Ann Thorac Surg 2002;73:48-56
© 2002 The Society of Thoracic Surgeons
Original article: cardiovascular
Apical ventricular septal defects: follow-up concerning anatomic and surgical considerations
Stella Van Praagh, MD*b,
John E. Mayer, Jr, MDa,
Norman B. Berman, MDc,
Michael F. Flanagan, MDc,
Tal Geva, MDb,
Richard Van Praagh, MDb
a Departments of Surgery, Cardiology, and Pathology, Children’s Hospital, Boston, Massachusetts, USA
b Harvard Medical School, Boston, Massachusetts, USA
c Division of Pediatric Cardiology, Children’s Hospital at Dartmouth, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, USA
Accepted for publication August 18, 2001.
* Address reprint requests to Dr Van Praagh, Cardiac Registry, Bader 138, Children’s Hospital, 300 Longwood Ave, Boston, MA 02115, USA
e-mail: gaskill{at}a1.tch.harvard.edu
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Abstract
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Background. Apical ventricular septal defects (VSDs) are difficult to visualize and close transatrially. We described their distinctive anatomic features, which have seldom been documented angiocardiographically and pathologically, in order to develop an effective approach for their surgical management.
Methods. Fourteen postmortem cases, two explanted hearts, 9 successfully operated patients, and 1 unoperated living patient were included in this report. Angiocardiographic documentation of the apical VSD was available in 14 of 16 (87.5%) of the postmortem and transplanted cases, and in 6 of 10 (60%) of the living patients. Echocardiograms were available in 23 of all 26 cases (88%).
Results. Severe associated malformations were present in 14 of 16 (87%) of the pathologically documented cases. Large VSDs allowed extensive communication between the left ventricular and the right ventricular sinuses in 4 patients. In 12 of the pathologically documented cases and in the 10 living patients, the left ventricular apex communicated with the right ventricular apical infundibular recess.
Conclusions. Extremely large apical VSDs with severe biventricular dysplasia and dysfunction may require cardiac transplantation. Large apical VSDs can be successfully closed through a small apical infundibulotomy. This approach, applicable even in small infants, can avoid pulmonary artery banding or left ventriculotomy.
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Introduction
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Apical ventricular septal defects (VSDs) are the most difficult to visualize through the tricuspid valve and to close transatrially. With our colleagues at the University of Padua, Italy, we described in a previous publication [1] the distinctive anatomic characteristics of apical VSDs and the short-term results of the surgical approach inspired by the understanding of these characteristics. In the present report, we present additional short-term and long-term results of the proposed surgical approach, thus providing further evidence of its efficacy. We have also documented for the first time the correlation between the distinctive angiocardiographic images of apical VSDs with the corresponding pathologic findings in postmortem cases. In addition, we report the anatomic findings of the heart specimens with apical VSDs preserved in the Cardiac Registry of the Boston Children’s Hospital, thus providing a more complete picture of the heart defects that may be associated with apical VSDs.
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Material and methods
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Among the 3,155 heart specimens with congenital structural defects preserved in the Cardiac Registry of the Boston Children’s Hospital, we identified 16 cases (0.5%) with hemodynamically significant apical VSDs (Table 1).
According to the computerized data of the Cardiology Department of the Boston Children’s Hospital, 7 patients with apical VSDs and congestive heart failure in early infancy have been operated by the same surgeon (J.E.M.) over a 16-year period (1985 to 2001) (Table 2).
Two other patients were operated on elsewhere after we suggested our approach to the respective surgeons. Case 8 (Table 2) was operated on by Dr Neirotti in Grand Rapids, Michigan, and case 9 (Table 2) was operated on by Dr Miguel Barbero Marcial in Rio de Janeiro, Brazil. One additional unoperated patient with an apical VSD and a restrictive exit of the infundibular recess was included in the present report. This patient (case 10, Table 2) was diagnosed and followed at the Dartmouth-Hitchcock Medical Center in Lebanon, New Hampshire.
Terminology
Infundibular apical recess (or infundibular apex) is the recess anterior, inferior, and to the left of the junction of the septal and moderator bands of the right ventricle (RV) [2–4]. It is present in all hearts that exhibit a moderator band and varies in size (Fig 1).
