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Ann Thorac Surg 2003;76:158-166
© 2003 The Society of Thoracic Surgeons

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Original article: cardiovascular

Closure of muscular ventricular septal defects guided by en face reconstruction and pictorial representation

^a Department of Pediatric Cardiology, Amrita Institute of Medical Sciences & Research Center, Kochi, India
^b Department of Pediatric Cardiac Surgery, Amrita Institute of Medical Sciences & Research Center, Kochi, India

Accepted for publication February 12, 2003.

^* Address reprint requests to Dr Kumar, Amrita Institute of Medical Sciences & Research Center, Kochi 682026, India
e-mail: rkrishnakumar{at}aimshospital.org

	Abstract

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BACKGROUND: A surface reconstruction of the location and dimensions of muscular ventricular septal defects (VSDs) on right ventricular (RV) septal surface could serve as a better guide to surgical closure amid different classifications and confusing terminologies.

METHODS: We reconstructed muscular VSD requiring surgery on an en-face view of the RV septal surface from echocardiographic orthogonal views in 34 consecutive patients. The location, dimensions of the defects, and relation to various RV septal landmarks are illustrated as a diagram. Recommendations are presented regarding surgical approach to the defects, along with predictions on the possibility of residual defects and heart block.

RESULTS: Surgical findings were as predicted by the diagram in the 27 patients who underwent VSD closure. Seven infants (2.5 to 4.9 kg) underwent pulmonary artery (PA) banding based on predictions of heart block or major residual defects. Two patients with predicted risk of heart block underwent VSD closure with heart block ensuing in one of them. Based on the diagram limited ventriculotomy (n = 2) or detachment of tricuspid leaflets (n = 6) aided access to the VSD. Among patients undergoing VSD closure only 1 patient had a major residual defect that required PA banding. There were clinically insignificant residual defects in 8 patients. Four patients (12%) were anticipated preoperatively because of surgical inaccessibility and intentionally left alone.

CONCLUSIONS: En-face reconstruction of single or multiple muscular VSDs is feasible from orthogonal echocardiographic views. It helps plan the surgical approach and predict the likelihood of heart block and residual defects after surgery.

	Introduction

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Muscular ventricular septal defects (VSD) are holes in the ventricular septum completely surrounded by muscle [1]. Surgically relevant peculiarities of these defects include diverse locations, traversing muscle bars and tricuspid chordo-papillary apparatus, and multiplicity [2]. Surgical approaches vary depending upon their location [3, 4]. Residual defects after surgery are usually related to surgically inaccessible location, defects hidden by hypertrophied muscle bars, or traversed by muscle bands and large tricuspid papillary muscle structures [5–7]. The proximity of the margins of a muscular defect in the inlet septum to the atrioventricular (AV) conduction tissues determines the risk of postoperative heart block [8, 9].

There is no uniformity in nomenclature and a number of classifications exist for muscular VSDs [10–12]. Amid confusing classifications, a pictorial reconstruction of the location and dimensions of the VSD on the right ventricular (RV) septal surface and its relation to RV septal structures should give a better understanding and provide an accurate road map for the surgery. This illustration would be a lot more informative than a verbal description based on conventional two-dimensional echocardiography [13].

This report describes the technique of echocardiographic en-face reconstruction and surgical results guided by the reconstruction. We also examined the utility of this approach to guide surgical access and predict risk of heart block and the likelihood of residual VSD after surgical closure.

	Material and methods

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Study design
En-face reconstruction was routinely performed between January 2000 and April 2002 on consecutive patients undergoing surgical treatment of single or multiple muscular VSDs at our institution. The records of all these patients were reviewed. Patients with additional perimembranous defects were also included; however, isolated perimembranous VSD with muscular extensions were not included. Patients with associated atrial septal defect, patent ductus arteriosus, and coarctation were included. Patients with muscular VSD that were a part of a more complex defect (such as tetralogy of Fallot, double outlet right ventricle, and transposition) were excluded in this study.

Right ventricular anatomy
Certain distinct anatomic landmarks clearly identifiable on echocardiography were used to characterize the RV septal surface (Fig 1).

