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Ann Thorac Surg 2008;86:142-146. doi:10.1016/j.athoracsur.2008.03.058
© 2008 The Society of Thoracic Surgeons
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Original Articles: Pediatric Cardiac

Perventricular Device Closure of Ventricular Septal Defects: Six Months Results in 30 Young Children

Changping Gan, MSa, Qi An, MDa,*, Ke Lin, MDa, Hong Tang, MDb, Raphael C. Lui, MD, FRCSC, FACSa, Kaiyu Tao, MSa, Wencheng Pan, MSa, Yingkang Shi, MDa

a Department of Thoracic and Cardiovascular Surgery, West China Hospital, Sichuan University, Chengdu, Sichuan, People's Republic of China
b Department of Echocardiography, West China Hospital, Sichuan University, Chengdu, Sichuan, People's Republic of China

Accepted for publication March 25, 2008.

* Address correspondence to Dr An, Department of Thoracic and Cardiovascular Surgery, West China Hospital, Sichuan University, Chengdu, Sichuan, 610041, People's Republic of China (Email: anqi8890{at}163.com).


   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 
Background: Both surgical repair and transcatheter closure of isolated ventricular septal defects are known to have limitations in children. This report describes the short-term results of perventricular device closure of nonmuscular ventricular septal defects without cardiopulmonary bypass in young children.

Methods: Thirty patients who had nonmuscular ventricular septal defects underwent perventricular closure by minimally invasive technique without cardiopulmonary bypass. A subxiphoid minimally invasive incision was performed. Under the continuous guidance of transesophageal echocardiography, the free wall of the right ventricle was punctured and a guidewire was introduced into the left ventricle through the defect. A delivery sheath was advanced over the wire and through the defect into the left ventricle. The device was released.

Results: Closure was successful in 27 patients (90%). There was no mortality or atrioventricular block perioperatively or during the entire follow-up period. Three patients developed incomplete right bundle branch blocks and seven patients developed new trace or mild tricuspid regurgitation after the closure. The mean hospital stay was 3.6 ± 0.7 days (range, 3 to 5 days) and no patient needed any blood or blood products. Follow-up at 6 months showed that two of the three patients had persistent incomplete right bundle branch block and three of the seven patients had persistent closure-related trace or mild tricuspid regurgitation.

Conclusions: Perventricular device closure of isolated ventricular septal defects without cardiopulmonary bypass appeared to be safe and efficacious in selected young children. The outcomes of short-term follow-up are acceptable.


   Introduction
Top
 Abstract
 Introduction
Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 
Isolated ventricular septal defects (VSDs) are among the most common congenital heart defects, accounting for approximately 20% to 29% of all congenital heart disease [1, 2]. Early surgical repair is indicated for hemodynamically significant defects, especially for those young children who present with congestive heart failure. Conventional surgical repair requires cardiopulmonary bypass (CPB) with its inherent perioperative morbidity and infrequently mortality secondary to its systemic inflammatory response [3]. Transcatheter closure of perimembranous VSDs (PVSDs) has been described in recent years and considered as a valuable alternative to surgery [4–6], but this technique has its limitations in young children due to the large sheath size relative to the patients' small vessel size, and thus subsequent complications. Perventricular device closure (PVDC) of muscular VSDs has recently been successfully conducted on human beings [7, 8]. However, PVDC of nonmuscular VSDs has been previously described only in animal models [9, 10], and most recently in a relatively small series of 12 patients [11]. In this communication we describe our experience of PVDC of nonmuscular VSDs without CPB in 30 young children.


