Is Complete Heart Block After Surgical Closure of Ventricular Septum Defects Still an Issue? Henrik . Andersen, Marc R.

de Leval, Victor T. Tsang, Martin J. Elliott, Robert H. Anderson and Andrew C. Cook Ann Thorac Surg 2006;82:948-956 DOI: 10.1016/j.athoracsur.2006.04.030

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CARDIOVASCULAR

Is Complete Heart Block After Surgical Closure of Ventricular Septum Defects Still an Issue?
Henrik . Andersen, MD, PhD, Marc R. de Leval, MD, Victor T. Tsang, MD, MS, Martin J. Elliott, MD, Robert H. Anderson, MD, and Andrew C. Cook, PhD
Department of Cardiothoracic Surgery, Rigshospitalet, Denmark; Cardiothoracic Unit, Great Ormond Street Hospital for Children, National Health Service Trust, London, and Cardiac Unit, Institute of Child Health, London, United Kingdom

Background. A serious complication after surgical closure of ventricular septal defect (VSD) is complete heart block. In this retrospective study, we reviewed the incidence of complete heart block after surgical closure of a VSD at Great Ormond Street Hospital from 1976 to 2001 to identify any particular anatomic features that still predisposed patients to surgically-induced complete heart block and to provide anatomic guidelines to avoid this in future. Methods. Data were extracted from our local database for patients having (1) isolated VSD or VSD in the setting of (2) tetralogy of Fallot with pulmonary stenosis or (3) tetralogy of Fallot with pulmonary atresia; (4) absent pulmonary valve syndrome; (5 and 6) coarctation or interruption of the aortic arch; and (7) subaortic brous shelf. We carefully reviewed the operative notes from all patients with postoperative complete heart block to dis-

cover any predisposing anatomical reasons to explain the complication. Results. Two thousand seventy-nine patients had a VSD closure. Permanent complete heart block developed in 7 of 996 patients (0.7%) with an isolated defect and in 1 of 847 patients (0.1%) with tetralogy of Fallot. Four more patients had postoperative complete heart block. Conclusions. Instances of iatrogenic complete heart block continue to occur after surgical VSD closure, either because of unexpected biological variations or because of unawareness of the disposition of the atrioventricular conduction axis in particular circumstances. This report emphasizes the latter aspect in details and suggests a risk of iatrogenic complete heart block of less than 1%. (Ann Thorac Surg 2006;82:948 57) 2006 by The Society of Thoracic Surgeons

entricular septal defects (VSD) are the most frequent congenital cardiac malformations [1]. Surgical closure of such defects was rst performed in 1954, using cross-circulation [2]. Since then, closure by the surgeon has become routine. Over the intervening period, however, there have been signicant changes in the surgical strategy for closure. Thus, priority has shifted from a two-stage approach, with initial banding of the pulmonary trunk to limit the ow of blood to the lungs, with subsequent surgical closure of the defect, to a singlestage approach, with radical surgery performed at an early age [3, 4]. The strategy for perfusion has also changed, from the use of total circulatory arrest with cooling to 18C, to an approach without any, or only mild, cooling and standard cardiopulmonary bypass. Finally, the surgical procedure itself has changed, from a transventricular procedure [5] to a transatrial procedure, thereby limiting the potential damage to the right ventricle [4, 6]. Complications are now rare, but still include serious problems such as cerebral damage, or even death. In certain circumstances, such problems may still be unavoidable. Another serious complication, nonetheless,
Accepted for publication April 7, 2006. Address correspondence to Dr Andersen, Department of Cardiothoracic Surgery, The Heart Centre, Rigshospitalet, Blegdamsvej 9, Copenhagen 2100, Denmark; e-mail: hoandersen@dadlnet.dk.