The right ventricular sinus is the part of the RV to which the tensor apparatus of the tricuspid valve (TV) attaches [3]. The RV sinus is inferior and posterior to the parietal band, the conal septum, the septal band, and the moderator band—all of which are infundibular outflow tract structures. The apex of the infundibular recess is superoanterior and to the left of the apex of the RV sinus (Fig 1). The apical ventricular septum separates the left ventricular (LV) apex from the infundibular apex rather than the RV sinus apex (Fig 2A). The infundibular apex is separated from the RV sinus apex by a septumlike structure that may include the moderator band and that may exhibit some intertrabecular spaces. This muscular structure represents the apical infundibulosinus partition (Figs 1 and 2A).
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Fig 1. (A) Opened normal right ventricle (RV). The apex of the infundibular recess is anterior and to the left of the moderator band (MB). The apex of the RV inflow is inferior and to the right of the infundibular apex. The two apices are separated by a muscular ridge, which in some cases may exhibit some intertrabecular spaces. (Reproduced and modified with permission from Van Praagh R, Plett JA, Van Praagh S. Single ventricle: pathology, embryology, terminology, and classification. Herz 1979;4:113–50 [Copyright Urban & Vogel].) (B) A normal RV showing the relative positions of the RV sinus apex and of the infundibular apical recess. A muscular ridge, the infundibulosinus partition, separates those two areas in the normal RV. (PB = parietal band; PV = pulmonary valve; SB = septal band; TV = tricuspid valve.)
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Fig 2. The heart of a 2.5-month-old girl with apical ventricular septal defect (VSD), coarctation of the aorta, and patent ductus arteriosus (case 5, Table 1). (A) Opened right ventricle (RV). The apical VSD is located in the area of the ventricular septum, which lies between the left ventricle (LV) and the apical infundibular (Inf) recess. A muscular partition separates the apical Inf recess from the RV apex. In the exit of the Inf recess there is a small remnant of the patch, which was placed transatrially. (B) Opened LV showing the large apical VSD (25% of the left ventricular septal length, Table 1). (C) Angiocardiogram of same case at 17 days of age. Left anterior oblique view of an LV injection after coarctation repair, patent ductus arteriosus ligation, and main pulmonary artery banding. Note how the dye enters the Inf apical recess adjacent to the apical VSD (white arrows), which has a nonrestrictive exit (gray arrows). (Ao = aorta.)
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Apical muscular VSDs are defects that occupy the most apical portion of the ventricular septum and are usually distal to the moderator band from the RV side (Fig 2). In postmortem specimens we expressed VSD size as a percentage of the left ventricular septal length (LVSL), that is, maximal apicobasilar dimension of the VSD/LVSL x 100. Ventricular septal defect size was indexed to LVSL because of the great differences in the sizes of the heart specimens (Table 1). In the living patients the largest dimension of the VSD was assessed echocardiographically or angiocardiographically or at the time of operation (Table 2).
Operative technique
All patients underwent median sternotomy. Cardiopulmonary bypass was established with a single arterial cannula in the distal ascending aorta. In cases 1 and 2 (Table 2), a single cannula for venous return and deep hypothermia with circulatory arrest were used. In cases 3 to 7, two venous cannulas were used and hypothermic circulatory arrest was used only for aortic arch repair. Single-dose cardioplegia was used in all cases. The apical VSD was approached through an RV incision that was placed rightward of the anterior descending coronary artery and just superior to the cardiac apex (Fig 3).
Muscle bundles crossing the space between the ventriculotomy and the margin of the VSD were divided. The moderator band was never transected. The VSDs were closed with Dacron (C. R. Bard, Haverhill, PA) patches, which were secured with multiple interrupted pledgeted horizontal mattress sutures. In some cases in which there was no muscular rim between the defect and the free wall of the RV, the sutures were placed through the full thickness of the ventricular wall. In all but one case, the ventriculotomy was closed primarily. A pericardial patch was used to close the ventriculotomy in case 3 (Table 2).