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Comment
 Acknowledgments
 References
 
Patients
Between April and July 2007, 252 patients were enrolled with the preoperative diagnosis of isolated nonmuscular VSDs by transthoracic echocardiography (TTE). Our selection criteria for PVDC were the following: (1) evidence of congestive heart failure indicating early intervention; and (2) age under 3 years or body weight less than 15 kg. Thirty patients qualified for PVDC by these criteria. None of the patients underwent cardiac catheterization, and therefore pulmonary to systemic blood flow ratio (Qp/Qs) values were not available. This study was approved by the hospital Ethics Committee. Individual informed consents were obtained from both parents of all the patients after explaining to them the nature, the advantages, and the disadvantages of the procedure when compared with the conventional open repair with CPB. There were 16 males and 14 females with a mean age of 29.2 ± 7.3 months (range, 12 to 36 months) and a mean body weight of 12.0 ± 1.8 kg (range, 8.5 to 16 kg) in the series. Twenty-eight patients (93%) had PVSDs and 2 (7%) had subarterial VSDs. All patients underwent detailed transesophageal echocardiography (TEE) under general anesthesia before the procedure by the same echocardiographer. The following data were recorded: (1) the maximum diameter of the defect as assessed by multiple views; (2) the distance from the superior edge of the VSD to the aortic valve; (3) the end-diastolic diameter of the left ventricle; and (4) whether there was any septal aneurysm or prolapse of aortic valve leaflet. Patients with prolapse of the aortic valve leaflet would be excluded from the study. The mean diameter of the VSDs was 6.1 ± 1.7 mm (range, 3.5 to 11 mm). Eight patients with PVSDs were found to have septal aneurysms. The mean distance from the superior edge of the PVSDs to the aortic valve was 2.5 ± 1.2 mm (range, 0.3 to 5.0 mm), and the same distances were 0.5 mm and 0.7 mm in the two subarterial VSDs, respectively. The mean end-diastolic diameter of the left ventricle was 31.9 ± 3.0 mm (range, 28 to 38 mm). The TEE also demonstrated that 7 patients with PVSDs and 1 patient with subarterial VSD had trace or mild (1+) preoperative tricuspid regurgitations. No aortic incompetence or prolapse of the aortic valve leaflet were observed. No preoperative arrhythmia was recorded.

Devices
All the occluder devices (Shanghai Shape Memory Alloy Corporation, Shanghai, China) are made of 0.004-inch Nitinol wire mesh. The wires are shaped to form two discs, with a short connecting waist. The device is self-expandable and fully retrievable to the point of release. The size of the device corresponds to its waist. There are two categories of device; one is concentric and the other one is eccentric. The flanges of the concentric device are measured 2 mm around the waist, on both the right and left ventricular sides. In an eccentric device, the flange of the left ventricular disc, which faces the aortic valve, is only 0.5 mm or 0 mm larger than the waist, while the flange of the disc which is on the opposite side of the aortic valve is 5 mm larger than the waist. The right ventricular disc of the eccentric device is the same as the concentric device (ie, 2 mm larger than the waist all around). A female screw is welded in the center of the right disc for attachment to the delivery cable and a metallic marker is welded to the edge of the larger flange on the left, to indicate the direction opposite the aortic valve (Fig 1).


Figure 1
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  		Fig 1. (Top) The concentric occluder with 2-mm flanges around the waist, on both right and left ventricular sides. (Middle) The 0.5-mm eccentric occluder with the flange of the left ventricular disc that eventually faces the aortic valve, being 0.5 mm larger than the waist. (Bottom) The 0-mm eccentric occluder with the flange of the left ventricular disc that eventually faces the aortic valve, being the same size as the waist.

 
Perventricular Technique
The chest was opened through a 4- to 5-cm subxiphoid incision and lower partial sternotomy. The pericardium was opened longitudinally and suspended to expose the free wall of the right ventricle (RV). Under continuous TEE monitoring, the RV free wall was gently depressed with the index finger of the surgeon. This depression of the RV free wall could be clearly visualized by TEE and its spacial relationship to the defect was determined. By changing the location of the depression, a point that was closest to the defect was identified and a purse-string suture of 4-0 Prolene sutures (Ethicon Inc, Somerville, NJ) was placed at this location. After systemic heparinization (1 mg/kg), the RV free wall was punctured with a 20-gauge needle through the purse-string suture. Under continuous TEE monitoring and guidance, a flexible 0.035-inch guidewire was introduced into the RV, and subsequently the left ventricle (LV), through the defect. A deliver sheath was advanced over the wire into the LV, the wire was removed, and the sheath was allowed to back bleed to ensure that there was no air in the sheath. The occluder was screwed onto the delivery cable and the cable was inserted into a loader, which would be connected to the tail of the sheath in order to load the device into the sheath. The cable was pushed to allow deployment of the left ventricular disc. The whole system (cable and sheath) was then pulled back slightly so that the underside of the left ventricular disc lay snug against the septum. If an eccentric device was used, the device would be rotated gently to align the marker on the opposite side of the aortic valve. The sheath was then withdrawn further to allow the deployment of the right ventricular disc. The position of the device was checked again by TEE. The aortic and tricuspid valves were evaluated routinely for insufficiency. If any residual shunt, new aortic insufficiency, or more than mild tricuspid regurgitation were identified, the patient would be converted to conventional repair with CPB. If none of the above was found, the device was released by rotating the cable anticlockwise. The cable and the sheath were pulled out and the purse-string suture was tied. The pericardium was closed and a chest tube was placed in the mediastinum. The rest of the wound closure was routine. Broad spectrum second-generation cephalosporin was given intravenously for 3 days, and all the patients were put on aspirin daily (3 mg/kg) for 6 months.

