Eur J Cardio-thorac

Surg (1992) 6: 31-35

Surgery 0 SpringeTVerlag 1992

Late reoperations after repair of tetralogy of Fallot G. Pome I, C. Rossi I, V. Colucci ‘, L. Passini I, M. Morello I, C. Taglieri I, A. Pezzano ‘, A. Figini 3, A. Pellegrini ’ ’ Departments

of Cardiac Surgery, 2 Cardiology,

and 3 Pediatric Cardiology,

Niguarda

Ca’Granda

Hospital,

Milan, Italy

Abstract. Twenty-two patients underwent 23 late reoperations after total correction of tetralogy of Fallot from 1965 to 1990. Indications for reoperation included: isolated ventricular septal defect (VSD) in 9 patients (41%), isolated right ventricular outflow tract (RVOT) obstruction in 3 patients (13.7%), VSD associated with a RVOT obstruction in 7 patients (31.8%), aneurysm of the pericardial RVOT patch in 1 patient (4.5%), aortic insufficiency with a residual VSD in 1 patient (4.5%), and tricuspid regurgitation in 1 patient (4.5%). The reoperation consisted of closure of a residual VSD in 17 patients, relief of a RVOT gradient in 11, insertion of a RVOT valve in 4, tricuspid valve replacement in 1 (reoperated twice), aortic valve replacement in 1, and excision of a RVOT aneurysm in 1. Two patients died in hospital (9%) but there were no early deaths in the 11 patients reoperated upon after 1978. Mean follow-up period was 135 months. There were 2 late deaths. The actuarial 20-year survival was 87%. Of the surviving patients, 16 (89%) were in New York Heart Association class I, 1 (5.5%) was in class II, and one (5.5%) was in class III. One patient required a second reoperation for tricuspid bioprosthesis degeneration and 1 patient had moderate recurrent RVOT gradient due to calcified pulmonary bioprosthesis. This study tends to support the policy of recommending reoperation in the presence of surgically significant residual defects. Reoperation is associated with a low early mortality and good long-term results. [Eur J Cardio-thorac Surg (1992) 6:31-351 Key words:

Fallot’s tetralogy - Reoperation

The excellent operative results and the long-term survival of patients with tetralogy of Fallot are well documented up to three decades after repair [S, 14, 25, 30, 311. However, reports of late sudden death [lo, 211 and congestive heart failure (CHF) [22] serve as reminders that surgical repair of the tetralogy of Fallot may be imperfect in some cases. Fortunately, patients in whom CHF develops after initial repair usually have surgically correctable lesions [23]. It is difficult to determine what percentage of patients who have undergone such corrective operations for tetralogy of Fallot may subsequently require reoperation. Much depends on the anatomy of the individual lesion in each patient and on the type of surgical approach employed [I, 81. However, approximately 5% of patients will require reoperation for recurrent or residual lesions [5,6,29]. This study outlines our experience on late reoperations after surgical repair of tetralogy of Fallot over a 25year period.

Received for publication: Accepted for publication:

July 22. 1991 September 12. 1991

Material and methods Of 658 patients who underwent repair of tetralogy of Fallot at Niguarda Ca Granda Hospital in Milan between January 1965 and December 1990,22 patients (3.3%, 13 male and 9 female) required a total of 23 late reoperations. Patients were excluded from the study if they had tetralogy of Fallot with pulmonary atresia, complete atrioventricular canal, or other major associated lesions. The records were analyzed retrospectively for age at initial repair and subsequent reoperation, catheterisation data before each repair, management of right ventricular outflow tract (RVOT) obstruction at the initial repair, signs and symptoms prior to reoperation, associated procedures performed during reoperation, type of valves inserted, gradient across the pulmonary outflow tract before and after repair and hospital mortality. For the study group, the mean age was 13 + 11 years (range l-37 years) at the initial total repair and 17& 10 years (range 2-40 years) at the time of reoperation. The mean interval between operations was 51+48 months (range 2 months to 146 months). One patient required two late reoperations (at ages 37,46). Six patients (27%) had previous Blalock-Taussig shunts. At the initial open repair, RVOT obstruction was treated by infundibulectomy and pulmonary valvotomy in 2 patients (9.1%); by infundibulectomy and RVOT patch on the infundibulum only in 14 patients (63.7%: Dacron was used in 12 patients and pericardium in 2 patients); by

