originally closed by direct suture. There was one late postoperative death from unrelated causes. The results of primary closure of VSD in infancy are compared with those of preliminary pulmonary artery banding (PAB) and of VSD closure after PAB. Fifty-six patients with isolated VSD or with VSD associated with atrial septal defect. patent ductus arteriosus, or aortic arch anomalies underwent initial palliative PAB. There were 10 early postoperative deaths (17.8%). Four additional patients died in the late postoperative period. Severe elevation of PVR persisted in three patients despite PAB. Closure of VSD and pulmonary artery debanding was done in 43 patients. with four early postoperative deaths (9.3%). Distal migration of the band necessitated extensive reconstruction of one or both pulmonary arteries in four patients. Placement of the PAB too close to the pulmonary anulus necessitated transannular patching in three patients. The staged surgical management of symptomatic VSD in infancy carries significant mortality and complication rates. Early primary closure is the treatment of choice because of its lower postoperative mortality rate and superior long-term results.

Eduardo Arciniegas, M.D., Zia Q. Farooki, M.D., Mehdi Hakimi, M.D., Burton L. Perry, M.D., and Edward W. Green, M.D., Detroit, Mich.

Infants with a large ventricular septal defect (VSD) and congestive heart failure unresponsive to intensive medical therapy require prompt surgical intervention. Failure to thrive, recurrent respiratory infections and, less frequently, increasing pulmonary vascular resistance (PVR) are also indications for early operation. Previously, the preferred surgical approach consisted of initial pulmonary artery banding (PAB) followed at a later time by direct closure of the VSD and pulmonary artery debanding. This treatment plan, however, has been abandoned in most centers because of the significant mortality and morbidity associated with both From the Department of Cardiovascular Surgery and the Division of Cardiology, Children's Hospital of Michigan, Detroit, Mich. 48201. Received for publication April I, 1980. Accepted for publication April 22, 1980. Address for reprints: Eduardo Arciniegas, M.D., Department of Cardiovascular Surgery, Children's Hospital of Michigan, 3901 Beaubien, Detroit, Mich. 48201.

the banding and debanding procedures and the incidence of further deaths and complications between the two stages. Additionally, the preliminary banding often complicates the intracardiac repair and may adversely affect the late hemodynamic result. More recently, early primary closure has been advocated for all infants requiring operation in whom the VSD is the major intracardiac defect. In this report we review our experience with surgical closure of VSD during the first 12 months of life. In order to provide additional comparative data, we also analyze our results with PAB for symptomatic VSD in infancy as well as our experience with total intracardiac repair after PAB .

Patients and methods Primary surgical closure of VSD. Fifty-two infants in whom a large VSD was the major intracardiac lesion were treated by early surgical closure of the defect at Children's Hospital of Michigan from May, 1973, to

0022-5223/80/120921+08$00.80/0 © 1980 The C. V. Mosby Co.

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Table I. Age distribution and mortality rate among 52 infants who underwent primary surgical closure of VSD within the first 12 months of life Hospital deaths

Age (mo)

No. of patients

No.

<3 3-6 7-12

4 2127

2 2

9.5 7.4

Totals

52-

4

7.6

I

%

Legend: VSD, Ventricular septal defect.

"Includes two patients with early failure of pulmonary artery banding.

Table II. Preoperative catheterization data in 52 infants who underwent surgical closure of VSD within the first 12 months of life Pulmonary-systemic ratio

I

Flow Pressure Resistance

Range

Mean

1.1-6.8 0.35-1.07 0.07-0.72

3.54 0.86 0.25

Table III. Incidence of anatomic VSD types among 92 patients who underwent surgical closure No. of patients VSD

type

Primary closure

Closure after PAR

I

IV Multiple

40 7 2 3

Totals

52-

II III

%

5 25 6 4

5 65 13 6 3

5.4 70.6 14.1 6.5 3.2

40t

92

99.8

"Includes two patients with early failure of pulmonary artery band (PAB).

t Excludes three patients with spontaneous closure of VSD.

Table IV. Nonfatal postoperative complications following surgical closure of VSD in infancy Complication Low cardiac output Respiratory insufficiency Complete heart block Temporary A V dissociation S V tachycardia Bleeding Retained IP needle Bacteremia

I

No. of patients

12 15 0 2 2 I I I

'--'!i-V-23.0 28.8 3.8 3.8 1.9 1.9 1.9

Legend: AV, Atrioventricular, SV, Supraventricular. lP, lntrapericardial.