Follow-Up
A TTE and an electrocardiogram were routinely performed on all the patients at discharge and at 6 months follow-up as part of the study protocol. All the TTEs were done and interpreted by the same echocardiographer with specific attention to any new aortic or tricuspid valve regurgitation and residual shunt. Arrhythmia (if any) would be recorded. The end-diastolic diameter of the LV was measured only at discharge.

Statistics
Data are expressed as mean ± SD. Paired data of the end-diastolic diameter of the LV were analyzed using a 2-tailed paired t test. Values for p less than 0.05 were considered significant. Statistical significance was tested using SPSS 13.0 (SPSS Inc, Chicago, IL).


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Comment
 Acknowledgments
 References
 
The procedure was successful in 27 (90%) patients. There was no perioperative mortality or any late death during the entire follow-up period. There was no incidence of device embolization or atrioventricular block (AVB). In one case, the patient had an 8.5-mm PVSD, with its upper edge being 1.5-mm away from the aortic valve. We tried to close the defect with a 10-mm eccentric device (0.5 mm) first, but a moderate aortic regurgitation occurred. We then changed the device to another eccentric one, which was 10 mm in size but had no edge on the aortic side (0 mm). The aortic incompetence disappeared after deployment of the second device but a residual shunt was identified. In two other cases the PVSDs measured 7 mm and 8 mm in size. We decided to close them with 9-mm and 10-mm eccentric devices (0 mm), respectively, and aortic regurgitations occurred in both cases. We elected to convert all three cases to conventional open repair with CPB.

In the 27 successful cases, two PVSDs, whose upper edges were 1-mm and 1.5-mm away from the aortic valves, respectively, were both successfully closed by 0.5-mm eccentric devices. Both subarterial VSDs and a PVSD were successfully closed by 0-mm eccentric devices. The rest of the PVSDs were all closed by concentric devices. The mean size of the devices was 7.7 ± 1.8 mm (range, 4 to 12 mm). None of the eight preexisting tricuspid regurgitations worsened after the closures; in fact, two of them diminished from mild to trace immediately after the closures of the PVSDs. On the other hand, 7 patients with PVSDs developed new trace or mild tricuspid regurgitations, and 3 patients developed incomplete right bundle branch blocks (IRBBB) after the procedures in the operating room (OR).

At discharge, no new valvular problems or arrhythmia were observed; in fact, two of the seven closure-related tricuspid regurgitations (trace) and one IRBBB were found to have disappeared. No aortic incompetence was found. The mean end-diastolic diameter of the LV of 27 patients was 28.7 ± 2.6 mm (range, 25 to 35 mm), which was significantly smaller than that before the procedure (p < 0.05). Follow-up at 6 months with TTE revealed that another closure-related and two preexisting tricuspid regurgitations diminished in magnitude (from mild to trace). The two closure-related IRBBB remained and no aortic incompetence was observed. No AVB or residual shunt was found during the entire follow-up period.

Except for a one-year-old boy, who was mechanically ventilated for 2 hours after the procedure, all the patients were extubated in the OR. No children needed any blood or blood product transfusion at any time. The mean hospital stay was 3.6 ± 0.7 days (range, 3 to 5 days).


