Experience with Valved Conduits for Repair of Congenital Cardiac Lesions

Experience with Valved Conduits for Repair of Congenital Cardiac Lesions William I. Nonvood, M.D., Michael D. Freed, M.D., Albert I?. Rocchini, M.D., William F. Bernhard, M.D., and Aldo R. Castaneda, M.D. ABSTRACT Dacron valved conduits or aortic allografts were placed between the right heart and the pulmonary artery for repair of various complex congenital cardiac anomalies in 56 patients (aged 5 days to 33 years; median, years). Forty-four patients had a total of 56 previous palliative procedures, which contributed to postoperative morbidity and mortality. Six patients had a total of seven episodes of early or late sepsis involving the conduit. One patient, treated for early sepsis, again developed infection in the Hancock graft year postoperatively and died. Three other patients, 2 with calcified allografts, developed infections 4 months to 7 years following repair and required graft replacement. Hemodynamic data month to 5 years (mean,.6 years) following repair revealed mild to moderate obstruction (< 45 mm Hg gradient) at the Hancock conduit valve ring in 3 of 9 patients, while 5 had large pressure gradients (> 75 mm Hg). All aortic allografts had severe obstruction and calcification necessitating graft replacement. It is anticipated that improved technique. and appropriate timing of palliative and corrective operations will substantially reduce or eliminate these problems. While some forms of cyanotic congenital heart disease were corrected soon after the advent of cardiopulmonary bypass, lesions that lacked continuity between the systemic venous ventricle and the pulmonary artery remained a challenge until the mid 96s [4, 4. A valved con- From the Departments of Cardiovascular Surgery and Cardiology, The Children s Hospital Medical Center, and The Departments of Surgery and Pediatrics, Harvard Medical School, Boston, MA. Supported in part by project No. 26 from the Maternal and Child Health Service, Health Service and Mental Health Administration, United States Public Health Service, and by grants HL 5855-8 and 5 PO 436-OH from the National Institutes of Health. Presented at the Thirteenth Annual Meeting of The Society of Thoracic Surgeons, Jan 24-26, 977, San Francisco, CA. Address reprint requests to Dr. Nonvood, Department of Cardiovascular Surgery, The Children s Hospital Medical Center, 3 Longwood Ave, Boston, MA 25. duit to bridge the anatomical barrier was used in 966 by Ross [7] in a patient with ventricular septa defect (VSD) and pulmonary atresia (PA). This provided a conceptual breakthrough that was quickly extended to other complex congenital cardiac lesions such as truncus arteriosus communis (TAC) in 968 [5, {S,D,D}* transposition of the great arteries (d-tga), VSD and pulmonic stenosis one year later 33, and tricuspid atresia (TA) in 97 [2. In the years since valved conduits were first used, important advances have been made both in the understanding of these lesions and in surgical techniques. The purpose of this review is to make clear some of the present advantages and limitations of valved conduits in right heart reconstruction. Clinical Material Between October, 972, and November, 976,56 patients had a valved conduit placed from the right side of the heart to the pulmonary arteries at Children s Hospital Medical Center, Boston. The age of the patients at the time of repair ranged from 5 days to 33 years (mean, years) (Fig ). Two operations were performed in the first month of the patient s life, and 9 patients were 5 years of age or younger. Initially, 4 patients received a frozen irradiated aortic allograft. Since July, 973, all have had placement of a Dacron conduit containing a porcine aortic valve (Hancock Laboratories). The primary diagnosis in the 56 patients is listed in Table. Thirty-two patients had severe forms of tetralogy of Fallot, including 23 with infundibular or valvular atresia, 2 with anomalous origin of the left anterior descending coronary artery from the right coronary artery, and with either congenital or acquired absence of one pulmonary artery. There were 9 patients with *Situs solitus, o-loop of ventricle, D position of aorta. 223

