Ann Thorac Surg 2000;69:1496-1498
© 2000 The Society of Thoracic Surgeons
Original articles: Cardiovascular
Transaortic closure of residual intramural ventricular septal defect
Emre Belli, MDa,
Lucile Houyel, MDa,
Alain Serraf, MDa,
François Lacour-Gayet, MDa,
Jérôme Petit, MDa,
Claude Planché, MDa
a Marie Lannelongue Hospital, Le Plessis-Robinson, France
Address reprint requests to Dr Planché, Marie Lannelongue Hospital, 133, Ave de la Résistance, 92350 Le Plessis-Robinson, France
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Abstract
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Background. Residual intramural ventricular septal defect is an unusual cause of left-to-right shunt after biventricular repair of conotruncal anomalies. It results from the insertion of the patch within the trabeculated right ventricular free wall related to the ventriculoinfundibular fold creating a communication through the intertrabeculated spaces to the right ventricular cavity. This complication often leads to unsuccessful reoperations unless the exact mechanism of the shunt has been identified.
Methods and Results. Five patients presented with residual intramural ventricular septal defects. Three had double outlet right ventricle, one pulmonary atresia with ventricular septal defect, and one tetralogy of Fallot. One patient was unsuccessfully reoperated on for closure of the residual ventricular septal defect through the right ventricular approach. The surgical treatment, which consisted of patch closure of the residual intramural ventricular septal defect through aortotomy, was successful in 3 patients. In the 2 remaining patients the hemodynamically insignificant residual intramural ventricular septal defect remained untouched. No mortality or morbidity occurred.
Conclusions. Residual intramural ventricular septal defect should be suspected in presence of a residual ventricular septal defect after biventricular repair of conotruncal anomalies. It is not accessible through either atriotomy or right ventriculotomy. The transaortic approach allows an easy treatment of this rare complication.
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Introduction
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In most conotruncal anomalies including tetralogy of Fallot, double outlet right ventricle (DORV), and transposition of great arteries with ventricular septal defect (VSD) associated with pulmonary stenosis, the aorta arises entirely or partially from the right ventricle over a malalignment form of the VSD. The surgical biventricular repair involves the construction of an intracardiac baffle to tunnel the left ventricle to the aorta using the VSD, at least partially, for the egress of left ventricular flow. The left ventricular outflow pathway is formed by the baffle inserted at the right ventricle free wall to the aortic junction, also called ventriculoinfundibular fold [1]. In this particular group of anomalies the right ventricular free wall is often hypertrophied, containing parietal muscular bands and coarse trabeculations.
Residual interventricular communications after surgical biventricular repair of conotruncal anomalies represents a rare cause of early reoperation. They are most commonly from patch dehiscence, incomplete closure of the defect, or the presence of additional unrecognized VSDs.
As has been previously described by Preminger and coworkers [2], we have observed an unusual type of residual interventricular communication. These defects were difficult to localize and could be the cause of multiple reoperations with a high risk of morbidity and mortality. The left orifice was usually located under the aortic cusps. The defect coursed through intertrabecular spaces in the right ventricular free wall and gave rise, by definition, to multiple orifices on the right ventricular side. In fact, they can be defined as residual interventricular (right ventricle) communications, the distal part of the left ventricular outflow being partially created by the right ventricular free wall after the repair. The cause might result from the insertion of the VSD patch to trabeculae, far from the aortic valve. The surgical closure of these residual intramural ventricular septal defects (RIVSD) may be extremely difficult through conventional right atrial or right ventricular approaches.
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Patients and methods
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Between 1985 and 1998, at our department, 1,238 patients underwent anatomic repair of a conotruncal anomaly associated with a VSD. The latter included 294 transpositions of great arteries associated with VSD, 661 tetralogy of Fallot, 184 DORV, and 99 truncus arteriosus. The records of all patients who underwent reoperation for residual VSD (n = 27, 2%) were reviewed. The echocardiograms, cineangiograms, clinical and operative records of these patients were reviewed. Five patients presented with RIVSD. Three of them presented with cardiac failure and significant shunt (Qp/Qs >1.5) across the RIVSD. In the remaining 2 patients, the shunt diagnosed at angiography was of trivial nature and did not constitute alone an indication for reoperation. In all, the biventricular repair was performed through a right ventriculotomy, which was our standard surgical approach to repair the patients presenting with tetralogy of Fallot, truncus arteriosus, and the majority of the DORV cases.
Patient 1 presented with pulmonary atresia associated with VSD. The total repair was performed in the neonatal period using a valved right ventricle-to-pulmonary artery conduit. The postoperative course was complicated by inability to wean the patient off mechanical ventilation. A cardiac cathterization performed at that time showed a residual VSD with a significant shunt (QP/QS = 2) (Fig 1). An unsuccessful reoperation directed to residual VSD closure was performed. At 2 months postoperatively, he underwent a second reoperation with the diagnosis of RIVSD, which was closed with a patch inserted through the aorta.
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Fig 1. Angiocardiography of patient 4 showing residual intramural ventricular septal defect. (AO = aorta; LV = left ventricle; RV = right ventricle.) The arrow indicates the residual intramural ventricular septal defect.
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Patient 2 presented with DORV. The VSD was in subaortic position and was associated with two additional trabecular VSDs and pulmonary stenosis. He underwent palliation at 2 years of age with a left modified Blalock shunt. The biventricular repair was performed at 10 years of age: pulmonary infundibular dissection, intraventricular baffle repair, and closure of the trabecular VSDs were performed, and to avoid damage to the infundibular coronary artery, a right ventricle to pulmonary artery conduit (14 mm) was added to the restrictive pulmonary outflow. Both operations were performed at a different instutition. At 15 years of age, he presented to us with a RIVSD and a restrictive right ventricular outflow (Fig 2). At reoperation, the RIVSD was closed with a patch through the aorta and the right ventricular ouflow conduit was enlarged with a patch.