remains the production of complete heart block, and this is unequivocally linked to the conduct of the surgical procedure itself. Closure is usually achieved by insertion of a patch, anchoring the patch using either a continuous suture, or interrupted sutures. During this maneuver, be it performed through atrial, ventricular, or arterial access, traction and tension are needed to obtain good surgical exposure. The conduction system, specically the bundle of His and its branches, is almost always closely related to some part of the border of the defect, and is, therefore, at risk during the insertion of the individual stitches. Should heart block occur during or after the procedure, it is most often an indication for insertion of a permanent pacemaker, which may demand either a limited, partial sternotomy, performed by opening the lower part of epigastric portion of the wound, or in some occasions a full resternotomy, with insertion of epicardial pacemaker electrodes. There is a recognized increased risk of late death in such patients with postsurgical complete heart block [7]. In the account of the follow-up of Lilleheis pioneering open heart repairs [2], it is reported that complete heart block occurred in 4 of the 27 patients in whom closure was attempted. In reports collected from the last 30 years, describing series of from 23 to 265 patients, although some had no incidence of complete heart block [5, 8 14], this complication occurred in as many as 4% of the others [3, 4, 7, 1528], with an incidence of as high as 8%
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Table 1. Surgical Closure of Simple Ventricular Septal Defects Reported in the Literature Since 1971, With Details of the Incidence of Complete Heart Block and Mortality
Year Published 1971 1972 1976 1977 1978 1979 1979 1980 1980 1980 1982 1984 1984 1985 1990 1991 1991 1992 1992 1993 1994 1996 1996 2000 2001 2003 2005 Surgical Period 196070 196571 196776 195775 197176 197176 197376 196779 197479 197379 195875 197682 197381 197283 196087 195460 198589 198090 198691 198091 197182 199395 197492 197696 199699 199201 197601 Number of Patients 102 68 88 106 71 65 58 265 54 52 187 46 128 57 100 258 115 130 48 141 49 23 124 256 172 188 996 Complete Heart Block 2% 4% 1.5% 1% 0% 3% 2% 1% 3.7% 0% 3% 2% 2% 2% 4% 3.5% 0% 3% (2)a 0% 0% 0% 0% 8% 0% 1% 0.7% 5%, late death 9.8% 22% 4.2% 6% 15% 9.6% 4% 7.6%, transventricular access Pts selected by survival 6% 7.8% 7% Pts from pool of 262 pts, atrial/ventricular access 13% 1% 7.7%, isolated multiple VSDs 2% early, 4% late 0% 8% 0% 1.8% transaortic approach 10% 0.6%, tricuspid valve detachment 2% 1.5%

Author Ibach [15] Ziady [16] Blackstone [17] Sigman [18] Fisher [8] McNicholas [4] Hobbins [19] Rizzoli [20] Borsu [21] Arciniegas [5] Blake [22] Henze [23] Yeager [24] Doty [25] Houyel [26] Moller [7] McGrath [9] Serraf [27] Hardin [3] Backer [10] Kuribayashi [11] Mullen [12] Leao [13] Nygren [29] Gaynor [14] Bol-Raap [28] Andersen
a

Mortality 9%

One patient had intermittent atrioventricular block, but died day 4 postoperatively. patients; VSD ventricular septal defect.

Pts

reported in one series spanning a period of 21 years [29] (Table 1). The aim of our retrospective study, therefore, was to review the incidence of complete heart block in patients who had undergone surgical closure of a VSD at Great Ormond Street Hospital over a period of 26 years. We hoped to identify any particular anatomic features that still predisposed to surgically-induced heart block, if indeed it still occurred, and to provide anatomic guidelines to avoid this complication in future. We analysed only patients with concordant atrioventricular and ventriculoarterial connections, and with normally positioned chambers and arterial trunks.

Material and Methods

The data were collected from our local database, which covered the period from January 1, 1976, through December 31, 2001, a period of 26 years. The database contains information concerning date of birth, diagnosis, surgical procedures, date of operation, and so on. The study was approved by the local Institutional Review Board. Indi-

vidual patient consent was waived in this quality review study with no patient identiers used. We extracted data relevant to patients with otherwise isolated VSDs, along with those having interventricular communications in the setting of tetralogy of Fallot with pulmonary stenosis or atresia, absent pulmonary valve syndrome, coarctation or interruption of the aortic arch, and those having resection of a subaortic brous shelf. We included those with multiple as well as single defects. We excluded patients with discordant ventriculoarterial connections (transposition), double-outlet right ventricle, all forms of functionally single ventricle, including hypoplasia of the left heart, and those with single outlet from the heart except in the setting of tetralogy. We also excluded all patients having a common atrioventricular junction, irrespective of the level of shunting through the associated atrioventricular septal defect. So as to identify the patients who had suffered complete heart block, we matched the procedure VSD closure with the procedure insertion of pacemaker, dening complete heart block for the purposes of this review as the indication for insertion of a permanent