December, 1979. The patients are not consecutive because prior to 1975, when our current policy of routine early surgical closure of isolated VSD was adopted, PAB was done selectively in some of the smaller and younger infants. Two patients are included who underwent intracardiac repair at the ages of 3 and 6 months, respectively, following inadequate preliminary PAB. The ages of the patients ranged from 2 to 12 months, with a mean age of 6.9 months (Table I). The mean weight of the patients was 5.2 kg (range 3.1 to 8.1 kg). Congestive heart failure persisting despite intensive medical treatment was present in 39 patients (75%) and was the most common indication for operation. Early operation was also needed because of failure to thrive in nine patients (17.3%) and because of significant elevation of PVR (>8 units) in four other patients (7.6%). The clinical diagnosis of large VSD was confirmed by cardiac catheterization and cineangiograms in all patients. The hemodynamic data are summarized in Table II. The PVR was less than 4 units/rn 2 in 29 patients (55.7%), all of whom were in intractable congesti ve heart failure. Moderate elevation of PVR (4 to 8 units/rn") was present in 19 patients (36.5%) and a severe increase (>8 units/rn") was demonstrated in the remaining four infants (7.6%). Associated cardiovascular anomalies included atrial septal defect in 23 patients (44.2%), patent ductus arteriosus in seven patien ts (13.4%), aortic valvular stenosis in one patient (1.9%), and right aortic arch in two patients (3.8%). The most common anatomic VSD type.' was type II, which occured in 40 patients. The incidence of other types is listed in Table III. Surgical technique. During the earlier part of our experience intracardiac repair was done with high-flow normothermic cardiopulmonary bypass and intermittent aortic cross-clamping. More recently, moderate systemic hypothermia has been used routinely in conjunction with multidose injection of asanguineous cold cardioplegic solution and topical myocardial cooling for improved myocardial protection. The length of extracorporeal perfusion ranged from 40 to 95 minutes (mean 72 minutes). Deep hypothermic circulatory arrest was employed for better exposure only in the smallest infants and in some patients with type III and type IV defects. The VSD was exposed in all patients through a vertical right ventriculotomy, which avoided all major coronary artery branches. It was closed in all instances with a Dacron patch that was sutured in place with interrupted horizontal mattress sutures buttressed with Teflon pledgets. In the posteroinferior portion of type II and III defects, the sutures were placed caudal and to

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the right of its edge to avoid injury to the conduction system. Large muscular defects were also closed with a prosthetic patch. The atrial septum was routinely inspected through the tricuspid valve and associated atrial septal defects were closed by this approach or through a separate right atriotomy. The pulmonary artery was reconstructed with a pericardial patch in two infants who required early repair after failure of preliminary PAB. Associated aortic valvular stenosis was relieved by valvulotomy in a 6-week-old baby. A patent ductus arteriosus was ligated intrapericardially before initiation of cardiopulmonary bypass in seven patients. Postoperative care included careful maintenance of blood volume and replacement of blood losses from the chest. Right atrial, left atrial, and systemic arterial pressures were monitored in all patients during the first 48 hours after operation. Cardiac output was not routinely measured. The need for postoperative inotropic support has been reduced markedly since cold and cardioplegia were introduced for improved myocardial protection. Ventilation was assisted overnight in all patients and, thereafter, extubation was done according to the patient's individual ventilatory status. Early results. Four patients (7.6%) died in the immediate postoperative period (Table I). Low cardiac output was the cause of death in three patients. Intractable supraventricular tachycardia, which may have been related to an accidental digoxin overdose, was a contributing factor in one patient. Postmortem examination revealed a satisfactory repair in each instance. Another patient died on postoperative day 14 from ventilatory difficulties. This was a 5-month-old infant with pre-existing severe distal airway obstruction and bilateral lung hyperinflation. Major nonfatal complications are listed in Table IV. Low cardiac output was considered to be present if inotropic support was needed longer than 24 hours after operation. Respiratory insufficiency was felt to exist in patients requiring ventilatory support for more than 48 hours. Permanent complete heart block did not occur in any patient. Temporary atrioventricular dissociation, present in two infants, converted to normal sinus rhythm during the first postoperative day. One other patient required re-exploration on postoperative day 10 for removal of a retained intrapericardial suture needle. Late results. One patient died of pneumococcal meningitis 6 months after operation. Autopsy revealed the intracardiac repair to be satisfactory. One patient, whose parents are migrant farm workers, was lost to follow-up. All other patients (n = 47) are alive and well from 3 to 75 months postoperatively (mean follow-up 20.3 months).