32 Table 1. Management at initial repair

of right ventricular outflow tract obstruction

Procedure

n

Infundibulectomy

and valvotomy

Outflow patch on infimdibulum Transannular

only

2

9.1

14

63.7

5

22.7

1

4.5

outflow patch

RV-PA valveless conduit n = number of patients; PA = pulmonary ular

Table 2. Types and distribution reoperation in 22 patients

%

artery; RV = right ventric-

of residual defects responsible

for

Lesions

n

%

Isolated VSD

9

41

Isolated RVOTG

3

13.7

VSD + RVOTG

7

31.8

Aneurysm + RVOTG

1

4.5

Aortic insufficiency + VSD

1

4.5

Tricuspid regurgitation

1”

4.5

a Reoperated twice; n = number of patients; VSD = ventricular septal defect; RVOTG = right ventricular outflow tract gradient

infundibulectomy and transannular patch in 5 patients (22.7%, we used composite patches in these patients: pericardium distally to the pulmonary annulus and Dacron proximally); and insertion of a nonvalved extracardiac conduit from the right ventricle to the pulmonary artery in 1 patient (4.5%) with an anomalous left anterior descending coronary artery (Table 1). All patients, at the initial repair, had closure of the ventricular septal defect (VSD) with a prosthetic patch through a right ventricular approach; 1 patient underwent suture of the papillary muscle which had had an ischemic partial rupture causing severe tricuspid regurgitation [19]. All patients underwent cardiac catheterisation before reoperation. The indication for catheterisation after initial repair was disability in 19 instances and suspicion of a residual defect from lindings on the chest roentgenograms or physical examination in 3 asymptomatic patients. Prior to reoperation, 19 of 22 patients (86%) had symptoms of fatigue, reduced exercise tolerance or CHF and were in New York Heart Association (NYHA) functional class III or IV, and 3 (14%) were asymptomatic but had significant murmurs. The indications for reoperation included (Table 2): an isolated VSD in 9 patients (41%) (the pulmonary to systemic flow ration (QP/QS) was greater than 1.5 in 8 patients); an isolated RVOT obstruction with a gradient greater than 70 mmHg in 3 patients (13.7%); a VSD associated with a RVOT obstruction in 7 patients (31.8%); an aneurysm of the pericardial RVOT patch associated with a RVOT obstruction in 1 patient (4.5%); aortic insufftciency with a residual VSD in 1 patient (4.5%) and tricuspid regurgitation in 1 patient (4.5%) reoperated upon twice. Of the 17 patients with VSD, 15 (88%) had disruption of the patch suture line and the postero-inferior quandrant of VSD was involved in approximately 70% of these patients; 2 patients (12%) had a residual muscular VSD. The mean Qp/Qs was 2.4* 1.5 (range 1.4-4.3) in the isolated VSD group and 1.63 kO.51 (range 1.2-2.7) in the combined group (NS). In the group of 11 patients with RVOT obstruction, the residual or recurrent stenosis was due to a hypoplastic pulmonary valve annulus in 6 (54.6%) residual obstruction of the pulmonary bifurcation at the distal edge of the transannular patch in 4 (36.4%, in 2 of these patients, an obstruction of the left

main pulmonary artery was present), and calcification of a valveless conduit in 1 (9%). The peak systolic gradient at the time of catheterization before reoperation between the right ventricle and the main pulmonary artery ranged from 40 to 120 mm Hg (mean 67 mm Hg). No correlation was found between preoperative Qp/Qs or the severity of the RVOT gradient and the symptoms of the patients before reoperation. No reoperation was performed for isolated pulmonary valve insufficiency. Four patients who underwent reoperation for associated residual defects also underwent a procedure to relieve pulmonary insufficiency. The associated residual lesions were a residual VSD in 4, RVOT gradient in 3 and tricuspid insufficiency in all 4 patients. One patient twice underwent reoperation for isolated tricuspid insufficiency: the first was 14 months after correction because of reruptured papillary muscle repaired at that time and subsequently, 9 years later, for tricuspid bioprosthesis degeneration. One patient underwent reoperation 8 years after initial repair for a residual VSD and rheumatic aortic incompetence.