View larger version (99K): [in this window] [in a new window]   Fig 1. Right ventricular septal landmarks: 1 = tricuspid annulus at septal leaflet attachment; 2 = posterior margin of ventricular septum; 3 = apex of right ventricular sinus; 4 = septal band; 5 = moderator band; 6 = apex of right ventricular infundibulum; 7 = anterior margin of ventricular septum; 8 = outflow septum; and 9 = membranous septum.

View larger version (119K): [in this window] [in a new window]   Fig 2. Subxiphoid short axis sweeps from basal to apical septum. Frame 1 illustrates the inflow septum in close vicinity to the base of MV and TV and frame 2 cuts through the belly of the AV valves (arrows = a large posterior muscular VSD). Frame 3 cuts through the septum immediately below the tips of the AV valve leaflets. Here the dimension of the VSD has reduced, giving a clue of the shape of the VSD, reconstructed in the diagram (frame 5). Frame 4 is at the level of the papillary muscles and the septal band in trabecular septum. The VSD is not imaged in this plane. The arrows in the drawing of the right ventricular surface are numbered and indicate the planes of section for the corresponding frames. The shaded area in the diagram (frame 5) represents the VSD. (AV = atrioventricular; LV = left ventricle; MV = mitral valve; RV = right ventricle; TV = tricuspid valve; VSD = ventricular septal defect.)

View larger version (113K): [in this window] [in a new window]   Fig 3. Apical sweep from posterior to anterior plane (same patient as illustrated in Fig 2). Frame 1 cuts through the posterior-most portion of the ventricular septum. Frame 2 cuts through the mid portions of the AV valves, and frame 3 illustrates the anterior portions of the AV valves. The VSD is seen in all three frames. The arrows indicate the deficient juxta-tricuspid rim. Further anterior sweep (frame 4) through the membranous septum and aortic valve does not reveal the defect. The numbered arrows in the drawing (Frame 5) indicate the planes of section for the corresponding frames and the shaded area represents the VSD. The arrowheads on the echocardiogram frames 2 and 3 indicate the crux of the heart. (AV = atrioventricular; LV = left ventricle; RV = right ventricle; VSD = ventricular septal defect.)

View larger version (172K): [in this window] [in a new window]   Fig 4. Parasternal short-axis sweep in a patient with a large mid-muscular VSD. Frame 1 reveals the intact inlet septum at the levels of the belly of the MV and TV. Frame 2 cuts through the trabecular septum at the level of MB insertion site. Here, a hypertrophied septal band may render the margins of a VSD irregular. Frame 3 illustrates the most apical cut. The VSD is not visualized. The numbered arrows in the drawing (Frame 4) indicate the planes of section for the corresponding frames, and the shaded area represents the VSD. (LV = left ventricle; MB = moderator band; MV = mitral valve; RV = right ventricle; TV = tricuspid valve; VSD = ventricular septal defect.)

Surgical approach
All moderate to large mid-muscular VSDs were closed through tricuspid valve after right atriotomy using Gore-Tex patches (W.L. Gore & Associates, Flagstaff, AZ) and anchored with interrupted pledgetted sutures. Smaller additional defects were closed directly with pledgetted sutures. Sutures were placed away from the edge of the VSD and the anticipated location of the conduction bundle. Septal or posterior leaflets of the tricuspid valve were detached to obtain better visibility of the VSD margins, especially in instances of inlet or posterior muscular VSD. Other approaches included transpulmonary approach for outlet VSDs, and right ventriculotomy over the anticipated locations of the defects for anterior marginal and apical defects [7].

Pulmonary artery (PA) banding was advised in the following circumstances:

1. Proximity of margins of the defect to the AV nodal conduction tissues predicted a high possibility of AV block in a small infant (< 5 kg) where spatial constraints exist for placing a permanent pacemaker. The prospect of cost savings from avoiding a permanent pacemaker if these VSDs were closed at a later date was an important additional consideration in our environment.
   
2. Multiple apical VSDs.
   
3. Selected patients with large muscle bands traversing the defects that could interfere with complete closure.
   
4. During earlier period of the study, large muscular defects with associated coarctation of aorta in infants less than 2 months old.
   

	Results

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Demographic data
Thirty-four patients (median age 6 months old, range 1 to 54 months old; median weight: 4.3 kg, range 2.5 to 17 kg) formed the study group. The summary of the defects is illustrated in Table 1. The patients were grouped according to the location of the major defect under six descriptions (Table 2).