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Table 2. Numbers in the Various Groups, Along With the Incidence of Complete Heart Block and the Rates of Deaths, for Patients Undergoing Surgical Closure of a Ventricular Septal Defect at Great Ormond Street, London, During the Period of 26 Years From 1976 to 2001
Number of Patients 996 32 58 40 847 14 92 Complete Heart Block 7 (0.7%) 1 (6.4%) 2 (3,4%) 1 (2.5%) 1 (0.1%) 0 0 Number of Deaths 19762001 15 (1.5%) 1 (3.1%) 8 (13.8%) 12 (30%) 27 (3.2%) 2 (14.3%) 11 (12.0%) Number of Deaths 19972001 2/263 (0.7%) 0/10 (0%) 0/19 (0%) 1/10 (10%) 1/42 (2.5%)

Diagnostic Groups Isolated Subaortic shelf Previous repair of coarctation Interrupted aortic arch Tetralogy of Fallot Absent pulmonary valve syndrome Tetralogy of Fallot with pulmonary atresia

1/13 (8%)

pacemaker. We then reviewed in detail the operative notes from all patients found to have postoperative complete heart block to discover any predisposing anatomical reasons to explain the complication.

Results
During the period of 26 years spanning from 1976 to 2001, closure of a VSD was attempted in 2,079 patients with concordant atrioventricular and ventriculoarterial connections (Table 2). Of these, the defect in 996 patients was an isolated perimembranous, muscular, or doubly committed defect, whereas in 847 patients the defect was closed as part of the repair of tetralogy of Fallot. The numbers of patients with other complicating lesions, such as brous subaortic shelves, absent pulmonary valve syndrome, and so on, are shown in Table 2. In terms of the numbers of patients in the two major categories undergoing closure each year, the surgical activity has been relatively stable since 1988, with an average of 50 and 40 operations yearly for the two respective groups (Fig 1). The distribution of the ages of the patients in these groups is shown in Figure 2. Most patients underwent closure of isolated defects between the ages of 3 and 12 months, whereas the most frequent age at closure for those with tetralogy of Fallot was a little later, from 6 months to 2 years. The overall mortality for the patients with isolated defects was 1.5%, and that for the patients with tetralogy of Fallot was 3.2%. The major cause of postoperative death was low cardiac output. The rates of mortality for those with other complicating lesions are shown in Table 2. In the 996 patients with an isolated defect, permanent complete heart block developed postoperatively in 7, whereas only 1 of the 847 patients with tetralogy of Fallot suffered from this complication (Table 2). Another 4 patients also had heart block. Thus, among the 58 patients with previous repair of coarctation, 2 had heart block, whereas 1 patient among the 32 patients undergoing resection of a subaortic brous shelf had heart block. Heart block also developed in 1 of 40 patients who needed additional surgery for repair of an interrupted

aortic arch. It is noteworthy, however, that in closing the VSD in 92 patients needing procedures on the pulmonary arteries in the setting of tetralogy with pulmonary atresia, and 14 with absent pulmonary valve syndrome, there were no incidences of surgically-induced complete heart block (Table 2). The ndings from the detailed review of the operative and case notes are shown in Table 3. In 1 patient (no. 12), heart block occurred subsequent to resection of the subaortic brous shelf that was producing obstruction within the left ventricular outow tract. Such shelves are known to overlie the left bundle branch, albeit that the obstructing brous tissue can usually be enucleated without damaging the underlying conduction tissues, as occurred in the other 31 patients with such brous shelves. In 2 further patients (nos. 4 and 5), there was associated overriding and straddling of the tricuspid valve (Fig 3), including the only patient in our series in whom heart block occurred in the setting of tetralogy of Fallot. The

Fig 1. The graph shows the numbers of patients undergoing surgery in each year at Great Ormond Street Hospital in the period from 1976 to 2001 for patients having isolated ventricular septal defect (open columns) and patients with tetralogy of Fallot (shaded columns).