Operative procedures All reoperations were performed through a median stemotomy with cardiopulmonary bypass and hypothermia of 25”-30°C. Perfusion during the repair was at flow rates of 2.0-2.4 l/min per m2. Myocardial protection was achieved initially by releasing the aortic cross clamp every 15-20 min, but recently by cold potassium cardioplegia and topical hypothermia. The technique of closure of residual VSDs was resuture of the original patch to the septal rim in all patients with patch detachment and direct suture of additional muscular VSDs in 2 patients. Of the 11 patients with RVOT obstruction, 6 required distal extension of the RVOT patch to cross the annulus of the pulmonary valve. Four patients with original RVOT transannular patches required revision or extension of these patches and in 2 patients, an associated severe left pulmonary artery stenosis was treated with pericardial patch angioplasty. One patient underwent replacement of the calcified extracardiac conduit. Ultimately, 86% (19 of 22) of the entire population underwent RVOT patch enlargement; 50% (11 of 22) were transannular. Four patients with severe pulmonary valve insufticiency, tricuspid incompetence and dilatation of the right ventricle in association with other residual lesions had RVOT reconstruction with pulmonary valve replacement. Two had insertion of heterograft valves, 1, a mechanical valve and 1 received a homograft. In 1 patient with tricuspid insufftciency, a bioprosthesis was inserted twice. One patient with aortic incompetence received a mechanical valve, and 1 patient required the excision of the RVOT pericardial patch aneurysm and the enlargement of the RVOT with a new Dacron patch.

Results Early results

Two of the 22 reoperated patients (9%) died in hospital, but there were no early deaths in the 11 patients who underwent reoperation after 1978. A 7-year-old boy reoperated upon in 1965 for an isolated residual VSD died suddenly the day after operation. The death was presumed to have been due to ventricular arrhythmias. Postmortem examination revealed a technically satisfactory repair. The other patient was a 3-year-old boy reoperated upon in 1978 who remained in a low cardiac output state after closure of a large residual VSD and revision of the RVOT transannular patch associated with a pericardial patch angioplasty of the left main pulmonary artery. He died 12 days after operation. Postoperative cardiac

33

catheterization revealed residual stenosis of the left main pulmonary artery associated with previously unrecognized peripheral pulmonary branch stenosis. The postoperative course in most surviving patients was uneventful, and the average postoperative hospital stay was 15 days (range 9-30 days). A IO-year-old boy developed permanent complete heart block after closure of residual VSD. He now has a permanent implanted pacemaker. The intraoperative peak systolic gradient between the right ventricle and the pulmonary vascular bed measured after repair for the group of 11 patients with RVOT obstruction ranged from 30 to 5 mm Hg (mean 18.2 mm Hg).

current pulmonary stenosis (55 mm Hg gradient) due to a calcified pulmonary bioprosthesis; 1 patient had moderate tricuspid regurgitation due to bioprosthetic dysfunction 10 years after the second reoperation. Three of 20 hospital survivors later required implantation of a permanent pacemaker: in 1 patient 13 years after reoperation when intermittent complete A-V block developed, and in 2 other patients 9 and 10 years, respectively, after reoperation because of symptomatic atria1 fibrillation with low ventricular response. Three other patients had atria1 fibrillation, which was chronic in 1 and paroxysmal in 2 patients. None had bifascicular block. Among the 18 surviving patients, cardiac enlargement defined as a cardiothoracic ratio higher than 0.55, was observed in 8 (44%).