224 The Annals of Thoracic Surgery Vol 24 No 3 September 977 i died <2 2 4 6 8 2 4 6 8 2 22 >23 YEARS Fig I. Distribution of the56patients by age. d-tga, 7 with VSD and subpulmonic stenosis (PS), with a single ventricle, and with a hypoplastic right ventricle and overriding tricuspid valve. There were 8 children with truncus arteriosus. Two had previously had repair at another institution by means of an aortic allograft and required reoperation because of calcification, obstruction, and infection of the allograft. The other 7 patients had either double-outlet right ventricle (2 patients), {S,L,L}* TGA, VSD and PS (2 patients), PA with intact ventricular septum (IVS) ( patient), or TA (2 patients). Forty patients had a total of 52 palliative shunts performed prior to repair, and 2 with increased pulmonary blood flow had had previous pulmonary artery banding (Table 2). Ten patients had associated anomalies requiring correction (Table 3). Generally, the clinical indications for operation were increasing cyanosis and decreasing exercise tolerance secondary to diminished pulmonary flow. For those patients younger than 4 years of age, most of whom had truncus arteriosus, intractable congestive heart failure and increased pulmonary artery pressure were valuable determinants for operation. All operations were done on cardiopulmonary bypass with moderate hypothermia (3 C), except for 2 infants who underwent repair of TAC by means of deep hypothermic circulatory arrest. Five patients who were reoperated on for graft replace- *Situs solitus, L-loop of ventricle, L position of aorta. ment were placed on peripheral cardiopulmonary bypass using femoral vessels prior to opening the sternum. All VSDs were closed with a knitted Dacron patch. Initially, the proximal orifice for conduit reconstruction was created with a transverse ventriculotomy and excision of a small button of ventricular wall. However, in the last 8 months a smoother exit of the conduit without proximal angulation has been obtained with a vertical incision and little or no excision of ventricular muscle. Three patients, 2 with TA and with PA and IVS, had Hancock conduits interposed between the right atrium and pulmonary arteries. (Two patients with type Ib TA repaired with a nonvalved conduit are excluded from this review.) Two patients required a bifurcated conduit constructed by interposing a 2 mm Dacron graft between the Hancock conduit (distal to the valve) and the right pulmonary artery. One child had a partially thrombosed right pulmonary artery and the other had had a previous Glenn anastomosis. Routinely, at the time of operation we have placed left atrial, right atrial, and radial artery catheters to monitor blood pressure and ventricular filling pressures, and we recently have placed catheters through the right ventricular free wall, across the conduit, into the main pulmonary artery (23 patients). This allows measurement of residual left-to-right shunts (if present) as well as pressures and gradients in the conduit when the catheter is removed 24 to 48 hours postoperatively. Cardiac catheterization is routinely recommended for all patients year postoperatively. To date, hemodynamic data are available for 23 patients month to 5 years (mean,.6 years) after repair. All had right heart catheterization and right ventricular cineangiography and 6 had left heart studies. Early Results Hospital mortality was 2% (2 of 56 patients) and seemed to be related more to the severity of the underlying disease than to age (see Fig ). Four of 32 patients with tetralogy of Fallot died shortly after their corrective procedure. One 8-year-old girl had pulmonary vascular obstructive disease secondary to longstanding bilateral Blalock-Taussig shunts and had inter-

225 Nonvood et al: Valved Conduits for Repair of Congenital Cardiac Lesions Table. Distribution of Lesions Repaired Mortality No. of Lesion Defects Hospital Late Tetralogy of Fallot 32 4 Pulmonary atresia 23 a 2 9 Single pulmonary artery Double-outlet RV TGA {s,d,d} VSD + PS HRV + OTVb Single ventricle TGA {s,l,l}, VSD, + psc 2 Tricuspid atresia 2 Truncus arteriosus communis 8 4 Pulmonary atresia + IVS 7 Total 56 2 (2%) 3 (7%) patient had both pulmonary atresia and single pulmonary artery. Conduit interposed between RA and PA. cconduit interposed between LV and PA. TGA = transposition of the great arteries; VSD = ventricular septal defect; PS = subpulmonic stenosis; HRV = hypoplastic right ventricle; OTV = overriding tricuspid valve; IVS = intact ventricular septum; RV = right ventricle; PA = pulmonary artery; RA = right atrium; LV = left ventricle. Table 2. Previous Surgical Procedures in Patients Studied Procedure Previous shunts Blalock-Taussiga Waterston Potts Glenn Blalock + Glenn Blalock + Potts Blalock + Waterston Potts + Waterston Blalock-Hanlon Pulmonary artery banding Previous corrective procedures Total No. of Operation 22 (6 bilateral) 4 3 3 Two Blalock shunts were end-to-end anastomoses. 52 2 2 5 6 Table 3. Associated Cardiovascular Lesions Lesion Patent ductus arteriosus 2 Atrial septal defect 3 Truncal valve regurgitation 3 Aortopulmonary window Total anomalous pulmonary venous connection Total No. of Patients mittent severe hemoptysis postoperatively. She had a cerebrovascular accident month postoperatively and died. A 33-year-old man, the oldest patient in this series, had undergone a Blalock-Taussig shunt in 947 and had severe left ventricular failure and secondary renal insufficiency (BUN mglloo ml) preoperatively. He had low cardiac output syndrome postoperatively and died of combined renal and cardiac insufficiency. Two patients died from uncontrolled hemorrhage during operation: during dissection of a left Blalock-Taussig shunt and during dissection of the right limb of a throm-