N

E "-

10

2 9 w u 8

z i=! 7 en en w a: 6 a:
:J

u

en 4 ~

>a:
z

0

3 2

::!i'

...J

:J

a.

PRE-OP

POST-OP

Fig. 1. Postoperative changes in pulmonary vascular resistance in 15 infants who underwent early primary surgical closure of ventricular septal defect. Hemodynamic evaluation was done an average of 30.8 months after operation.

Relief of congestive heart failure was prompt in all patients following closure of the VSD. Weight gain has become normal for the respective age and height of each patient. The mean cardiothoracic ratio, measured at an average of 28 months postoperatively, was 0.57 as compared to 0.65 before operation. Review of the postoperative electrocardiographic tracings revealed complete right bundle branch block in all patients. Left anterior hemiblock was present before operation in two patients and developed postoperatively in nine additional patients (18.7 %). Hemodynamic evaluation has been done in 15 patients from 6 to 75 months (mean 30.8 months) following operation. The patients selected for postoperative cardiac catheterization were those with preoperative elevation of PVR (>4 units/m-) or with residual postoperative heart murmurs. Residual VSD (Qp/Qs 1.2) was found in only one patient with partial disruption of a muscular VSD closed by direct suture. Hemodynamically unimportant residual Ieft-to-right shunt at the atrial level was present in two patients. The postoperative pulmonary artery pressure was normal in all patients. The pulmonary-systemic artery pressure ratio after operation ranged from 0.1 to 0.25 (average 0.16) whereas, preoperatively, it had ranged from 0.62 to 1.07 (average 0.86). The PVR was normal postoperatively in all patients studied (Fig. 1). Pulmonary artery banding (PAB). Fifty-seven infants in whom a large VSD was the main intracardiac lesion underwent PAB during the first 12 months of life from 1972 to 1979 (Table V). The age of the patients ranged from 3 days to 12 months (mean age 2V2 months). The ratio of pulmonary-systemic flow (Qp/ Qs)

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924 Arciniegas et al.

Thoracic and Cardiovascular Surgery

Table V. Age distribution and mortality rate among 57 patients who underwent initial pulmonary artery banding VSD with associated lesions

I

Age (rno)

Isolated VSD


5 5 4

4 (3)*

14 0

5 (3) 60

With ASD

PDA

PDA

I

6 (3) 12 2 (I)

I

Totals Mortality rate (%)

+

I Coarct.

4 3 2

fAA

7 (3) I

I

21 (4) 19

9 0

8 (3) 37.5

Legend: VSD, Ventricular septal defect. ASD, atrial septal defect. PDA, patent ductus arteriosus. Coarct, Coarctation, lAA, Interrupted aortic arch. 'Numbers in parentheses represent postoperative deaths.

Table VI. Age distribution and mortality rate among 43 patients who underwent surgical VSD closure and pulmonary artery debanding Operative deaths Age (yr)

No. of patients

<2 2-5 >5

3 30 10

4

13.3

Totals

43*

4

9.3

No.

I

%

* Excludes two patients with early band failure. Includes three patients with spontaneous VSD closure after banding.

ranged from 0.94 to 9.60 with a mean flow ratio of 3.7. The ratio of pulmonary-systemic pressure (Pp/P s) ranged from 0.16 to 1.2 (average 0.83). Surgical technique. An anterolateral thoracotomy was used in patients with isolated VSD and in those with associated atrial septal defect. A posterolateral incision was preferred in patients with coexisting patent ductus arteriosus, coarctation, or aortic arch interruption. A Dacron band containing a radiopaque marker was passed around the main pulmonary artery and tightened until the pressure distal to it was reduced to between one half and one third of prebanding levels. This procedure usually was associated with a simultaneous rise in the systemic arterial pressure and a strong systolic thrill in the pulmonary artery beyond the band. Excessive constriction, as indicated by bradycardia or systemic arterial desaturation, was carefully avoided. The band was secured to the pulmonary artery wall with fine interrupted sutures to prevent distal migration. A small plastic catheter was routinely inserted into the