Surgical approach
Reconstruction in 6 patients with large posterior muscular defects (Groups I and II) revealed the defects in close proximity to tricuspid annulus with tricuspid chordal apparatus coursing across the defect. Surgical visualization of the defect margins was facilitated greatly by detachment of the septal (patients 1, 3, and 7) or posterior (patients 10, 11, and 16) tricuspid leaflet from its annular attachment. Among the 3 patients with anterior marginal defects (Group IV), anterior right ventriculotomy over the infundibulum aided closure in 2 patients (patients 28 and 29), but was not considered in the third (patient 27) because the defect was small. In all other patients, VSDs were seen and closed transatrially through the tricuspid valve.

Postoperative AV conduction
Five patients (Group II, patients 12–16) with large inlet VSD and a very thin separating muscle rim from the tricuspid annulus were predicted a higher risk for heart block. Patient 12 developed immediate postoperative complete heart block. Three patients weighing less than 5 kg (patients 13–15) were advised PA banding. One older patient (patient 16) had uneventful VSD patch closure with interrupted sutures away from the conduction tissues. Of the remaining 29 patients who were felt to be at little risk for development of heart block, patient 4 developed complete heart block. This patient had a 10-mm membranous defect and an 8-mm posterior muscular defect separated by a 6-mm muscular septal tissue. These defects were closed with two separate patches.

Pulmonary artery banding
Seven patients underwent PA banding. Three infants weighing less than 5 kg (patients 13–15) with large inlet muscular defects (Group II) were predicted to have a higher risk of heart block. One infant (Group III, patient 19) with large mid-muscular defect and muscle bands traversing the defect from left ventricular free wall to anterior tricuspid papillary muscle underwent PA banding in view of uncertainty about ventricular function after resection of these muscle bands. Two small infants (Group V, patients 30 and 31) with swiss cheese defects were predicted to have remote chances of closing all the defects. Early in our experience, one 2-month-old infant with a large VSD and coarctation (patient 23) initially underwent PA banding and arch repair.

Residual VSD
Among 27 patients who underwent primary closure for their VSD, 9 patients had residual defects on postoperative echocardiography. The residual defect was hemodynamically significant only in 1 patient (patient 1). Preoperative echocardiography diagnosed inlet muscular VSD and large muscle bundles traversing the apical end of the defect. During surgery, hypertrophied tricuspid chordopapillary apparatus straddling the apical margin of the VSD posed difficulties in placing interrupted sutures for patch closure. After surgical closure, there was a significant residual defect along this apical margin. After a PA banding on next day, this patient could be successfully extubated and discharged.

Four patients had tiny residual defects close to the margins of the main defect. In these patients, preoperative echocardiography had visualized the irregularity of the defect margins due to tricuspid chordopapillary apparatus (patients 3 and 8) and large muscle bands (patients 28 and 34). In 4 patients with small additional apical (patients 10 and 33) and anterior marginal defects (patients 12 and 27), poor visualization from the right atrial approach due to apical trabeculations and hypertrophied septal band could be predicted preoperatively, but the defects were felt to be too small to merit a ventriculotomy for clear surgical visualization. Because the estimated postoperative pulmonary to systemic flow ratio using superior venacava and pulmonary artery saturations in the operation room were less than 1.3:1 in all these patients, cardiac catheterization was not performed.

Surgical results and Follow-Up
There were two deaths. Patient 15 with a large inlet VSD, straddling tricuspid valve, severe tricuspid regurgitation, and additional large apical VSD presented with severe pneumonia requiring mechanical ventilation. Because pictorial reconstruction predicted risk to AV node (no juxta-tricuspid muscular rim) and possible residual defect (apical defect hidden in RV trabeculations), PA banding and tricuspid valve repair was done. The patient succumbed to sepsis after 7 days. Patient 24 had a muscular VSD anterior to the hypertrophied septal band, closed through a right ventriculotomy. The child was extubated after 2 days with no postoperative residual defects. On the third postoperative day, the child died of recurrent unexplained ventricular fibrillation.