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Fig 3. Diagrammatic presentation of apical infundibulotomy. The incision (dotted line) is parallel to and to the right of the distal part of the anterior descending coronary artery (LAD). The length of this incision, which extended close to the apex of the heart, varied from 1.5 to 2.5 cm. Inset shows the exposed apical ventricular septal defect (VSD). In this diagram and in some cases of this report the defect extends above and below the moderator band (MB). (Ao = aorta; LV = left ventricle; MPA = main pulmonary artery; RV = right ventricle; SB = septal band.) Reproduced with permission from The Society of Thoracic Surgeons (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.)
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Results
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Anatomic findings
The cardiac anatomic findings in the 14 postmortem cases and the two explanted hearts are presented in Table 1. In cases 1 to 4 (Table 1) the large apical VSD involved the septum of both the RV sinus and of the infundibular apical recess (Fig 4). All other apical VSDs of this study were invariably located on the septal surface of the infundibular recess (Fig 2). In three cases (case 7, Table 1 and cases 4 and 5, Table 2), the VSD was bisected by the moderator band so that it had one exit from the LV and two entrances into the RV (Fig 3). The associated malformations of most postmortem cases were multiple and severe (Table 1). By contrast, the associated malformations of the living patients were a patent ductus arteriosus (PDA) with or without hypoplasia and coarctation of the aortic isthmus or an additional membranous VSD (Table 2).
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Fig 4. The explanted heart of a 2.5-year-old boy with a large apical ventricular septal defect (VSD), abnormal tricuspid valve (TV), and biventricular dysplasia (case 1, Table 1). (A) Opened right ventricle (RV). The abnormal TV was both stenotic and regurgitant. The pulmonary valve (PV) was stenotic. The RV free wall shows extensive endocardial fibroelastosis. (B) The extremely large apical VSD (white arrows) occupies 60% of the left ventricular (LV) septal length. The mitral valve (MV) is seen through the VSD. Patchy endocardial sclerosis is seen in the LV free wall.
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Case 8 had a persistent left superior vena cava to a partly unroofed coronary sinus. The presence of a well-developed innominate vein permitted the ligation of the left superior vena cava during the operation for VSD closure.
Clinical data
The sex was known in 15 of the 16 postmortem and transplanted cases. The male/female ratio was 2. In the 10 living patients, the male/female ratio was 4. The median age at death or cardiac transplantation of the postmortem and transplanted cases was 14 months (range 12 days to 28 years 11 months). The median age at operation for VSD closure in the living patients was 7 months (range 4 days to 3.5 years).
All but one of the postmortem cases (case 13, Table 1) and 9 of the 10 living patients (cases 1 to 9, Table 2) had signs of congestive heart failure and failure to thrive preoperatively.
Cardiac catheterization was performed before the operation in cases 1 to 3, 5, and 7 to 16 (Table 1). Except for cases 9, 13, and 14 who had pulmonary stenosis or atresia, all other postmortem cases had severe pulmonary hypertension. The 9 living patients who underwent surgical closure of the apical VSD had evidence of severe pulmonary hypertension measured by cardiac catheterization or two-dimensional (2D) echo-Doppler study (Table 2). Case 10 (Table 2) had a stenotic exit of the infundibular apical recess. Hence, despite the presence of a large-sized apical VSD, the pulmonary artery pressure was not elevated, the Qp:Qs = 1.3, and the pulmonary resistance was normal (Fig 5).
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Fig 5. The angiocardiogram of a 5-year-old boy with an apical ventricular septal defect (VSD) and restrictive exit from the apical infundibular (Inf) recess (case 10, Table 2). (A) Left anterior oblique projection of a left ventricular (LV) injection. The dye entered the apical Inf recess through the apical VSD (white arrowheads). The exit of the Inf recess (white arrowheads) was restrictive, minimizing the left-to-right shunt and preventing right ventricular hypertension. (B) Lateral projection of the angiocardiogram of the same patient with an injection into the Inf recess where the pressure was similar to that of the LV. The dye flowed into the LV through the apical VSD (white arrowheads) and a small amount escaped around the catheter, which almost occluded the exit of the Inf recess.