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Fig 2. The graph shows the distribution of ages at the time of surgical closure of the patients with isolated ventricular septal defect (open columns) and patients with tetralogy of Fallot (shaded columns) operated on in the period from 1976 to 2001. (mth months; yrs years.)

operative notes give no indication that the technique used to close the interventricular communication was modied once the surgeon had noted the presence of straddling of the tricuspid valve, yet the conduction axis is known to be abnormally located when there is straddling and overriding of the tricuspid valve (see discussion). In another 2 cases (nos. 1 and 8), heart block occurred after closure of multiple muscular defects. This is another known risk factor for heart block, yet in one instance (patient no. 8), the muscular bar separating the defects was purposely removed. This maneuver is almost certain to induce surgical heart block (see discussion). Heart block also occurred in 1 patient (no. 3) when a muscular defect opening to the inlet was closed with sutures placed close to the muscular margins. This is another known danger situation (see discussion). When closing a perimembranous defect in 1 further patient (no. 9), the surgeon commented in his operative note that he was suspicious about a suture placed in the brous tissue forming the central brous body, yet he did not remove the suture. This patient also had postoperative complete heart block. In the other 3 patients (nos. 2, 7, and 10) with perimembranous defects, and 2 (nos. 6 and 11) with muscular defects, there were no obvious anatomical reasons why the patient should have had complete heart block. The mean time from closure of the defect to insertion of the pacemaker was 27 days, with a range from 6 to 96 days. In 2 patients, however, the course was unusual. Our rst patient (no. 1) initially had sinus rhythm, which converted to complete atrioventricular dissociation 9 days after closure of the defect. The other patient (no. 2) suffered a serious postoperative infection, and the pacemaker was not inserted until 96 days after surgery.

Excluding these 2 patients, the mean period for insertion of the pacemaker was 17 days after surgery, with a range from 6 to 42 days.

Comment
It is salutary to note that, when Lillehei rst performed surgical closure of VSDs, conventional wisdom [30, 31] suggested that there was no single axis responsible for atrioventricular conduction, despite the earlier exemplary description of the atrioventricular bundle provided by Tawara [32]. It was Lev [33], in fact, who claried the course of the atrioventricular bundle in hearts with the typical VSD, with Copenhaver and Truex [34] shortly thereafter showing the distinction between the course of the conduction axis in the setting of what we now call perimembranous as opposed to muscular defects opening to the inlet of the right ventricle. Had the rules established by Copenhaver and Truex [34] been respected, these subsequently being conrmed by Latham and Anderson [35] in 1972, before the commencement of our current series, then heart block could at least have been avoided in our patient with a muscular defect opening close to the annulus of the tricuspid valve (patient no. 1). Indeed, on the basis of these early studies, the disposition of the atrioventricular conduction axis has been well established for all the various types of VSD [36], and surgeons are well aware of the signicance of these anatomical ndings [37]. Despite this knowledge, as our analysis shows, occasional instances of iatrogenic complete heart block continue to occur after surgical closure of VSD, either because of unexpected biological variations, or because of unawareness of the known disposition of the atrioventricular conduction axis in

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Table 3. Details of the 12 Patients From 2,079 Who Had Complete Heart Block After Surgical Closure of an Interventricular Communication
Patient No. and Age at Surgery (1) 7 years Date of Surgery 9/6/77 Description of Defect and Signicant Lesions One defect just underneath the aortic valve in close proximity to the tricuspid valve, with additional apical defects. All 3 apical defects were covered with one patch placed through left ventriculotomy. Small perimembranous defect opening toward apex and large ASD. Description of Surgery Access through right atrium and left ventriculotomy. Upper defect closed with interrupted sutures inferiorly and with running suture superiorly. Access through right atrium. Standard closure. Time of Pacemaker Insertion PM 42 days after surgery

Diagnosis Multiple muscular VSDs, earlier PAB

(2) 6 months

5/13/85

Perimembranous VSD

(3) 1 1/2 years

3/22/90

Muscular VSD, earlier PAB

Muscular defect opening to RV inlet.

(4) 2 1/2 years

4/11/94

Perimembranous VSD

Overriding of tricuspid valve and straddling tricuspid valve papillary muscle.

(5) 1 year

1/30/95

Tetralogy of Fallot

Huge conuent perimembranous defect. Large papillary muscle to tricuspid valve was straddling the septum and arising from the left ventricular surface.

(6) 6 months

3/16/95

Muscular VSD

Large muscular defect. Abnormal AV conduction with left bundle branch block.

Access through right atrium. Sutures placed close to the margins of muscular defect. Access through right atrium. In the vicinity of the straddling papillary muscle to the septal leaet of the tricuspid valve, a small cut was made in the patch. The stitches were then brought out through the annulus of the tricuspid valve. Access through right atrium. Running suture, patch split and draped around the papillary muscle. Right ventricular muscle bundles resected. Access through right atrium. Standard closure. CHB noted at end of bypass.