226 The Annals of Thoracic Surgery Vol 24 No 3 September 977 Table 4. Complications Not Related to Conduit Complication No. of Patients J L 2 3 v) s Excluding hospital deaths *Overall 6 2 24 3 36 42 4 54 MONTHS Fig2. Actuarialsurviual curves. Fifteen patients have now reached at least 3 months following repair. bosed bifurcated graft 33 months after the initial repair. Two patients with d-tga died: of unrecognized cardiac tamponade and of low cardiac output syndrome following septation repair of a type A2 single ventricle. There were 2 deaths early in the series following graft interposition from the right atrium to the pulmonary artery: a 4-year-old patient had PA, IVS, a Waterston shunt, and a high left ventricular end-diastolic pressure, while the other had TA, a Potts shunt, and mild to moderate pulmonary vascular obstructive disease. Neither patient would be considered for this repair by today's criteria. Four patients with truncus arteriosus died. Two were less than month of age and, aged 7 months, had pulmonary vascular obstructive disease. Another developed acute tubular necrosis and a hemorrhagic diathesis postoperatively. Major complications not directly related to the conduit occurred in 27 of the 56 patients (Table 4). Five patients (Table 5) had early sepsis (< 6 days following repair). Two patients developed a mediastinal abscess; was cured by antibiotics and open drainage. Three patients had early graft infections (more than 6 days following repair), all of which were treated with antibiotics alone. Following a 2-month asymptomatic interval, of these patients died from late infection of the Hancock conduit. Cardiac Tamponade Arrhythmias a Transient CHB Permanent CHB Pulmonary 5 Hemopty sis Respiratory insufficiency and atelectasis Phrenic nerve palsy Renal ATN 2 CNS CVA Hepatic Hepatitis Total 27 allwee patients had transient supraventricular tachycardias, a transient nodal bradycardia, and persistent premature ventricular contractions. CHB = complete heart block; ATN = acute tubular necrosis; CVA = cerebrovascular accident; CNS = central nervous system. Table 5. Management of Sepsis Sepsis A A+D A+GR Mediastinal abscess 2 () Early graft infection Late graft infection () 3 () "One patient, treated for presumed early graft infection, died of an infection of the prosthesis 2 months later. Numbers in parentheses represent deaths. A = antibiotics; D = drainage of abscess; GR = graft replacement. Twenty-three patients had pulmonary artery or right ventricular pressure determinations within the first 48 hours postoperatively using the indwelling catheters. Mean pulmonary artery pressure was available in 8, and peak systolic pressure was greater than 35 mm Hg in 9 (5%) (Fig 3). The mean right ventricular systolic pressure was 47 mm Hg in 23 patients, with 7 having a pressure greater than 35 mm Hg. Nine of 8 patients had peak systolic gradients from

227 Norwood et al: Valved Conduits for Repair of Congenital Cardiac Lesions 8 E 6 8 I Shunts No Shunts "3 N=5 Fig3. Early (24 hours) postoperative pulmonary artery pressure in 8 patients. Thirteen patients had had previous palliative shunts preoperatively; 5 had not. pulmonary artery to right ventricle ranging from 6 to 78 mm Hg (mean, 23 mm Hg), and 9 had no gradient. Five patients had evidence of a residual left-to-right shunt, and 2 of these underwent early reoperation in the first postoperative week for closure of a residual VSD. Both survived reoperation and are well. The other 3 had small residual shunts (Q,/Q, <.5). Lute Results The actuarial survival rate for44 patients leaving the hospital after repair is 93%. Duration of follow-up ranges from to 5 months (mean, 25.3 months), with 5 patients now followed more than 3 months postoperatively. All late complications have been related to the valved conduit. There have been 4 late graft infections (see Table 5). One patient, treated with antibiotics alone for early Hancock conduit infection, developed septicemia again year later and died during antibiotic therapy. Two others developed infections in their calcified stenotic aortic allografts and were managed by antibiotics and graft replacement. Both survived and are well. One patient with a Hancock conduit developed late infection but died of persistent sepsis after graft replacement. Follow-up hemodynamic data are available for 23 patients month to 5 years (mean,.6 years) after repair. A4 patients with aortic allografts had marked stenosis of the graft. Two had suprasystemic pressure in the right ventricle, and 3 had right ventricular failure. None of the ; 2 n QP 8 8 A 8 RV-conduit Valve Conduit-PA Total N =ll N=5 N = N=8 Fig4. Late postoperative pressuregradients across the Hancock conduits. Six patients hadgradients at multiple levels. 