radial artery for intraoperative and postoperative measurement of blood pressure and arterial blood gases. Early results. There were no deaths within 30 days following PAB among 23 patients with VSD alone or in association with patent ductus arteriosus (Table V). Ten deaths occurred among 34 patients with coexisting atrial septal defect or aortic arch anomalies. Low cardiac output was the cause of death in eight patients. Severe pulmonary vascular obstructive disease was present at autopsy in another patient, aged 5 t/2 months, who died at operation. One additional patient, a 2-month-old infant, died on postoperative day 24 from Staphylococcus aureus septicemia. At postmortem examination the band had cut through the pulmonary artery wall and produced a false aneurysm. Late results. All patients but one were available for follow-up. There were four late postoperative deaths. Three infants died on post-banding days 42, 50, and 120 from persistent ventilatory difficulty, distal airway obstruction, and bilateral pulmonary hyperinflation. Another infant died at home 6 months after operation from an undetermined cause. Insufficient band constriction caused persistent congestive heart failure in five infants, three of whom underwent successful band revision early in our experience; the other two patients were subjected, more recently, to direct VSD closure and pulmonary artery debanding. Severe elevation of PVR persisted in three patients who underwent PAB at the ages of 8 months, 22 days and 8 months; the condition precludes further surgical treatment. The VSD has closed almost completely in an 8-year-old girl with only moderate constriction at the band level (30 mm Hg systolic pressure gradient); no further operation is currently contemplated. Twenty-nine patients have undergone VSD closure and pulmonary artery angioplasty in our hospital, with three postoperative deaths. One additional patient underwent subsequent intracardiac repair successfully elsewhere. Closure of VSD and pulmonary artery debanding. Forty-three patients have undergone VSD closure following PAB (Table VI). The initial banding operation was done in our institution in 29 patients and elsewhere in the other 14 patients. Two infants are excluded who underwent total repair at the ages of 3 and 6 months, respectively, after unsuccessful banding. The ages of the patients at the time of intracardiac repair ranged from 16 months to 12.4 years (mean age 52.1 months). The average interval between banding and definitive correction was 44.8 months. All patients were evaluated by cardiac catheterization and cineangiograms prior to closure of the VSD and pulmonary artery debanding. Preoperative herno-

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dynamic data in these patients are summarized in Table VII. Associated cardiovascular anomalies included atrial septal defect in nine patients (20.9%), fibromembranous subaortic stenosis in two patients (4.6%), persistent left superior vena cava in one patient (2.3%), and congenital heart block in one patient (2.3%). In the latter patient, a permanent pacemaker had been inserted at the time of the preliminary banding. Intracardiac repair was done with an operative technique and postoperative support methods similar to those employed in the patients undergoing primary VSD closure. The pulmonary artery constriction was relieved in all patients by insertion of a generous pericardial patch. The incision in the pulmonary artery extended to the origin of the left pulmonary artery in 39 patients. Distal migration of the band required right pulmonary artery angioplasty in three patients and bilateral pulmonary artery reconstruction in one additional patient. Transannular patching was necessary in three patients in whom the band was located too close to the pulmonary valve anulus. Acquired thickening of the pulmonary valve leaflets and valvular stenosis necessitated valvulotomy in one other patient. Marked muscular hypertrophy of the right ventricular outflow tract necessitating resection was present in 32 patients. Spontaneous VSD closure occurred in three patients. Intracardiac pressures were measured intraoperatively following termination of cardiopulmonary bypass and after hemodynamic stabilization in all patients (Table VIII). There was no residual systolic pressure gradient across the right ventricular outflow tract in 28 patients (65.1%). Moderate gradients «40 mm Hg) were found in the remaining 15 patients. Early results. Four patients (9.5%) died in the early postoperative period. One died as a result of severe diffuse brain damage, presumably related to intraoperative systemic air embolization. Low cardiac output was the cause of death in three other patients. One of these patients, a 3 1/2-year-old girl who had undergone PAB at the age of 10 months, was found at autopsy to have severe pulmonary vascular obstructive disease. Postmortem examination revealed the intracardiac repair to be satisfactory in each instance. Early nonfatal complications included low cardiac output in 12 patients. Severe postintubation laryngeal edema necessitated tracheostomy in one patient. Persistent bleeding from the chest necessitated early reexploration in three patients. One patient had a superficial wound infection and another patient had moderate congestive heart failure which responded to appropriate medical therapy. Heart block did not occur in any patient.