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Echocardiography
Preoperative 2D echocardiograms were available for review in cases 1, 3, 5, and 8 through 16 (Table 1) and in all 10 living patients (Table 2). The echocardiographic technique has been described previously [4]. Briefly, to fully characterize the location, size, and relationships of the VSD with neighboring structures, the interventricular septum was scanned from the apical four-chamber plane and from at least one short-axis plane. The apical four-chamber sweep demonstrates the apex-to-base location of the VSD, its relationship to the moderator band, apicobasilar diameter, and distance from the cardiac apex (Fig 6A). The short-axis sweep delineates the relationship of the VSD to the RV and infundibular apices as well as the lateral dimension of the defect (Fig 6B). The short-axis sweep can be performed from the subxiphoid or parasternal windows. Transthoracic 2D echo with color Doppler flow mapping clearly delineated the anatomic features and flow characteristics in all patients studied after 1985.
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Fig 6. Two-dimensional echocardiogram in case 3 (Table 2). (A) Preoperative examination at 3 months of age. Diastolic frame from the apical four-chamber view showing a large muscular defect between the left ventricular (LV) apex and the infundibular (Inf) recess. The ventricular septal defect (VSD) extends from inferior to the moderator band (MB) to the cardiac apex (arrows). (B) Postoperative scan at 7 months of age from the subxiphoid short-axis view. The patch extends across the junction between the Inf recess and the right ventricular outflow tract (RVOT), leaving the Inf recess incorporated with the LV through the VSD (arrows). (LA = left atrium; RA = right atrium; RV = right ventricle.)
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Angiocardiography
Left ventricular injection in the left anterior oblique view with cranial angulation provides a most characteristic angiocardiographic picture of apical VSDs. The infundibular recess and its exit are demonstrated clearly (Figs 2C, 5, and 7).
In some cases small intertrabecular spaces may be present in the partition between the infundibular recess and the RV sinus apex (Fig 7B). If 2D-echocardiographic and Doppler study is not pathognomonic for a large apical VSD, angiocardiogram is indicated to help plan the appropriate surgical approach for its closure.
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Fig 7. Angiocardiogram of a 3-month-old boy with a single apical ventricular septal defect (VSD; case 3, Table 2). At the time of this cardiac catheterization he had severe left ventricular (LV) dysfunction and his LV free wall showed an increased stratum spongiosum and a diminished stratum compactum. (A) Left anterior oblique projection with cranial angulation of an LV injection. The dye is beginning to cross the apical VSD. (B) The infundibular (Inf) apical recess next to the apical VSD is now visualized and the dye escapes through its unobstructed exit into the right ventricle. Note a tiny jet of dye (white arrow), which shows a narrow intertrabecular space in the muscular partition between the Inf recess and the right ventricular sinus.
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Surgical treatment
Because of associated malformations, various surgical procedures were performed in all but 2 (cases 4 and 6, Table 1) of the postmortem and transplanted cases. Cases 1 and 16 underwent orthotopic heart transplantation. Case 1 died 16 days after cardiac transplantation. Case 16 is alive and well 1.5 years after cardiac transplantation. Cases 12 and 15 had a transcatheter VSD occluding device placed in the operating room with partial success. Transcatheter occluding devices were also placed during cardiac catheterization in cases 13 and 16, or while the patient was on extracorporeal membrane oxygenator (case 11). Closure of the apical VSD by the method outlined in this report was not attempted in any of the postmortem cases.
Cases 1, 2, 3, and 5 (Table 2) underwent surgical closure of the apical VSD through an RV apical infundibulotomy (Fig 3). The large PDA in case 2 was also ligated at the time of the VSD closure. In case 3 the Dacron patch was unintentionally placed over the exit of the infundibular recess, instead of on the true VSD (Fig 6). Postoperatively the patient improved dramatically although he had echocardiographic evidence of a small residual left-to-right shunt, which probably was a result of the small intertrabecular space in the infundibulosinus partition separating the infundibular and RV sinus apices that was seen in his preoperative angiogram (Fig 7B). In his most recent echocardiogram, 23 months postoperatively, this shunt has disappeared.