9 patients with Hancock conduits had calcification on chest roentgenogram or by fluoroscopy, but 2 have angiographic evidence of thrombus in the graft. The patient with tricuspid atresia and a right atrial-pulmonary artery conduit had no pressure gradient across the graft; however, the 8 others with Hancock conduits had some degree of obstruction between the right ventricle and pulmonary artery. Eleven patients had gradients at the distal end of the conduit (4-98 mm Hg; mean, 3 mm Hg), 5 at the valve (-42 mm Hg; mean, 23 mm Hg) and at the distal anastomosis (4-6 mm Hg; mean, 35 mm Hg) (Fig 4). Six had gradients at multiple levels. In the majority (3 of 8) the total gradient was less than 45 mm Hg. Only 3 of 8 patients had elevated right ventricular end-diastolic pressures, and all had normal cardiac output. Two patients, with a gradient at the level of the valve and another with pulmonary artery hypertension, have murmurs of pulmonary insufficiency. A significant residual VSD (QJQ, > 2) was present in of 22 patients (4.5%), while 5 others had small residual defects (QJQ,<.5). Only2 patients have both early and late hemodynamic data for comparison. Neither patient demonstrated a change in the right ventricular pressure or gradient across the conduit and 2 years following repair. Comment The initial results from the use of valved conduits in this difficult group of complex lesions is

228 The Annals of Thoracic Surgery Vol 24 No 3 September 977 encouraging [6, 7. Nevertheless, the complications and hemodynamic residua following repair are important. The purpose of reviewing our experience with the use of valved conduits was, at least in part, to discern those problems inherent in the conduit itself from those that are technical and thus potentially subject to improvement. The advantage of inserting a valved conduit rather than patching the right ventricular outflow tract is that the hemodynamic burden on the right ventricle from acute and longstanding pulmonary regurgitation is reduced, especially in patients with pulmonary hypertension. Ten patients in our series had congenital or acquired absence of one pulmonary artery in association with severe tetralogy of Fallot, and all had at least some degree of pulmonary artery hypertension preoperatively. While the mortality following repair without a valved conduit of such patients is reported to be high [l, 2, all patients with a valved conduit in our series are alive and well, suggesting that a valve may contribute to improved survival [9]. Pulmonary artery hypertension may also be present in these patients secondary to either large palliative shunts, thrombosis of pulmonary arterioles secondary to cyanosis and polycythemia, or hypoplasia of the pulmonary arterial system. Of the 8 patients in whom pulmonary artery pressure was measured in the immediate postoperative period, 3 had some degree of pulmonary artery hypertension. These patients all had systemic-pulmonary artery shunts preoperatively, whereas none of the 5 without palliative shunts had pulmonary artery hypertension (see Fig 3). While palliative shunts certainly extend survival of patients whose malformations limit pulmonary blood flow, the detrimental effects of chronic volume overload may eventually lead to left ventricular dysfunction, and the increased flow to the development of pulmonary vascular obstructive disease. This contributed largely to the morbidity and mortality in our series. In addition, obstruction or complete loss of the pulmonary artery at the level of anastomosis may occur. Two deaths in our series were directly attributable to the takedown or repair of a shunt. Our data support the conclusion of Moore and associates [ who, on the basis of 75 patients who had a valved conduit placed, believe the primary cause of mortality and morbidity is the anatomical and physiological changes secondary to systemic-pulmonary artery shunts. On the other hand, the use of valved conduits in infants must be considered palliative in the sense