925

Table VII. Preoperative hemodynamic data in 43 patients who underwent closure of VSD and pulmonary artery debanding Ratio

I---R-a-ng-e----.--M-e-a-n-0.4-3.0 0.08-0.65 0.01-0.45 40-123

Flow Pressure* Resistance Pressure gradient

* Pulmonary artery pressure

1.34 0.22 0.12 76.8

measured distal to band.

Table VIII. Residual intraoperative systolic pressure gradients across right ventricular outflow tract following pulmonary artery debanding Gradient (mm Hg) None

<10 10-20 21-40 Totals

I

No. of patients 28 3

1--0;;-0--

II I

65.1 6.9 25.5 2.3

43

99.8

Late results. Two patients have been lost to followup. There have been no late deaths. Functional results have been good in all late survivors. Postoperative hemodynamic evaluation has been done in only three patients. Significant elevation of PVR persisted 3 years after intracardiac repair in a 6-year-old girl. Marked aneurysmal dilatation of the pericardial patch used for the pulmonary artery angioplasty was present in another patient in whom successful corrective reoperation has been done. No residual abnormalities were found in the remaining patient. Discussion VSD is the most common congenital heart lesion. According to Keith and associates," it occurs once in every 1,000 live births and, as an isolated defect, it is found in about 30% of children with congenital heart disease." Congestive heart failure develops during the first year of life in about 25% of infants with a large VSD,4 and another 20% are at risk from progressive pulmonary vascular disease." Because medical treatment alone in this group of critically ill infants carries a high mortality rate," surgical intervention is frequently indicated. In the past, controversy existed as to the superiority of PAB over early routine surgical VSD closure. PAB gained initial popularity as a palliative procedure because, in many instances, it effectively reduced the excessive pulmonary blood flow and provided clini-

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926 Arciniegas et al.

cal improvement." By contrast, the earlier attempts at direct closure of VSD carried a high mortality rate, especially during the first 6 months of Iife. 7- 1O However, PAB is an unsatisfactory operation, partly because of the intraoperative difficulties encountered in judging the optimal degree of arterial constriction required. This is evidenced by the numerous criteria of banding adequacy which have been advocated. Some of these criteria include decreasing the pulmonary artery diameter to 50% or less, II reducing the pulmonary artery circumference according to predetermined formulas related to the patient's body weight,'! lowering the pulmonary artery pressure by one half or more while maintaining normal systemic oxygen saturation and increasing the systemic arterial pressure.r" " and producing a strong systolic thrill distal to the band without causing myocardial cyanosis or impaired cardiac action. 16 None of these guidelines, either alone or in combination, is entirely reliable. This was demonstrated in our own experience by persistence of excessive pulmonary blood flow and congestive heart failure in five of our patients whose initial banding was judged to be adequate by several of these criteria. Similar experience has been previously reported. 14, 17 In other instances, 18 excessive tightening of the band has caused early cyanosis and polycythemia. PAB is also unsatisfactory because of significant early and late operative mortality rates and the development of band-related complications which add to the technical complexity of the subsequent intracardiac repair and, in some instances, adversely affect the quality of the ultimate hemodynamic result. 19 Although there were no early deaths following PAB among our patients with isolated VSD or VSD associated with patent ductus arteriosus, postoperative mortality rates ranging from 7% to 53% have been reported by others'< 19-21 in comparable groups of patients. The early post-banding mortality rate is increased by additional deaths occurring prior to and following closure of VSD and pulmonary artery debanding. Four of our patients died between the first and second stages and three other patients, among those who underwent the initial PAB in our institution, died after intracardiac repair. Adding these seven deaths to the 10 early deaths which occurred after the preliminary banding, the overall mortality rate in our experience with the two-stage approach was 29.8% (17/57 patients). Moreover, three additional patients were found to be unable to undergo operation because of severe elevation of PVR, which was not prevented by PAB. Most of the late complications which occurred in our patients following PAB have been described by others