Late results All 20 surviving patients were followed from 3 to 20 years postoperatively (mean follow-up period 135 months). Follow-up included physical examination, electrocardiography, chest roentgenography and two dimensional echocardiography. There were 2 late deaths, so that the actuarial 20-year survival was 87% (Fig. 1). One unexplained sudden death occurred in a 40-year-old man, 57 months after reoperation. He was found dead in bed when he was known to have been in NYHA class I. Whether the death was caused by an arrhythmia or a non cardiac cause is not clear. Autopsy was not performed. A 29-year-old man, known to be in moderate chronic CHF and who had required implantation of a permanent pacemaker because of symptomatic bradyarrhythmias, died one month later of right ventricular failure 9 years postoperatively. Post-mortem examination showed acute tricuspid endocarditis. Of the surviving patients, 16 (89% of 18 patients) were in NYHA class I, 1 (5.5%) was in class II, and 1 (5.5%) was in class III. The latter was a 59-year-old patient requiring digoxin and diuretics for a biventricular cardiomyopathy associated with moderate tricuspid bioprosthesis insufficiency. Two women had become pregnant and both had normal babies. Residual anatomical defects were diagnosed by clinical examination and echocardiography. No patient underwent cardiac catheterization after reoperation. Two of 18 patients had trivial VSDs; 1 patient remained asymptomatic IO years after reoperation but had moderate re100-r-

90% Cl: 0.75-0.9s

a

n

.z 80> 5 IJl

60-

87

s

2

& a

LO2007 0

10 Time

Fig. 1. Cumulative

20

(years)

actuarial survival of patients discharged

Discussion

The concept of feasibility of reoperation after an unsuccessful repair of tetralogy of Fallot [15, 181 appeared 5 years after the first report of intracardiac repair by Lillehei in 1955 [13]. Mortality at reoperation in these two early reports was high (100% and 29% respectively), but reoperation is currently associated with risks no greater than the original operation [5-7, 311. The presence of severe residual or recurrent anatomic and hemodynamic abnormalities is associated with biventricular dysfunction [20, 23, 241 and can be the harbinger of late sudden death [9]. Although routine late catheterisation has not been the practice at our institution, we recommended that every symptomatic or asymptomatic patient who has evidence of a residual defect undergo restudy. In our series, 14% of patients who underwent reoperation were asymptomatic. With the advent of echocardiography, better periodical out-patient evaluation of those who have residual murmurs due to either regurgitation or stenosis or shunt is possible. The frequency and distribution of residual lesions responsible for reoperation in this series were similar to those reported in other papers [5, 161. A reasonable estimate of the true incidence of significant residual shunts at the ventricular level is probably less than 5%. The incidence of residual VSDs with a QplQs 2 1.5 was 3.6% of 221 patients catheterized by Ruzyllo [26]. Rieker [22] who catheterized more than 70% of their operative survivors, found that the incidence was 4%. Our policy is to advise reoperation for closure of residual or recurrent VSD if the Qp/Qs is greater than 1.5, but absolute criteria are difficult to establish. In our series, no strict correlation was found between preoperative Qp/Qs and symptomatic status: 1 of the reoperated patients who was in NYHA class III had a Qp/Qs of 1.4 and became asymptomatic after reoperation. Every patient should be evaluated individually as, even in the presence of a small residual shunt, signs of CHF may appear especially if it is associated with other defects. Detachment of the VSD patch most frequently occurred along its posteroinferior margin near the fibrous base of the tricuspid valve. This is probably due to the difficulty of exposing that corner of VSD and the