CHB postoperatively; temporary PM wires due to infection in postoperative course; nal PM 96 days after surgery CHB postoperatively; PM 12 days after surgery Postoperative CHB; PM 7 days after surgery

PM 23 days after surgery

PM 9 days after surgery

particular circumstances. It is the latter circumstance that are the focus of our current review, since in more than half of our own cases, it is possible that damage to the conduction axis could have been avoided had full advantage been taken of the extant anatomical knowledge. In this respect, our own experience, coupled with that culled from review of the literature, shows that the incidence of complete heart block is independent of the route

of surgical access, and whether or not the surgeon chooses to detach the septal leaet of the tricuspid valve [14]. Some of our own patients, nonetheless, would not have had heart block if knowledge about the course of the atrioventricular bundle had been respected [36, 37]. Thus, in 1 patient (no. 8) with both perimembranous and muscular defects, the surgeon chose to divide the muscle bar between the defects. It is well established that the bundle of His almost certainly

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Table 3. (Continued)
Patient No. and Age at Surgery (7) 6 months Date of Surgery 3/27/95 Description of Defect and Signicant Lesions Large perimembranous inlet defect. Description of Surgery Access through right atrium. Standard closure. CHB peroperative. Access through right atrium. Defects joined by cutting the muscle between them, and the holes were closed as one. Access through right atrium. There was a zone of deciency of valvar tissue, and sutures were placed in the brous rim of this defect in the belief that this was far away from the conduction tissue. Access through right atrium. Defect larger than aorta. Standard closure. Access through right atrium. Sutures were placed deeply into the left side of the outlet septum in an attempt to pull it to the right side. Access through right atrium. Subaortic shelf resected from aortotomy.
interrupted aortic arch; PAB

Diagnosis Perimembranous VSD Earlier PAB CoA Perimembranous and muscular VSDs Previous PAB CoA

Time of Pacemaker Insertion PM 12 days after surgery

(8) 3 1/2 years

6/6/96

Enormous defect. Septum almost absent, but 2 defects.

PM 6 days after surgery

(9) 6 months

10/17/ 96

Perimembranous VSD

Large perimembranous outlet defect with an aortic valve prolapsing through the superior margin of the defect. The suture in the brous rim was suspected by surgeon to be suspicious, but he did not remove in spite of 2:1 block.

PM 36 days after surgery; Had a short-termed occurrence of SR then CHB

(10) 2 1/2 months

21.01.99

Perimembranous VSD

Inlet VSD extending to the subaortic area, diameter larger than the aorta.

(11) 1 year

02.03.00

IAA (type A) and muscular VSD

Large muscular outlet defect with posterior deviation of the infundibular septum, producing a signicant narrowing of the subaortic area. Large perimembranous defect and subaortic shelf.
CoA Coarctation; IAA ventricular septal defect.

CHB noted. February 1, 1999; PM 60 days after surgery CHB during operation; PM 12 days after surgery

(12) 6 months

08.01.01

Perimembranous VSD and subaortic shelf

CHB postoperatively; PM 8 days after surgery

pulmonary artery

ASD band;

atrial septal defect; PM pacemaker;

CHB complete heart block; SR sinus rhythm; VSD

will traverse such a muscle bar (Fig 4) [36]. In another patient (no. 9), a zone of deciency was noted between the septal and antero-superior leaets of the tricuspid valve. A suture was placed in the brous rim at this point, which almost certainly was the site at which the atrioventricular bundle is known to penetrate from the apex of the triangle of Koch to the crest of the muscular ventricular septum (Figs 5 and 6) [6, 36]. In 2 further cases, the surgeon recognized the presence of straddling and overriding of the tricuspid valve (patient nos. 4 and 5). Overriding of the right atrioventricular junction, with consequent malalignment between the atrial and ventricular septal components, is known to be the one situation in which, with a perimembranous defect, the conduction axis does not arise from the regular atrioventricular node, but instead arises from an

anomalous node. The node is formed at the site where the malaligned ventricular septum meets the right atrioventricular junction (Fig 3) [38]. In this respect, it is surely signicant that 1 of the patients with straddling and overriding of the tricuspid valve was the only 1 among 847 patients with pulmonary stenosis, and a further 92 with pulmonary atresia, who had complete heart block in the setting of tetralogy of Fallot. This difference between the incidence of heart block between otherwise isolated defects, and that occurring in the setting of tetralogy, was highly signicant (p 0.04, Fishers test). It almost certainly reects the fact that the bundle of His is better protected in the setting of tetralogy of Fallot, the known danger situations being combined perimembranous and muscular defects [36], and straddling and overriding of the tricuspid valve [38].