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Fig 2. Preoperative echocardiographic view of patient 1.(AO = aorta; LV = left ventricle; RV = right ventricle.) The arrow indicates the residual intramural ventricular septal defect.
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Patient 3 presented with DORV with noncommitted VSD. There was no pulmonary stenosis. He underwent biventricular repair at 4 months of age. The baffle construction was associated with an anterocaudal VSD enlargement. Two years later he underwent reoperation for subaortic stenosis and residual VSD (Qp/Qs 1.8). An extended septoplasty with subaortic fibromuscular resection was performed [3]. The diagnosis and treatment of RIVSD were made intraoperatively through aortotomy.
Patient 4 also presented with DORV. The VSD was in the subaortic position. The biventricular repair was performed at 3 months of age and included infundibular dissection, division of the abnormally attached tricuspid chordae at their muscular insertion, baffle construction, and reimplantation of the chordae to the baffle patch. The right ventriculotomy was closed by means of a patch. Eight years later he presented with both left and right ventricular outflow obstruction and RIVSD with trivial shunt. At reoperation, the tunnel was obstructed by deposed fibrocalcified material. The treatment consisted of the resection of deposed material associated wih an extended septoplasty [3]. The left orifice of the RIVSD could not be identified.
Patient 5 had tetralogy of Fallot and underwent repair at 3 months of age. Not to damage the large infundibular coronary artery, the operation was performed through a lower right ventriculotomy. The patient required an early reoperation (13th postoperative day) for residual pulmonary stenosis in which an 8-mm conduit was added to the native restrictive pulmonary outflow. At 4 years of age, right ventricle outflow gradient of 80 mm Hg and a small RIVSD without a significant shunt at angiography developed. The treatment was limited to the pulmonary outflow reconstruction by means of transannular patch performed without aortic cross-clamp.
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Results
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No mortality or morbidity occurred. Postoperarive echocardiography showed the absence of residual shunt in the 3 patients in whom the RIVSD was closed. At last visit all patients were asymptomatic and without medication.
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Comment
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In conotruncal anomalies, the right ventricle, even in the absence of pulmonary infundibular stenosis, is frequently hypertrophic and its free wall contains muscular bands and coarse trabeculations. The surgical biventricular repair involves the construction of an intracardiac baffle to tunnel the left ventricle to the aorta. Intraventricular baffle (or VSD) patch must be inserted at its posterosuperior border to the junction between the right ventricular free wall and the semilunar attachment of the aortic valve leaflets, which is corresponding to the ventriculoinfundibular fold. The RIVSD appears to result from suturing the patch to trabeculations within the ventriculoinfundibular fold. Consequently, blood can flow from the new left ventricular outflow tract, between the trabeculae, into the right ventricle (Fig 3). These channels are usually multiple at their right ventricular end. Because of the absence of residual significant shunt in the early postoperative echocardiography (except for patient 1), we suspect that they are small early after initial surgical repair of the conotruncal anomaly as a result of right ventricular hypertrophy and become larger after a variable time period with the regression of hypertrophy after right ventricular decompression. To prevent these residual defects, the surgeon must initially divide major parietal muscular bands, which will also allow an adequate visualization of this area. Then, he or she must insert the patch close to the aortic valve as much as possible, with the inclusion of possible trabecular orifices into the suture line.
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Fig 3. Postmortem right ventricular view of a heart specimen presenting with double outlet right ventricle and pulmonary stenosis. (AO = aorta.) The arrow indicates the ventricular septal defect. The probe crosses the intretrabecular spaces at the right ventricular free wall from which residual intramural ventricular septal defect can potentially develop.
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Preminger and coworkers [2] previously reported umbrella closure in 7 patients with modest results. They proposed removal and reattachment of the anterior portion of the patch as the surgical solution. In light of our experience of both transventricular and transaortic approaches for the surgical treatment of secondary left ventricle outflow obstruction of this goup of anomalies [3, 4], we propose the transaortic approach as the adequate solution to treat these defects. We performed successful RIVSD closure in 3 patients. In 1 of the remaining 2 patients presenting with RIVSD with trivial shunt, the small left orifice could not be identified within the deposed fibrocalcified material and in the other patient, we preferred the conservative approach avoiding aortic cross-clamp.
Residual intramural ventricular septal defects represent an extremely rare cause of residual shunt after biventricular repair of conotruncal anomalies. These defects, when hemodynamically significant, may cause major morbidity. They should be suspected when the echocardiographic and the catheter evaluation show a residual shunt that does not lie in the plane of the interventricular septum and also, intraoperatively, when transatrial and transventricular inspection fails to identify the residual defect. The RIVSD is not accessible through either atriotomy or right ventriculotomy. The transaortic approach allows an easy treatment of this complication.
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References
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Anderson R.H., Becker A.E., Van Mierop L.H.S. What should we call the "crista"?. Br Heart J 1977;39:856-859.[Abstract/Free Full Text]
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Preminger T.J., Sanders S.P., Van Der Velde M.E., Castaneda A.R., Lock J.E. "Intramural" residual interventricular defects after repair of conotruncal malformations. Circulation 1994;89:236-242.[Abstract/Free Full Text]
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Accepted for publication November 11, 1999.
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Abstract
Introduction