Case 4 (Table 2) had repair of the severe coarctation with aortic isthmus hypoplasia and PDA ligation at the time of the apical VSD closure at the age of 4 days. The area of the coarctation was resected and the aortic arch incision was augmented with a patch of pulmonary artery homograft. The augmented proximal aorta was sewn in an end-to-end fashion to the descending aorta. Restenosis of the aortic isthmus developed in this patient and she underwent successful balloon dilatation of the stenotic segment at the age of 4 months. Progressive fibrous subaortic stenosis also developed with a 60 mm Hg gradient across the LV outflow tract. At the age of 19 months she underwent successful resection of the subaortic fibrous ridge and myomectomy. At her last follow-up visit 8 months later, she was asymptomatic with normal growth and development.
Case 6 (Table 2) was diagnosed as having a membranous and an apical VSD as well as mitral and subaortic stenosis after cardiac catheterization and angiocardiography at the age of 9.5 months. Although he did not have the usual auscultatory findings of mitral stenosis, his elevated left atrial pressure (29 mm Hg mean) led to the performance of atrial septectomy when he underwent banding of his main pulmonary artery (MPA) at the age of 9.5 months. He was referred to our hospital at the age of 2 years for cardiac catheterization and possible further surgical procedures. 2D-echocardiography showed an apical VSD of approximately 10 mm in diameter, a membranous VSD of 7 mm in diameter, and a large aneurysm of the membranous septum protruding into and partly obstructing the LV outflow. The mitral valve had two well-spaced papillary muscles and a mildly small orifice, but did not appear congenitally malformed. A left-to-right shunt was present through the surgically created atrial septal defect and bidirectional flow occurred through both VSDs. The RV-to-MPA maximum instantaneous gradient was 100 to 120 mm Hg. It was concluded that the mitral valve and LV could handle normal cardiac output. When the patient was 2.5 years old, the surgical atrial septal defect and the membranous VSD were closed transatrially. The MPA band was resected and the proximal and distal parts of the MPA were anastomosed directly. The apical VSD was visualized through a 1.5-cm RV apical infundibulotomy and closed with a knitted Dacron patch. The patient’s recovery was uneventful. Additional membranous VSDs were also present in cases 8 and 9, and aortic coarctation in case 8 (Table 2).
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Comment
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The findings of this report provide a spectrum of the various sizes of apical VSDs and some of the malformations that may be associated with these defects (Tables 1 and 2). The size of the apical muscular VSD in 14 patients with pathologic confirmation (Table 1) averaged (± 1 standard deviation) 10.71 (± 10.19) mm, with a median of 6 mm and a range from 3 to 35 mm. The average size of the apical VSD in the 9 operated and living patients (Table 2) averaged 10.43 (± 2.07) mm, with a median of 10 mm and a range from 7 to 15 mm. Hence, the average size of the apical muscular VSD did not differ significantly between the living and dead/transplanted groups, although the range in the dead/transplanted group was greater than in the living group.
Very large apical VSDs in cases 1 to 4 (Table 1) always occurred in association with downward displacement of the septal leaflet of the TV and deformities of the other TV leaflets resulting in tricuspid stenosis or regurgitation. Although the TV showed some similarities with the TV in Ebstein’s malformation, the RV myocardium was dysplastic but not abnormally thin (Fig 4). An additional small membranous VSD was present in cases 1 and 2 and a conoventricular VSD with conal septal malalignment occurred in case 4.
When the apical VSD is extremely large and is associated with abnormalities of the TV and with dysplasia of the RV and the LV myocardium (Fig 4), orthotopic heart transplantation may be the most likely therapeutic option. Many of the large- and small-sized apical VSDs of the postmortem cases were associated with complex malformations. Corrective surgical treatment was probably possible only in cases 5, 7, 11, and 15 (Table 1) in whom the associated malformations consisted of hypoplasia of the aortic isthmus, coarctation of the aorta, and PDA.
The difficulty in visualizing and surgically closing apical VSDs has precipitated the introduction of various surgical innovations [5] and transcatheter device closure in the catheterization laboratory or in the operating room [4, 6, 7]. Most of the reported cases [4] had additional midmuscular VSDs; hence they do not represent cases similar to those of this report.