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Fig 3. The drawing shows the known disposition of the conduction axis, as seen by the surgeon operating through the right atrium, when there is straddling and overriding of the tricuspid valve [38]. Note that the bundle does not originate from the regular atrioventricular node located at the apex of the triangle of Koch.

Fig 5. The drawing shows the expected site of the conduction axis when a ventricular septal defect (VSD) is perimembranous [36], as it would be seen by the surgeon lifting up the septal leaet of the tricuspid valve having approached the defect through the right atrium.

The choice and timing of insertion, of a permanent pacemaker after closure of a VSD can be difcult. Insertion of a permanent pacemaker may introduce increased morbidity, and even mortality [22, 39]. Furthermore, on the one hand, recovery of atrioventricular conduction after temporary postoperative block has been seen up to 6 weeks after surgery, and on the other hand, occurrence of block has been seen as late as 25 years after closure of the septal defect [7]. One study, investigating patients after surgery for congenital heart disease, reported that two thirds of patients with temporary postoperative block regained atrioventricular conduction, and that in 97%, this occurred within 9 days [40]. They also reported that of the patients who needed a permanent pacemaker, 11 of 31 patients had recovery of atrioventricular conduction after insertion of the pacemaker [40]. This sequence occurred in 1 of our own patients, who had a pacemaker inserted 6 days

after surgery, and then regained atrioventricular conduction 2 days later. Temporary pacemakers, placed epicardially during surgery, normally should function for at least 3 weeks after surgery. Thus, in this respect, the therapeutic window for placement of a permanent epicardial system extends between 9 and 21 days after surgery. That is also a period during which postsurgical adherences are not fully developed. Most would prefer to insert an epicardial system with steroid-eluting electrodes, which should have a lifespan similar to permanent endocardial systems [39]. Our mean time for insertion of the permanent pacemaker was 17 days. It is also the case, of course, that patients suffering transient postoperative block should always be followed carefully in order to detect any possible later development of complete heart block [7, 22].

Limitations of the Study

In this study, we chose to focus only on the development of complete heart block after surgical closure of so-called

Fig 4. The drawings show the known disposition of the conduction system when the atrioventricular conduction axis descends through a muscle bar separating perimembranous and muscular inlet defects [36]. In (a), the leaets of the tricuspid valve are shown in-situ, whereas they are retracted in (b). (VSD ventricular septal defect.)

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ate to expect rates of mortality at around 0%, and the risk of iatrogenic heart block at less than 1%. It is against these results that cardiologists should now evaluate the anticipated results from interventional closure.
Research at the Great Ormond Street Hospital for Children, National Health Service Trust, and the Institute of Child Health and benets from research and development funding were received from the NHS Executive. Andrew C. Cook, PhD, and Robert H. Anderson, MD, are supported by grants from the British Heart Foundation, together with the Joseph Levy Foundation in the case of Dr Anderson.