34

reluctance to make deep sutures in this area near the conduction tissue. In 2 patients (12% of patients with residual VSD in this series), a preoperative unrecognized muscular VSD was responsible for residual shunts. At the present time, multiple VSDs are easily identified on angled views of biplane cineangiography with proper proliling of the ventricular septum [3]. The problem of residual RVOT gradient after correction of tetralogy of Fallot is an important one. A 2%9% incidence of RVOT obstruction has been reported in literature [2,22,26], and in our series, 50% of the reoperations also involved an RVOT gradient. The decision about when to reoperate for residual or recurrent RVOT obstruction depends on both the symptomatic state of the patient and the gradient. We recommend reoperation in the presence of a surgically relievable obstruction with peak systolic RVOT gradient of 70 mm Hg or even higher in asymptomatic patients. We advise reoperation in patients with gradients (approximately moderate 50 mm Hg) when signs of CHF appear. In the majority of our patients, the obstruction was at the pulmonary valve annulus. Even the use of a transannular patch does not guarantee complete relief of RVOT obstruction, since 4 patients in our series, despite insertion of a transannular patch during the primary repair, had RVOT gradients of 40, 70, 90 and 120 mm Hg, respectively, before reoperation. In agreement with Ruzyllo [26], who identified the distal edge of the RVOT patch as a major site of obstruction, we believe that the broadest portion of the transannular patch should be located at the pulmonary valve annulus and that the distal end of the patch should be broad and rounded to avoid narrowing the artery. At the present time, we endorse liberal utilisation of transannular RVOT patches coupled with infundibuloplasty and pulmonary valvectomy. This trend has become more pronounced in recent years because intracardiac repair is now being performed more frequently in young ages. In our last 100 patients with tetralogy of Fallot, we used transannular RVOT patches in approximately 80% of cases. Our preferred technique for inserting a transannular RVOT patch is to extend the incision to the bifurcation of the pulmonary artery. We use routinely composite patches in the reconstruction of RVOT; pericardium distally to the pulmonary annulus and Dacron proximally. To avoid residual RVOT stenosis, we now measure the pulmonary valve annulus and artery sizes both from the preoperative angiocardiogram and by intraoperative sizing with Hegar dilators and compare these measurements with the normal values for the age of the patient, corrected for weight and height [1 1,271. After repair, if intraoperative pulmonary arterial pressure is elevated and right ventricular-left ventricular peak systolic pressure ratio is 0.70 or greater, we customarily resume extracorporeal circulation and revise the RVOT enlargement. Ample evidence [8, 201 exists that significant residual RVOT obstruction adversely affects the hospital survival and the late results. On the other hand, our experience and previous reports by others [l, 4,8,12,20] suggest that both acute and chronic forms of isolated pulmonary insufficiency appear to be well tolerated for many years. Based on the observa-

tions we continue to deal aggressively with the RVOT obstruction and to use transannular patching liberally in the presence of significant annular hypoplasia. Furthermore, we were unable to find any patient in our series whose results were classified as less than ideal because of isolated pulmonary valvular insufficiency. We recommend the use of a valve in the pulmonary position when reoperation is required after repair of tetralogy of Fallot for residual lesions that include severe pulmonary insufficiency and right ventricular failure associated with tricuspid incompetence due to dilation of the right ventricular annulus. It is known that the combination of pulmonary and tricuspid regurgitation leads to persistent right ventricular failure that is difficult to manage with drugs. All our 4 patients with residual defects associated with pulmonary valve insufficiency, tricuspid incompetence and dilation of right ventricle showed clinical improvement after RVOT reconstruction with pulmonary valve replacement. We believe that at least one right-sided cardiac valve must be functioning normally if CHF is to be avoided. Which valve is best in the RVOT is not clear. Whether the heterograft valve in the RVOT of a child will have the same poor prognosis as one in the left side of the heart is not known. In 1 patient, due to size limitations, we chose a mechanical valve. Use of fresh or cryopreserved homografts may improve the longevity of tissue valves in the pulmonary position and so probably reduce the percentage of reoperation due to bioprosthesis degeneration [ 171. Late tricuspid valve replacement was carried out in 1 patient in our series after an attempt to repair an ischemic rupture of the papillary muscle [19]. The use of pericardium for the RVOT patch and its role in the formation of aneurysms are controversial [ 12, 281. In our series, only 1 patient with pericardial patch RVOT reconstruction at the first operation and with suprasystemic pressure in right ventricle before reoperation, developed an aneurysm of the patch. At the present time, we prefer Dacron proximal to the pulmonary annulus when RVOT reconstruction is required. Increasing experience and refinements in the operative procedures have progressively reduced the incidence of residual defects after repair of tetralogy of Fallot. In the presence of surgically relievable significant residual defects we believe that reoperation is mandatory. Our policy is based not only on our experience but also on ample evidence suggesting that residual defects adversely affect the hospital survival and represent an important risk factor for late premature death. Reoperation currently can be performed with low mortality, probably no greater than that of the initial repair. The long-term results of reoperation are good, and most patients return to an asymptomatic status, but a minority of these patients continue to have recurrent problems that may require an additional operation. References 1.

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Giuseppe Porn&, MD Divisibne di Chirurgia Cardiaca Niguarda Ca’ Granda Hospital P.zza Ospedale Maggiore, 3 I-20162 Milan Italy