After transcatheter device closure, a small residual left-to-right shunt was almost always present [4]. Transcatheter device closure of muscular VSDs during cardiac catheterization requires general anesthesia, an experienced interventionist, and often more than one device [4]. Reported morbidity of the procedure includes blood loss requiring transfusion, hypotension (greater than 20% decrease of systolic pressure), prolonged exposure to radiation, heart block requiring short-term treatment, significant ventricular dysrhythmias or ventricular tachycardia, and cardiac arrest requiring resuscitation [8].
Although transcatheter device closure remains a therapeutic option for selected cases of lesions that are difficult to manage operatively [9], the present report demonstrated that apical VSDs in the infundibular apical recess can be approached surgically with good results.
The excellent postoperative results of cases 1 to 5 and 7 (Table 2) who underwent closure of their apical VSD through an RV apical infundibulotomy in early infancy (4 days to 7 months) support the effectiveness and safety of this approach. All 6 had no previous operations and all had preoperative evidence of severe pulmonary hypertension and heart failure (Table 2). Case 7 had the combination of an apical VSD with common atrioventricular canal and Trisomy 21. Attention should be given to the possibility of unintentional placement of the VSD patch over the exit from the infundibular apical recess, instead of on the true VSD. If any intertrabecular spaces exist in the infundibulosinus partition a small left-to-right shunt will persist (case 3, Table 2, and Fig 7B). Such a shunt may or may not disappear eventually.
Cases 6, 8, and 9 (Table 2) indicate that this approach can also be used successfully in patients who have an additional membranous VSD and who have undergone MPA banding. Case 6 also exemplifies mild underdevelopment of the mitral valve and LV relative to the marked hypertrophy of the RV after banding of the MPA. Such cases run the risk of being misdiagnosed as congenital mitral stenosis. Postoperatively in case 6 the mean left atrial pressure was 10 mm Hg, indicating absence of anatomic congenital mitral stenosis.
A large left-to-right shunt prenatally is probably responsible for the hypoplasia of the aortic isthmus and preductal coarctation that is present in some patients with apical VSDs. When isthmus hypoplasia is present, to avoid recoarctation it may be necessary to repair the defect as if aortic arch interruption were present, using an extended end-to-end anastomosis between the transected end of the descending aorta and the underside of the aortic arch. The efficacy and safety of surgical treatment of symptomatic apical VSDs in early infancy through RV apical infundibulotomy is strongly supported by the 4 cases previously reported [1], and by the 9 cases of the present report.
Conclusions
- The relatively small number of apical VSDs found in the postmortem material of the Cardiac Registry of the Boston Children’s Hospital, which extends over the last 50 years, would suggest that hemodynamically significant apical VSDs are not common.
- The proposed surgical treatment is not indicated in cases of midmuscular (single or multiple) VSDs. Midmuscular VSDs usually can be approached transatrially.
- Single large apical VSDs may be associated with a PDA, coarctation of the aorta, an additional membranous VSD, or common atrioventricular canal. Our experience indicates that it is possible to correct these additional defects at the same time, thus avoiding pulmonary artery banding.
- The data of this report and of reference 1 indicate that large single apical VSDs can be closed successfully through a small RV apical infundibulotomy with excellent short- and long-term results. The success of this approach makes apical left ventriculotomy unnecessary [10–12].
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Acknowledgments
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This study was supported in part by the Karen Arbia Scholarship Fund of Boston, Massachusetts.
We thank Drs M. S. Florentine and R. A. Neirotti of Grand Rapids, MI, and Drs Rosa C. Barbosa and M. B. Marcial of Rio de Janeiro, Brazil, who provided the information and cared for cases 8 and 9 (Table 2), Emily and Bill McIntosh for artwork and photography, and Gloria Gaskill for typing the manuscript.
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References
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E. A. Bacha, Q.-L. Cao, J. P. Starr, D. Waight, M. R. Ebeid, and Z. M. Hijazi
Perventricular device closure of muscular ventricular septal defects on the beating heart: technique and results
J. Thorac. Cardiovasc. Surg.,
December 1, 2003;
126(6):
1718 - 1723.
[Abstract]
[Full Text]
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Abstract
Introduction