that grafts of limited size require replacement to accommodate increased cardiac output with growth. However, early repair has the potential advantage of minimizing the irreversible anatomical and functional changes resultant from chronic systemic-pulmonary artery shunts. With these considerations in mind, we now prefer repair at age 4 to 5 years (or approximately 2 kg body weight), when one can generally use a large conduit (No. 8 Hancock). In younger children we would create a palliative shunt and replace it with a conduit at about that age. Sepsis is a potential hazard following repair with prosthetic material [9. Although mediastinal infection occurred in 3 patients in the immediate postoperative period early in our series, no mediastinal abscess has occurred since 974 (in the last 28 patients). We are concerned with the risk of primary infection of the conduit (early or late) since it is prosthetic material on the right side of the heart proximal to protective bacterial filtering mechanisms of the lungs [2. However, other than Thompson and associates, who documented 4 instances of endocarditis in 28 patients repaired with an aortic allograft and Dacron extension, there are few reports of graft infections [MI. In our series, patient treated successfully for sepsis in the immediate postoperative period again developed infection of the Hancock conduit year postoperatively and died of septicemia and respiratory insufficiency during antibiotic therapy. Three other patients, 2 with aortic allografts, developed late infections and needed graft replacement for infected prostheses 4 months to 7 years following initial repair. Whether calcification of the allograft influences susceptibility to infection has not yet been determined. All 4 patients repaired with an aortic allograft had marked obstruction to flow and heavy calcification of the conduit. While all centers using aortic allografts report at least some calcification

229 Nonvood et al: Valved Conduits for Repair of Congenital Cardiac Lesions 7-6- 5-2.- 4- E - 7 6 - - 5-2 4- v 3-.- s 2- \ -I 3- : 2- Q - 8 I I I I 6 8 2 22 24 26 Conduit Valve Diameter (mm) Fig5. Distribution of Hancock conduit size in 7 patients according to body weight (see Fig 6). The solid line was derived by linear regression with a correlation constant of.78. lo pressure gradient ono pressure gradient ~ ~ ~ l 6 8 2 22 Conduit Valve Diameter (mm) Fig 6. Distribution of pulmonary bloodflow (PBF) determinedlate postoperatively in 8 patients with Hancock conduits of various size. The closed circles represent patients with pressure gradients at the level of the conduit valve ring. The solid line is generated by the fourth power of the conduit radius (r4) and is positioned to isolate those with gradients. of the graft, the degree of calcification and its hemodynamic sequelae appear to be related to the method of graft preparation [lo]. The allografts used in our series were frozen and sterilized with gamma irradiation. The walls of fresh, antibiotic-preserved allografts also calcify, but this calcification has not yet resulted in impaired function of the valve (follow-up now more than 8 years) [ill. Patients with severe allograft obstruction in our series were all improved by replacement of the aortic allograft with a Hancock conduit. To date we have no evidence of deterioration of the Hancock conduits. Despite the now widespread use of valved conduits, little is known about the long-term hemodynamic result in these patients [5,6. In our series, 8 patients had some degree of obstruction between the right ventricle and the pulmonary artery. Thirteen of 8 had pressure gradients less than 45 mm Hg, while 5 had severe obstruction (PSEG > 75 mm Hg) (see Fig 4). The obstruction has been found at three sites: the junction of the conduit with the right ventricle, the level of the valve ring, and the conduitpulmonary artery anastomosis. Several reports conclude that stenosis at or near the proximal anastomosis can result from compression of the conduit by the sternum or from severe posterior angulation resulting from the position of the pulmonary artery in d-tga [8,]. In only of our patients were we able to document compression by the sternum, and only of 2 patients with d-tga had a high proximal gradient. We now think that the primary determinant of proximal gradients in our patients is the manner in which the ventricular orifice was fashioned. Since August, 975, the proximal orifice has been created by a vertical ventriculotomy with little or no excision of ventricular muscle. As yet, only patient so treated has been restudied, and she has an mm Hg gradient at the proximal anastomosis. We anticipate that proximal