Thoracic and Cardiovascular Surgery

and represent additional undesirable features of this procedure. Distal band migration causes stenosis of the origin of one or both pulmonary artery branches.I''- 20 which may not always be relieved by extensive angioplastic procedures. Band placement too close to the pulmonary valve anulus may demand proximal extension of the pulmonary arteriotomy into the right ventricular outflow tract and insertion of a transannular patch for effective debanding. Thickening and stenosis of the pulmonary valve leaflets, presumably caused by trauma against the band;'? may necessitate pulmonary valvulotomy. Excessive muscular hypertrophy of the right ventricular outflow tract frequently necessitates extensive resection, Pressure necrosis of the pulmonary artery at the band site with partial intraluminal band migration and false aneurysm formation occurred in one of our patients and has also been described by Idriss.!" Hunt," and their co-workers. Thrombosis of the pulmonary artery proximal to the band developed in one case reported by Osborn and colleagues.F Spontaneous VSD closure was documented in three of our patients and, although not strictly a complication because it is also seen in non banded patients, its occurrence may be fostered by band-induced myocardial hypertrophy, Such mechanism has been invoked by Freed and associates'" to explain the development of acquired left ventricular outflow tract obstruction in four of their patients. PAB currently is reserved in our institution for patients with complex intracardiac anomalies associated with increased pulmonary blood flow which are not amenable to safe early repair. PAB also has been used in the initial management of infants with VSD and coarctation and of infants with multiple muscular VSDs. The high operative mortality rate in the group of patients with VSD associated with aortic arch anomalies has prompted us and others" to question the role of PAB in this subset of patients and to consider the possibility of repairing only the coarctation at the initial operation. The hemodynamic effect of the VSD can be better evaluated subsequently and the defect treated by early direct closure if clinical improvement is not complete. Otherwise, elective closure may be carried out between 12 and 24 months of age, if the lesion remains clinically significant. Early surgical closure of a large VSD in infants not responding to maximal medical treatment was recommended previously, 8, 9 but high mortality rates, especially in children under 6 months of age, hampered the general acceptance of this otherwise most appealing one-stage treatment concept. More recently, improvements in perfusion techniques and perioperative man-

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Ventricular septal defect

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agement of infants with complex intracardiac defects also have resulted in lower postoperative death rates in infants with a large VSD.25-30 Ptoper surgical technique and careful attention to detail should result in an incidence of postoperative residual VSD and heart block no greater than that encountered when the repair is done in older children. Normalization of pulmonary artery pressure and resistance following early surgical closure of VSD was demonstrated in our patients at late cardiac catheterization. This supports previous observations by DuShane and Kirklin'" and contrasts with the failure of PAB consistently to prevent the progress of pulmonary vascular obstructive disease. Our low mortality rate and good late results following surgical closure of VSD in infancy confirm the superiority of this treatment policy over the two-stage approach. We are grateful to Ms. Diane Pannette for her valuable assistance. REFERENCES Kirklin rw, Harshbarger HG, Donald DE, Edwards JE: Surgical correction of ventricular septal defects. Anatomic and technical considerations. 1 THoRAc SURG 33:45-59, 1957 2 Keith ID, Rose V, Collins G, Kidd BSL; Ventricular septal defect. Incidence, morbidity and mortality in various age groups. Br Heart 1 33:81-87, 1971 3 Hoffman JIE, Rudolph AM: The natural history of ventricular septal defects in infancy. Am 1 Cardiol 16:634653, 1965 4 Ritter DG, Feldt RH, Weidman WH, DuShane lW: Ventricular septal defect. Circulation 31, 32:Suppl 3:42-52, 1965 5 Collins G, Calder L, Rose V, Kidd L, Keith 1: Ventricular septal defect. Clinical and hemodynamic changes in the first five years of life. Am Heart 1 84:695-705, 1972 6 Muller WH, Dammann IF: The treatment of certain congenital malformations of the heart by the creation of pulmonic stenosis to reduce pulmonary hypertension and excessive pulmonary blood flow. A preliminary report. Surg Gynecol Obstet 95:213-219, 1952 7 Hallman GL, Cooley DA, Wolfe RR, McNamara DG: Surgical treatment of ventricular septal defect associated with pulmonary hypertension. 1 THoRAc CARDIOVASC SURG 48:588-600, 1964 8 Sigmann 1M, Stem AM, Sloan HE: Early surgical correction of large ventricular septal defects. Pediatrics 39:4-13, 1967 9 Cartmill TB, DuShane JW, McGoon DC, Kirklin JW: Results of repair of ventricular septal defect. J THORAC CARDIOVASC SURG 52:486-499, 1966 10 Ching E, DuShane JW, McGoon DC, Danielson GK: Total correction of ventricular septal defect in infancy using extracorporeal circulation. Surgical considerations and results of operation. Ann Thorac Surg 12: 1-10, 1971