   Comment
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
Acknowledgments
 References
 
Transcatheter closure of VSDs has been proven to be efficacious, and it was preferred because of its minimally invasive nature [5, 6]. However, this technique has significant complications when used in young children, because the patients' vessels are relatively small compared to the large size of the sheath, resulting in trauma to vessels with subsequent compromised circulation. In addition, the prolonged exposure to radiation required by this procedure carries long-term undesirable and potentially detrimental side effects. All these limitations realistically prevent the application of this minimally invasive technique in younger children. Perventricular closure of VSDs was reported in 1998 [12], and it appeared that the age and size of patients were not limiting factors for this technique. The youngest patients in our series were a one-year-old who weighed 8.5 kg, and another 14-month-old baby who weighed 10 kg with an 11-mm PVSD. Both patients underwent PVDC successfully and eventfully. These 2 patients would have presented significant challenges in the catheterization laboratory. Another distinct advantage of PVDC compared with transcatheter treatment is the fact that the former procedure is entirely guided by TEE, thus avoiding altogether prolonged radiation that might entail deleterious effect to the patients in the long run. Finally, during PVDC, any procedure-related valve insufficiencies can be readily detected and dealt with.

Compared with the conventional VSD repair, the unequivocal advantage of PVDC lies in the avoidance of CPB. The deleterious effects of CPB in pediatric patients, especially on brain development, have been well-documented [13, 14]. A more recent study [15] also showed that avoiding CPB in children might decrease postoperative morbidity and mortality. In addition, the PVDC requires a much shorter operating time and hospital stay. It also markedly reduces, if not eliminates altogether, the need for blood and blood product transfusion. In our series, we performed the PVDC through a subxiphoid minimally invasive incision, which allows the direct extension of the same incision to a full sternotomy in the event that conversion to CPB is needed.

Unlike muscular VSDs, the perimembranous and subarterial VSDs lie much closer to the conductive tissues and aortic valve; therefore, AVB and aortic incompetence are potential complications for PVDC. Similar to the results reported previously [9–11], there was no AVB in our series. This compares favorably with the reported incidence of complete AVB after transcatheter device closure of VSDs [6]. This might be due to the fact that during PVDC the sheath carrying the device approaches the plane of the defect at a more or less perpendicular angle; thus minimizing if not avoiding compression with subsequent trauma to the tricuspid annulus, where the atrioventricular node is located. Transcatheter device closure, on the other hand, necessitates the passage of the cable with the device through the tricuspid annulus to reach the defect; thus potential damage to the atrioventricular node. Three patients in our series developed IRBBB after PVDC. One possible reason might be the edema of the adjacent tissues caused by the friction between the tissue and the device. This may explain why one IRBBB disappeared at discharge without any treatment when the tissue edema may have subsided. The possible injury of the conductive tissues located at the inferoposterior aspect of the defect caused by the guidewire or the device itself might also be another reason. However, the incidence of arrhythmia in our series compared favorably with that reported by transcatheter treatment [16].

Amin and colleagues [10] concluded in their experiment that an eccentric device might have better success rate than a concentric device. In our study, however, all the concentric devices (22 of 22) completed the closures without any aortic insufficiency, whereas only five out of eight eccentric devices were deployed successfully. The concentric devices were used for all VSDs whose upper edges were more than 2 mm from the aortic valve. When the distance was between 1 and 2 mm, an eccentric device with a 0.5-mm flange on the aortic side was used, and a device without an edge (0 mm) on that side would be used if the distance was less than 1 mm. The success rates of these three different devices were 100%, 67%, and 60%, respectively. We feel strongly that the choice of the device used should be based on the distance between the upper edge of the defect and the aortic valve. The only residual shunt after deployment of an eccentric device occurred in a 0-mm device with which we attempted to close a relatively large defect (8.5 mm). We failed to close another two defects because of aortic insufficiencies; even eccentric devices (0 mm) were deployed. We speculate that there might be mild aortic prolapses that were not detected by the preprocedural TEE, and the regurgitations might be caused by the devices compressing on the already prolapsed aortic valve leaflets making them more incompetent. This would suggest that PVSDs or subarterial VSDs associated with even mild aortic prolapse should not be considered for PVDC. Otherwise, clinically significant aortic regurgitation might occur.