gradients can be substantially reduced or eliminated by technical improvements. Gradients at the valve level are primarily a function of pulmonary blood flow and conduit size. While we use no specific formula to ascertain the appropriate size of conduit for each individual patient, the largest size accommodated within the mediastinum and by the pulmonary arteries is selected for each patient. As might be expected, a direct relationship between body weight and the size of the Hancock conduit used is generated by such a procedure (Fig 5). Of the 9 patients with late hemodynamic follow-up, only 5 had a pressure gradient at the level of the porcine valve ranging from to 42 mm Hg (mean, 23). All 5 patients had increased pulmonary blood flow from a residual VSD (QJQ, range,.4 : to.8 : ) (Fig 6). With normal pulmonary flow the gradients would be reduced or eliminated. The distal anastomosis, at the time of opera-

23 The Annals of Thoracic Surgery Vol 24 No 3 September 977 tion, was generally believed to be widely patent. Nevertheless, of the 8 patients had gradients between the distal conduit and pulmonary arteries. While the anastomotic site did not appear kinked or otherwise compromised on cineangiography, 8 of the patients with distal pressure gradients had a narrowed or deformed main or right pulmonary artery secondary to a previous systemic-pulmonary artery shunt. Since it is often difficult to determine precisely the level of the distal anastomosis during pressure determinations, the distal gradients may in part be related to anatomical abnormalities of the pulmonary arteries. The concept of external valved conduits has greatly expanded the scope of surgical management of patients with a variety of complex congenital cardiac malformations. While the initial results are encouraging, there is a high incidence of complications and persistent hemodynamic abnormalities. From this early experience it appears that the hemodynamic residua, morbidity, and mortality stem in large part from anatomical and functional changes in the pulmonary arteries and left ventricle caused by palliative shunts, and from the mechanical problem of positioning the conduit in a smooth course from the right heart to the pulmonary arteries. It is anticipated that improved technique and appropriate timing of operation will substantially reduce or eliminate these problems. The potential of late sepsis of the conduit is real, and careful attention to antibiotic prophylaxis is mandatory. References. Donahoo JS, Brawley RK, Haller JA, et al: Correction of tetralogy of Fallot in patients with one pulmonary artery in continuity with the right ventricular outflow tract. Surgery 74:887, 973 2. Fontan F, Baudet E: Surgical repair of tricuspid atresia. Thorax 26:24, 97 3. LaFarge CG, Miettinen s: The estimation of oxygen consumption. Cardiovasc Res 4:23, 97 4. Lillehei CW, Cohn M, Warden HE, et al: Direct vision intracardiac surgical correction of the tetralogy of Fallot, pentalogy of Fallot and pulmonary atresia defects: report of the first ten cases. Ann Surg 42:48, 955 5. McGoon DC, Rastelli GC, Ongley PA: An operation for the correction of truncus arteriosus. JAMA 25:69, 968 6. 7. 8. 9... 2. 3. 4. 5. 6. 7. 8. 9. 2. McGoon DC, Rastelli GC, Wallace RB: Discontinuity between the right ventricle and pulmonary artery: surgical treatment. Ann Surg 72:68, 97 McGoon DC, Wallace RB, Danielson GK: The Rastelli operation: its indications and results. J Thorac Cardiovasc Surg 65:65, 973 MerinM, McGoonDC: Reoperationafter insertion of aortic homografts as a right ventricular outflow tract. Ann Thorac Surg 6:22, 973 Mistrot JJ, Bernhard WF, Rosenthal A, et al: Tetralogy of Fallot with a single pulmonary artery: operative repair. Ann Thorac Surg 23:249, 977 Moodie DS, Mair DD, Fulton RE, et al: Aortic homograft obstruction. J Thorac Cardiovasc Surg 72:553, 976 Moore CH, Valentine M, Ross DN, et al: Reconstruction of right ventricular outflow tract with a valved conduit in 75 cases of congenital heart disease. J Thorac Cardiovasc Surg 7:, 976 Pazin GJ, Peterson KL, Griff FW, et al: Determination of site of infection in endocarditis. Ann Intern Med 82:746, 975 Rastelli GC, McGoon DC, Wallace RB: Anatomic correction of transposition of the great arteries with ventricular septa defect and subpulmonic stenosis. J Thorac Cardiovasc Surg 58:545, 969 Rastelli GC, Ongley PA, Davis GD, et al: Surgical repair for pulmonary valve atresia with coronary artery fistula: report of a case. Mayo Clin Proc 4:52, 965 Rocchini AP, Rosenthal A, Castaneda AR, et al: Subaortic obstruction after the use of an intracardiac baffle to tunnel the left ventricle to the aorta. Circulation 54:957, 976 Rocchini