Ann Thorac Surg 2006;82:948-956
© 2006 The Society of Thoracic Surgeons
Original article: Cardiovascular
Is Complete Heart Block After Surgical Closure of Ventricular Septum Defects Still an Issue?
Henrik Ø. Andersen, MD, PhDa,*,
Marc R. de Leval, MDb,
Victor T. Tsang, MD, MSb,
Martin J. Elliott, MDb,
Robert H. Anderson, MDc,
Andrew C. Cook, PhDc
a Department of Cardiothoracic Surgery, Rigshospitalet, Denmark
b Cardiothoracic Unit, Great Ormond Street Hospital for Children, National Health Service Trust, London
c Cardiac Unit, Institute of Child Health, London, United Kingdom
Accepted for publication April 7, 2006.
* Address correspondence to Dr Andersen, Department of Cardiothoracic Surgery, The Heart Centre, Rigshospitalet, Blegdamsvej 9, Copenhagen 2100, Denmark. (Email: hoandersen{at}dadlnet.dk).
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Abstract
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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 fibrous shelf. We carefully reviewed the operative notes from all patients with postoperative complete heart block to discover 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%.
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Introduction
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Ventricular septal defects (VSD) are the most frequent congenital cardiac malformations [1]. Surgical closure of such defects was first performed in 1954, using cross-circulation [2]. Since then, closure by the surgeon has become routine. Over the intervening period, however, there have been significant 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 flow of blood to the lungs, with subsequent surgical closure of the defect, to a single-stage 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 18°C, 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, 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, specifically 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 Lillehei's 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, 15–28], with an incidence of as high as 8% reported in one series spanning a period of 21 years [29] (Table 1).
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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
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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.
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Material and Methods
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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. Individual patient consent was waived in this quality review study with no patient identifiers 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 fibrous 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," defining complete heart block for the purposes of this review as the indication for insertion of a permanent 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.
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Results
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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 fibrous subaortic shelves, absent pulmonary valve syndrome, and so on, are shown in Table 2.
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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
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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.
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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.)
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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 fibrous 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 findings 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 fibrous shelf that was producing obstruction within the left ventricular outflow tract. Such shelves are known to overlie the left bundle branch, albeit that the obstructing fibrous tissue can usually be enucleated without damaging the underlying conduction tissues, as occurred in the other 31 patients with such fibrous shelves.
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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
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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 operative notes give no indication that the technique used to close the interventricular communication was modified 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 fibrous tissue forming the central fibrous 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.
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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.
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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 first 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.
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Comment
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It is salutary to note that, when Lillehei first 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 clarified 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 confirmed 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 significance of these anatomical findings [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 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 leaflet 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 will traverse such a muscle bar (Fig 4) [36]. In another patient (no. 9), a zone of deficiency was noted between the septal and antero-superior leaflets of the tricuspid valve. A suture was placed in the fibrous 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].
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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 leaflets of the tricuspid valve are shown in-situ, whereas they are retracted in (b). (VSD = ventricular septal defect.)
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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 leaflet of the tricuspid valve having approached the defect through the right atrium.
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Fig 6. The drawing shows how the conduction axis penetrates through the central fibrous 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 deficiency of leaflet tissue at the zone of apposition between the septal and anterosuperior leaflets of the tricuspid valve.
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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 significant 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 significant (p = 0.04, Fishers test). It almost certainly reflects 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].
The choice and timing of insertion, of a permanent pacemaker after closure of a VSD can be difficult. 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 "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 difficult 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 reflect surgical experience worldwide for closure of VSDs. Thus, our review of literature suggests that it is now appropriate 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.
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The Society of Thoracic Surgeons: Forty-Third Annual Meeting
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Please mark your calendars for the Forty-Third Annual Meeting of The Society of Thoracic Surgeons, to be held in San Diego, California, from January 29–31, 2007. The program will provide in-depth coverage of thoracic surgical topics selected to enhance and broaden the knowledge of cardiothoracic surgeons. Attendees will benefit from traditional Abstract Presentations, as well as Surgical Forums, Breakfast Sessions, Surgical Motion Pictures, and Town Hall Meetings on specific topics.
Advance registration forms, hotel reservation forms, and details regarding transportation arrangements, as well as the complete meeting program, will be mailed to Society members this fall. Also, complete meeting information will be available on the Society's Web site at www.sts.org. Nonmembers who wish to receive information on the Annual Meeting may contact the Society's secretary, Douglas E. Wood.
Douglas E. Wood, MD
Secretary
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Chicago, IL 60611-3658
Telephone: (312) 202-5800
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Acknowledgments
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Research at the Great Ormond Street Hospital for Children, National Health Service Trust, and the Institute of Child Health and benefits 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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E. M. Tucker, L. A. Pyles, J. L. Bass, and J. H. Moller
Permanent Pacemaker for Atrioventricular Conduction Block After Operative Repair of Perimembranous Ventricular Septal Defect
J. Am. Coll. Cardiol.,
September 18, 2007;
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[Abstract]
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I. D Sullivan
Transcatheter closure of perimembranous ventricular septal defect: is the risk of heart block too high a price?
Heart,
March 1, 2007;
93(3):
284 - 286.
[Abstract]
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A. Azakie
Invited commentary.
Ann. Thorac. Surg.,
September 1, 2006;
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956 - 957.
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Abstract
Introduction