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1. Hoffman JIE. Incidence, mortality and natural history. In: Anderson RH, Baker EJ, Macartney FJ, Rigby ML, Shinebourne EA, eds. Paediatric cardiology. 2nd ed. Edinburgh: Churchill Livingstone, 2005:111 40. 2. Lillehei CW, Varco RL, Cohen M, Warden HE, Patton C, Moller JH. The rst open-heart repairs of ventricular septal defect, atrioventricular communis, and tetralogy of Fallot using extracorporeal circulation by cross-circulation: a 30year follow-up. Ann Thorac Surg 1986;41:4 21. 3. Hardin.J.T., Muskett AD, Canter CE, Martin TC, Spray TL. Primary surgical closure of large ventricular septal defects in small infants. Ann Thorac Surg 1992;53:397 401. 4. McNicholas K, de Leval M, Stark J, Taylor JFN, Macartney FJ. Surgical treatment of ventricular septal defect in infancy. Primary repair versus banding of pulmonary artery and later repair. Br Heart J 1979;41:133 8. 5. Arciniegas E, Farooki ZQ, Hakimi M, Perry BL, Green EW. Surgical closure of ventricular septal defect during the rst twelve months of life. J Thorac Cardiovasc Surg 1980;80: 921 8. 6. de Leval M. Transatrial closure of perimembranous ventricular septal defect in infancy [Letter]. J Thorac Cardiovasc Surg 1984;87:640 2. 7. Moller JH, Patton C, Varco RL, Lillehei CW. Late results (30 to 35 years) after operative closure of isolated ventricular septal defect from 1954 to 1960. Am J Cardiol 1991;68:14917. 8. Fisher RD, Faulkner SL, Sell CG, Graham TP, Bender HW. Operative closure of isolated defectsof the ventricular septum: planned delay. Ann Thorac Surg 1978;26:351 6. 9. McGrath LB. Methods for repair of simple isolated ventricular septal defects. J Card Surg 1991;6:1323. 10. Backer CL, Winters RC, Zales VR, et al. Restrictive ventricular septal defect: how small is too small to close? Ann Thorac Surg 1993;56:1014 8. 11. Kuribayashi R, Sekine S, Aida H, et al. Long-term results of primary closure for ventricular septal defects in the rst year of life. Surg Today 1994;24:389 92. 12. Mullen JC, Lemermeyer G, Schipper SA, Bentley MJ. Perimembranous ventricular septal defect repair: keeping it simple. Can J Cardiol 1996;12:81721. 13. Leao LE, Buffolo E, Coto AE, Maluf MA, Andrade JC. Transaortic approach has a role in the surgical treatment of ventricular septal defects. Cardiovasc Surg 1996;4:250 4. 14. Gaynor JW, OBrien JE Jr, Rychik J, Sanchez GR, DeCampli WM, Spray TL. Outcome following tricuspid valve detachment for ventricular septal defects closure. Eur J Cardiothorac Surg 2001;19:279 82. 15. Ibach JR Jr, Bartley TD, Daicoff GR, et al. Correction of ventricular septal defect in childhood. Ann Thorac Surg 1971;11:499 507. 16. Ziady GM, Hallidie-Smith KA, Goodwin JF. Conduction disturbances after surgical closure of ventricular septal defect. Br Heart J 1972;34:1199 204. 17. Blackstone EH, Kirklin JW, Bradley EL, DuShane JW, Appelbaum A. Optimal age and results in repair of large

Fig 6. The drawing shows how the conduction axis penetrates through the central brous body at the apex of the triangle of Koch when a defect is perimembranous [36], and how this is more obvious to the surgeon when there is a deciency of leaet tissue at the zone of apposition between the septal and anterosuperior leaets of the tricuspid valve.

simple VSDs. Other diagnostic groups with VSDs might also have been included in the survey. Such groups would be those with interventricular communications in the setting of regular or congenitally corrected transposition, double-outlet right ventricle, atrioventricular septal defect with common atrioventricular junction, and common arterial trunk. In our opinion, however, inclusion of these groups would have unduly confounded the data. Furthermore, there are differences in the course of the atrioventricular bundle in congenitally corrected transposition and atrioventricular septal defects when compared with isolated defects. Patients with double-outlet right ventricle constitute a very heterogeneous group, with a spectrum from double-outlet right ventricle of the Fallot type to the Taussig-Bing malformation, and in a retrospective review, it would be difcult to distinguish between these different anatomic types. To limit our population, therefore, we included only patients with concordant atrioventricular and ventriculoarterial connections. In the process of selection , we matched the procedures of closure of VSD with insertion of a pacemaker. In some patients, of course, complete heart block could have developed at a time when they were no longer under the surveillance of our unit, and a pacemaker could have been inserted elsewhere. Such patients, nonetheless, most likely would have been readmitted to our unit. We also chose to omit any considerations of transient heart block, information that might also have been of interest, but which was not uniformly available. In conclusion, we see no reason to suppose that our experience at Great Ormond Street does not reect surgical experience worldwide for closure of VSDs. Thus, our review of literature suggests that it is now appropri-