AP, Rosenthal A, Keane JF, et al: Hemodynamics after surgical repair with right ventricle to pulmonary artery conduit. Circulation 54:95, 976 Ross DN, Somerville J: Correction of pulmonary atresia with a homograft aortic valve. Lancet 2:446, 966 Thompson J, DirksenT, Nube A, et al: Prosthesis endocarditis: treatment of a case occurring five years after a Rastelli-Ross operation. J Thorac Cardiovasc Surg 72:28, 976 Weinstein L, Rubin RH: Infective endocarditis-973. Prog Cardiovasc Dis 6:239,973 Williams GD, Dungan WT, Campbell GS: Surgical treatment of tetralogy of Fallot with unilateral absence of a pulmonary artery. Ann Thorac Surg 4:483, 972 Discussion DR. GORDON K. DANIELSON (Rochester, MN): I have analyzed this excellent series in great detail. Perhaps the only surprise for me was the finding of several instances of late infection in the Hancock conduit

23 Norwood et al: Valved Conduits for Repair of Congenital Cardiac Lesions series. I say surprising, because to my knowledge we have not seen late infection in our series. However, it is known that prosthetic woven grafts in general probably never heal in the sense that they develop an endothelium, and therefore are always at risk of infection from a bacteremia. The authors suggestion that these patients receive endocarditis prophylaxis seems appropriate. More than half of their patients had tetralogy of Fallot. While we would agree to the use of a conduit for complex forms of tetralogy of Fallot, including those associated with absent pulmonary artery, for the syndrome of absent pulmonary valve with aneurysmal pulmonary arteries, for tetralogy with pulmonary vascular obstructive disease due to previous systemic-pulmonary shunts, and for those with an anomalous left anterior descending coronary artery arising from the right coronary artery, we probably would not use a conduit for those patients withvalvular or subvalvular atresia, favoring, instead, the timetested outflow tract of pericardium. Whether or not conduits will be extended for every instance of tetralogy of Fallot that requires a patch across the outflow tract and pulmonary annulus will depend in large part on the long-term performance of conduits as revealed by studies such as those presented by Dr. Norwood. The only point of disagreement that we might have with respect to technique is that we would use larger, or even oversize, conduits for our younger patients. For example, in the 5-year-old patient we would try to place a 22 or 25 mm conduit instead of an 8 mm conduit. This practice decreases the gradient across the valve in the conduit and perhaps also reduces the proximal and distal anastomotic gradients. It obviates the need for conduit replacement with further growth of the patient. Finally, it is interesting to note the total mortality over the last three years for the three most common lesions requiring conduit reconstruction: pulmonary atresia, %; truncus arteriosus, 9%; transposition, 8%-total patients, 4. These risks are now approximating those for repair of tetralogy of Fallot. DR. ROBERT J. SZARNICKI (London, England): We have used conduits since 97 at the Hospital for Sick Children, London. Sixty-four patients were operated on. Thirty-four had transposition complexes. Fourteen had truncus arteriosus, while the remainder had pulmonary atresia, double outlet ventricles, tricuspid atresia, and tetralogy of Fallot. It is interesting to note that the spectrum of patients treated with conduits is quite different in our series than in the Boston series. Thus 53% of our patients were transposition complexes. Our next largest group is truncus arteriosus, which includes 3 patients with hemitruncus anatomy. Only 2 patients, or 3% of the total, had tetralogy of Fallot, whereas in the series presented, tetralogy of Fallot comprised 57% of the total. We continue to use an outflow patch in tetralogy of Fallot. Exceptions are made in the presence of abnormal coronary artery distribution, which prevents adequate enlargement of the outflow tract without injury to the major coronary vessels, and for those patients in whom pulmonary hypertension has resulted from a previous aortopulmonary shunt. I would like to ask the authors what their specific indications are for the use of conduits in tetralogy of Fallot. The second point I would like to raise is that of the incidence of gradients at the proximal anastomosis. Although we have not restudied all patients yet, in those we have restudied, the gradient between the right ventricle and the conduit was 3 mm Hg in and less than mm Hg in the remaining 7. We always make a wide anastomosis, and we are careful that the conduit is placed well to the left or right of midline