All others had an uneventful course. The patients with small residual defects were discharged after a mean intensive care unit stay of 5.8 ± 2.7 days and mean hospital stay of 12 ± 7.2 days (4.2 ± 1.9 days and 9.5 ± 5.8 days, respectively, in the patients with no residual defects, p value not significant). The residual defect in patient 1, who underwent postoperative PA banding, became restrictive after 18 months due to hypertrophy of muscle bands along apical margin of the patch. Two patients (patients 13 and 23), who underwent initial PA banding, underwent VSD closure and debanding and the surgical anatomy was as predicted.

	Comment

Top Abstract Introduction Material and methods Results Comment References

 
Between 5% and 20% of all VSDs are muscular [1, 15, 16]. Unique features of muscular defects include diverse locations, multiplicity, hypertrophied muscle bars traversing the defect, and varying numbers of orifices on left and right ventricular surfaces [2]. Differences in nomenclature and various classifications further complicate the understanding of muscular VSDs [10–12]. Based on location, as many as 13 different types of VSDs have been described [3]. The congenital heart surgery nomenclature and database project supported by the Society of Thoracic Surgeons and the European Association for Cardiothoracic Surgery recently concluded that pictorial representation of the VSD location on the RV septal surface allowed better understanding of the anatomy because the information is unambiguous and the stress on nomenclature is avoided [13].

This study demonstrates the feasibility of creating a pictorial representation based on en-face reconstruction of muscular VSDs on the right ventricular septal surface using transthoracic echocardiography. We could provide an en-face reconstruction in all the 34 patients with single or multiple muscular defects (62 defects). The picture provided a clear perspective for the cardiac surgeon about the dimensions, shape and relation of the defect to various RV septal structures, allowed planning of surgical approach, and helped anticipate heart block and residual defects.

Although most VSDs are repaired through the right atrium [3], selected patients may require detachment of the septal or posterior tricuspid leaflet from its annulus. Additional approaches include right ventriculotomy for apical and mid-muscular defects, and infundibulotomy for anterior marginal and outlet defects [3]. Left ventriculotomy for apical muscular defects is seldom recommended due to its impact on left ventricular function [4]. In our patient group, pictorial reconstruction helped the surgeons to plan the access for the defect (Table 2). Although a transatrial approach was used for most patients, additional anterior defects in 2 patients were accessed through ventriculotomy over the RV infundibulum. Six patients with posterior defects required detachment of the septal or posterior tricuspid leaflets for better visualization.

Knowledge of the anatomy of the AV conduction tissues and its relation to the rims of VSDs in various locations has improved prediction of the postoperative heart block [8]. In VSDs that are not juxta-tricuspid, a muscle bar separates the borders of the VSD from the tricuspid annulus and this protects the His bundle from lying along the free edge of the VSD [9]. Echocardiographic identification of this muscle bar that separates the VSD borders from the tricuspid annulus helps predict heart block [9].

We predicted higher risk of AV block in 5 patients with inlet muscular VSD with a very thin separating muscle rim from the anticipated site of course of conduction tissues. One patient developed postoperative complete heart block. In 3 patients weighing less than 5 kg, we chose to perform PA banding because we felt that the risk of heart block may be reduced if these VSDs were closed at an older age in a larger heart. We were unable to anticipate the occurrence of heart block in 1 patient with a large perimembranous defect and an adjacent posterior muscular VSD. The posterior muscular defect had a good juxta-tricuspid rim but the AV block presumably resulted from injury to the bundle of His at the posteroinferior rim of the perimembranous VSD.

Large residual defects may lead to heart failure and failed extubation, and small defects are a substrate for infective endocarditis. Revealing the location of the additional defects in relation to the main defect en-face reconstruction may allow complete closure of all surgically accessible defects. However, certain defects with large muscle bars traversing them and apical or marginal defects with irregular edges resulting from hypertrophied muscle bands carry a higher risk of residual defects after attempted primary closure [5, 14]. A higher prediction of residual defect in three infants altered our strategy from primary closure to PA banding.

Defects predicted in surgically inaccessible areas pose challenges to the surgeons and may be addressed by transcatheter or intraoperative device placement [14, 17]. Cost constraints precluded the use of devices in our patients.

Study limitations
The en-face reconstruction could not predict the occurrence of heart block in 1 patient and one major residual defect could not be anticipated. The relative merit of this technique can only be tested with a control cohort of patients with muscular VSD without en-face pictorial reconstruction. In older patients, poor echocardiographic windows may not allow clear delineation of the defect. Newer imaging modalities, such as fast gradient magnetic resonance cardiac imaging and real-time three-dimensional echocardiography, may allow pictorial reconstructions in the future with greater ease.