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29. Nygren A, Sunnegardh J, Berggren H. Preoperative evaluation and surgery in isolated ventricular septal defects: a 21 year perspective. Heart 2000;83:198 204. 30. Glomsett DJ, Glomsett ATA. A morphologic study of the conduction system in ungulates, dog and man: I, the sinoatrial node. Am Heart J 1940;20:389 98. 31. Glomsett DJ, Glomsett ATA. A morphologic study of the conduction system in ungulates, dog and man: II, the Purkinje system. Am Heart J 1940;20:677700. 32. Tawara S. Das Reizleitungssystem des Saugetierherzens: Eine anatomisch-histologischeStudie ber das Atrioventrikularbundel und die Purkinjeschen Faden. Jena, Germany: Gustav Fischer, 1906:9-70. 33. Lev M. The architecture of the conduction system in congenital heart disease: III, ventricular septal defect. Arch Pathol 1960;70:530 49. 34. Copenhaver WM, Truex RC. Histology of the atrial portion of the cardiac conduction system in man and other mammals. Anat Rec 1952;114:60125. 35. Latham RA, Anderson RH. Anatomical variations in atrioventricular conduction system with reference to ventricular septal defects. Br Heart J 1972;34:18590. 36. Anderson RH, Becker AE. The anatomy of ventricular septal defects and their conduction tissues. In: Stark J, de Leval M, eds. Surgery for congenital heart defects. 2nd ed. Philadelphia: WB Saunders, 1983:11538. 37. de Leval M. Ventricular septal defects. In: Stark J, de Leval M, eds. Surgery for congenital heart defects. 2nd ed. Philadelphia: WB Saunders, 1983:35571. 38. Milo S, Ho SY, Macartney FJ, et al. Straddling and overriding atrioventricular valves: morphology and classication. Am J Cardiol 1979;44:112234. 39. Thomson JD, Blackburn ME, Van Doorn C, Nicholls A, Watterson KG. Pacing activity, patient and lead survival over 20 years of permanent epicardial pacing in children. Ann Thorac Surg 2004;77:1366 70. 40. Weindling SN, Saul JP, Gamble WJ, Mayer JE, Wessel D, Walsh EP. Duration of complete atrioventricular block after congenital heart disease surgery. Am J Cardiol 1998;82:5257.

INVITED COMMENTARY
Andersen and colleagues [1] report the incidence of complete atrioventricular (AV) conduction block in a selected group of patients who had surgical closure of ventricular septal defect (VSD) at Great Ormond Street during a 26-year period. The results are excellent with an overall incidence of less than 1% for pacemaker insertions after postsurgical AV conduction block. Based on important anatomic and morphologic data, the authors make recommendations to further reduce the risk of injury to the AV conduction axis, supporting the notion that the incidence of the postoperative need for a pacemaker may in fact be less than 0.5%. The anatomy of the conduction tissue in congenital heart disease is fundamental to surgical practice. Thanks to the many contributions of Anderson and colleagues [1], Becker, Kurosawa, de Leval, and others, many of the morphologic details of the AV conduction axis in congenital heart disease have been dened. Biologic studies of morphologists are a good example of how basic science can impact clinical practice and outcomes. The principles of surgical closure of perimembranous VSD, in general, should include the use of oversized patches, suturing to
2006 by The Society of Thoracic Surgeons Published by Elsevier Inc

the right septal surface at least 2 mm away from the rim of the ventricular septum, especially around danger zones, and placement of supercial sutures when transitioning around the posterior inferior rim or crest. Uncomplicated closure of septation defects also requires an understanding of the anatomic variations of special situations including atrial ventricular septal defect (AVSD), double outlet right ventricle (DORV), AV discordance, straddling or overriding AV valves, as well as malaligned VSDs and trabecular, inlet or outlet extensions of perimembranous defects. Surgical AV conduction block necessitating pacemaker insertion should only occur due to undened anatomic variants or in patients who have a genetic predisposition to AV conduction delay such as in Tbx 5 or Nkx 2.5 mutations. Both Tbx-5 and Nkx 2.5 are important for the development, maturation, and maintenance of the conduction system and haploinssufciency or heterozygous mutations result in AV conduction block. The study may demonstrate some biases due to (1) the database search criteria matching VSD closure to pacemaker insertion, (2) the decision not to include septal
0003-4975/06/$32.00 doi:10.1016/j.athoracsur.2006.06.027

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Is Complete Heart Block After Surgical Closure of Ventricular Septum Defects Still an Issue? Henrik . Andersen, Marc R. de Leval, Victor T. Tsang, Martin J. Elliott, Robert H. Anderson and Andrew C. Cook Ann Thorac Surg 2006;82:948-956 DOI: 10.1016/j.athoracsur.2006.04.030
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