to avoid sternal compression. To facilitate this, the pleural space is opened widely and the pericardium is incised anterior to the phrenic nerve. In addition, partial thymectomy has been performed recently to further reduce the risk of compression at the distal anastomosis. DR. FREDERICK. BOWMAN (New York, NY): Beginning in March, 967, we have had experience with 66 patients who required restoration of right ventricular-pulmonary artery continuity. In 22 instances an aortic homograft was used; in 44 instances, a Hancock valved conduit. Since implanting the first conduit in May, 97, I have found the Hancock conduit to be a very satisfactory prosthesis, which has withstood high residual pulmonary artery pressure. The proximal gradients, as mentioned by the previous discussants, have not been a problem in our series as far as we know. We believe this is partially due to a vertical right ventriculotomy and a very wide proximal anastomosis. The valve gradients, as they have also mentioned, have been minimal, provided that an adequate size prosthesis can be used. Residual distal gradients have been found to relate to technical anastomotic problems such as the size of the vessels. And we also have noted no late valve or graft failures, and to our knowledge there have been no late infections. An example of the versatility of the Hancock conduit is seen in a patient with truncus arteriosus, type IV, and partially stenotic pulmonary arteries arising from the descending aorta. In using a right thoracotomy and a median sternotomy, an 8 cm segment of descending aorta containing the pulmonary arteries was isolated and replaced with a Dacron graft. The VSD was closed. Right ventricular-pulmonary artery continuity was reestablished with a long valved conduit to the isolated aortic segment (now part of the main pulmonary artery). While only one such repair has been performed, and only early follow-up results are available, we think this technique may be beneficial in certain of these difficult cases.

232 The Annals of Thoracic Surgery Vol 24 No 3 September 977 DR. DONALD R. KAHN (Madison, WI): During the past 4 years, 32 children with severe tetralogy of Fallot had their hypoplastic outflow tract enlarged: 5 children with a valved conduit and 7 with the conventional outflow patch. There were3 operative deaths (2 after a conduit and. after outflow patch repair) and no late deaths. All surviving patients in both groups are clinically asymptomatic, with the exception of patient with a residual VSD. Eleven patients were recatheterized 2 to 28 months postoperatively. With an outflow patch, the immediate postoperative right ventricular-pulmonary artery (RV-PA) gradients were to 2 mm Hg and did not change on recatheterization. The gradient is probably due to the large total flow across the RV outflow, because all patients have major pulmonary regurgitation. With the valved conduit, the immediate postoperative RV-PA gradients were also 5 to 2 mm Hg, but late studies in 2 patients revealed that their gradients had increased to 35 and 6 mm Hg, respectively. The gradients appear to be at the xenograft valve. There is no major pulmonary insufficiency with the conduit. The outflow tract patch is our present choice because the long-term risk of obstruction of the valved conduit outweighs the disadvantage of pulmonary insufficiency. The valved conduit is used when the patient has a large bronchial flow and pulmonary hypertension or when important coronary arteries cross the right ventricular outflow. DR. NORWOOD: I thank the discussants for their comments. I think the issue raised is primarily a matter of terminology. We concur with van Praagh that pulmonary atresia with VSD is simply an extreme form of tetralogy of Fallot. In fact, in most of these patients the pulmonary atresia is acquired. Of the32 patients with tetralogy of Fallot, all had either pulmonary atresia or congenital or acquired absence of one pulmonary artery. Generally, these patients had longstanding palliative shunts and pulmonary artery hypertension. We certainly are not recommending routine repair of simple tetralogy of Fallot using an external conduit. The gradients across the proximal anastomosis have been disturbing to us. We agree with all the discussants that the widest possible anastomosis, using a vertical incision, should reduce or eliminate these gradients. In fact, since adopting this technique we have seen a large reduction in gradients. Recently, only of 33 patients had a pressure difference of mm Hgin the immediate postoperative period. However, these patients have not yet come to late followup cardiac catheterization, which is why they were not mentioned in the paper.