In summary, pictorial representation of en-face reconstruction of single or multiple muscular ventricular septal defects are feasible through meticulous echocardiography in different orthogonal views. The picture generated allows unambiguous communication about the location and dimensions of the defect or defects. The picture of the reconstruction can guide surgical approach and help predicting possibility of residual defects and heart block after attempted primary closure of defect.

	References

Top Abstract Introduction Material and methods Results Comment References

 

1. Mavroudis C., Backer C.L., Idriss F.S. Ventricular septal defect. In: Mavroudis C., Backer C.L., eds. Pediatric cardiac surgery, Second edition. St Louis, MO: Mosby, 1994:201-224.
2. Wennick A.C.G., Oppenheimer D.A., Moulaert A.J. Muscular ventricular septal defects, a reappraisal of the anatomy. Am J Cardiol 1979;43:259-264.[Medline]
3. Kirklin J.W., Barratt-Boyes B.G. Ventricular septal defects. In Cardiac Surgery, Volume 1, Second edition. New York: Churchill Livingstone, 1993:749-824.
4. Griffiths S.P., Turi G.K., Ellis K., Krongrad E., Smith L.H., Gersony W.M. Muscular ventricular septal defects repaired through left ventriculotomy. Am J Cardiol 1981;48:877-883.[Medline]
5. Tsang V.T., Hsia T.Y., Yates R.W., Anderson R.H. Surgical repair of supposedly multiple defects within the apical part of the muscular ventricular septum. Ann Thorac Surg 2002;73:58-62.[Abstract/Free Full Text]
6. Black M.D., Shukla V., Rao V., Smallhorn J.F., Freedom R.M. Repair of isolated multiple muscular ventricular septal defects: the septal obliteration technique. Ann Thorac Surg 2000;70:106-110.[Abstract/Free Full Text]
7. Stellin G., Padalino M., Milanesi O., et al. Surgical closure of apical ventricular septal defects through a right ventricular apical infundibulotomy. Ann Thorac Surg 2000;69:597-601.[Abstract/Free Full Text]
8. Milo S., Ho S.Y., Wilkinson J.L., Anderson R.H. Surgical anatomy and atrioventricular conduction tissues of hearts with isolated ventricular septal defects. J Thorac Cardiovasc Surg 1980;79:244-255.[Medline]
9. Anderson R.H., Becker A.E. The anatomy of VSDs and their conduction tissues. In: Stark J., de Laval M.R., eds. Surgery for congenital heart defects, Second edition. Philadelphia: Saunders, 1994:115-138.
10. Soto B., Becker A.E., Moulaert A.J., Lie J.T., Anderson R.H. Classification of ventricular septal defects. Br Heart J 1980;43:332-343.[Abstract/Free Full Text]
11. Geva T., Kreutzer J., Van Praagh R. Ventricular septal defect, how shall we describe, name and classify them. J Am Coll Cardiol 1989;14:1298-1304.[Medline]
12. Soto B., Ceballos R., Kirklin J.W. Ventricular septal defects. A surgical viewpoint. J Am Coll Cardiol 1989;14:1291-1297.[Abstract]
13. Jacobs J.P., Burke R.P., Quintessenza J.A., Mavroudis C. Congenital heart surgery nomenclature and database project: ventricular septal defect. Ann Thorac Surg 2000;69:S25-S35.[Abstract/Free Full Text]
14. Kumar K., Lock J.E., Geva T. Ventricular septal defects between infundibular and left ventricular apices: imaging and interventional considerations. Circulation 1997;95:1207-1213.[Abstract/Free Full Text]
15. Graham T.P., Gutgessel H.P. Ventricular septal defects. In: Moss A.J., Adams F.H., eds. Heart disease in infants, children and adolescents, Fifth edition. Baltimore, MD: Williams and Wilkins, 1995:724-744.
16. Perloff J.K. The clinical recognition of congenital heart disease, Fourth edition. Philadelphia: W. B. Saunders, 1989:396-439.
17. Okubo M., Benson L.N., Nykanen D. Outcomes of intraoperative device closure of muscular ventricular septal defects. Ann Thorac Surg 2001;72:416-423.[Abstract/Free Full Text]

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