11 Reid JM, Barclay RS, Coleman EN, Stevenson IG, Welsh TM, McSwan N: Pulmonary artery banding in congenital heart disease associated with pulmonary hypertension. Thorax 23:385-391, 1968 12 Trusler GA, Mustard WT: A method of banding the pulmonary artery for large isolated ventricular septal defect with and without transposition of the great arteries. Ann Thorac Surg 13:351-355, 1972 13 Grainger RG, Nagle RE, Pawidapha C, Robertson DS, Taylor DG, Thornton JA, Verel D, Zachary RB: Pulmonary artery banding for ventricular septal defect. Br Heart 129:289-298, 1967 14 Stark J, Aberdeen E, Waterston DJ, Bonham-Carter RE, Tynan M: Pulmonary artery constriction (banding). A report of 146 cases. Surgery 65:808-818, 1969 15 Coles lC, Gergely NF, Buttigliero J: Banding the pulmonary artery. Clin Pediatr 2:316-322, 1963 16 Hallman GL, Cooley DA, Bloodwell RD: Two-stage surgical treatment of ventricular septal defect. Results of pulmonary artery banding in infants and subsequent open-heart repair. 1 THoRAc CARDIOVASC SURG 52:476485, 1966 17 Takahashi M, Lurie PR, Petry EL, King N: Clinical and hemodynamic effects of pulmonary artery banding. Am J Cardiol 21:174-184, 1968 18 Idriss FS, Riker WL, Paul MH: Banding of the pulmonary artery. A palliative surgical procedure. J Pediatr Surg 3:465-474, 1968 19 Hunt CE, Formanek G, Levine MA, Castaneda A, Moller IH: Banding of the pulmonary artery. Results in III children. Circulation 43:395-406, 1971 20 Henry 1, Kaplan S, Helmsworth JA, Schreiber IT: Management of infants with large ventricular septal defects. Results with two-stage surgical treatment. Ann Thorac Surg 15:109-119, 1973 21 Horsley BL, Zuberbuhler lR, Bahnson HT: Factors influencing survival after banding of the pulmonary artery. A review of 89 cases. Arch Surg 101:776-779, 1970 22 Osborn lR, Hall Rl, Winn DF, Capper RS, Black HA: An unusual late complication of pulmonary artery banding. Circulation 34:61-64, 1966 23 Freed MD, Rosenthal A, Plauth WH, Nadas AS: Development of subaortic stenosis after pulmonary artery banding. Circulation 47, 48:Suppl 3:7- 10, 1973 24 Strafford M, Hayes CJ, Griffiths SP, Hordof AJ, Edie RN, Bowman FO, Maim JR, Gersony WM: Management of the infant with coarctation of the aorta and ventricular septal defect (abstr). Am 1 Cardiol 45:450, 1980 25 Barratt-Boyes BG, Neutze JM, Clarkson PM, Shardey GC, Brandt PWT: Repair of ventricular septal defect in the first two years of life using profound hypothermiacirculatory arrest techniques. Ann Surg 184:376-390, 1976 26 Agosti J, Subramanian S: Corrective treatment of isolated ventricular septal defect in infancy. 1 Pediatr Surg 10:785-793, 1975 27 Blackstone EH, Kirklin rw, Bradley EL, DuShane JW,

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Appelbaum A: Optimal age and results in repair of large ventricular septal defects. J THoRAc CARDIOVASC SURG 72:661-679, 1976 28 Johnson DC, Cartmill TB, Celermajer JM, Hawker RE, Stuckey OS, Bowdler JD, Overton J: Intracardiac repair of large ventricular septal defect in the first year of life. Med J Aust 2:193-196, 1974 29 McNicholas KW, Bowman FO, Hayes CJ, Edie RN, Maim JR: Surgical management of ventricular septal de-

Thoracic and Cardiovascular Surgery

fects in infants. J THoRAc CARDIOVASC SURG 75:346353, 1978 30 Rein JG, Freed MD, Norwood WI, Castaneda AR: Early and late results of closure of ventricular septal defect in infancy. Ann Thorac Surg 24: 19-27, 1977 31 DuShane JW, Kirklin JW: Late results of the repair of ventricular septal defect on pulmonary vascular disease, Advances in Cardiovascular Surgery, JW Kirklin, ed., New York, 1973, Grune & Stratton, Inc., p 9