The occurrence of seven new tricuspid regurgitations after the closures of PVSDs did not seem to have any relationship with the presence or absence of septal aneurysms because only two out of the seven patients who developed new tricuspid regurgitations had septal aneurysms. Rather, the new tricuspid regurgitations might very well be caused by the newly deployed device, which might have distorted the subvalvular apparatus. Two preexisting tricuspid regurgitations diminished from mild to trace in the OR after PVDC. The possible explanation for this occurrence is that part of the regurgitant stream coming from the LV was immediately stopped after deployment of the device. At 6-month follow-up, one procedure-related and two preexisting tricuspid regurgitations further diminished in magnitude. This is most likely due to the fact that with successful PVDC the RV is no longer subjected to chronic volume overload. As the RV volume decreases with time, as documented by our follow-up TTE, so does the diameter of the dilated tricuspid annulus, rendering the tricuspid valve more competent.

In summary, the PVDC of isolated VSDs without CPB appeared to be safe and efficacious in a select group of young children, with acceptable short-term outcomes. However, further studies and long-term follow-up are necessary to evaluate the natural course of the closure-related tricuspid regurgitations and the long-term effect of the device on the left ventricular outflow tract and the aortic valve before PVDC can be recommended as an acceptable alternative to the treatment of isolated VSDs.


   Acknowledgments
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
References
 
This work was supported in part by a grant (2006BAI01A08) from The Ministry of Science and Technology of The People's Republic of China.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 

  1. Mitchell SC, Korones SB, Berendes HW. Congenital heart disease in 56,109 births Circulation 1971;43:323-332.[Abstract/Free Full Text]
  2. Kirklin JW, Barrat-Boyes BG. Ventricular septal defectsIn: Kirklin JW, Barrat-Boyes BG, editors. Cardiac Surgery. 3rd ed.. New York, NY: Churchill Livingstone; 1993. pp. 948-950.
  3. Rose EA. Off-pump coronary artery bypass surgery N Engl J Med 2003;348:379-380.[Free Full Text]
  4. Rigby ML, Redington AN. Primary transcatheter umbrella closure of perimembranous ventricular septal defect Br Heart J 1994;72:368-371.[Abstract/Free Full Text]
  5. Thanopoulos BD, Tsaousis GS, Karanasios E, Eleftherakis NG, Paphitis C. Transcatheter closure of perimembranous ventricular septal defects with the Amplatzer asymmetric ventricular septal defect occluder: preliminary experience in children Heart 2003;89:918-922.[Abstract/Free Full Text]
  6. Butera G, Carminati M, Chessa M, et al. Transcatheter closure of perimembranous ventricular septal defects: early and long-term results J Am Coll Cardiol 2007;50:1189-1195.[Abstract/Free Full Text]
  7. Bacha EA, Cao QL, Starr JP, Waight D, Ebeid MR, Hijazi ZM. Perventricular device closure of muscular ventricular septal defects on the beating heart: technique and results J Thorac Cardiovasc Surg 2003;126:1718-1723.[Abstract/Free Full Text]
  8. Diab KA, Hijazi ZM, Cao QL, Bacha EA. A truly hybrid approach to perventricular closure of multiple muscular ventricular septal defects J Thorac Cardiovasc Surg 2005;130:892-893.[Free Full Text]
  9. Amin Z, Gu X, Berry JM, Titus JL, Gidding SS, Rocchini AP. Periventricular closure of ventricular septal defects without cardiopulmonary bypass Ann Thorac Surg 1999;68:149-154.[Abstract/Free Full Text]
  10. Amin Z, Danford DA, Lof J, Duncan KF, Froemming S. Intraoperative device closure of perimembranous ventricular septal defects without cardiopulmonary bypass: preliminary results with the perventricular technique J Thorac Cardiovasc Surg 2004;127:234-241.[Abstract/Free Full Text]
  11. Zeng XJ, Sun SQ, Chen XF, et al. Device closure of perimembranous ventricular septal defects with a minimally invasive technique in 12 patients Ann Thorac Surg 2008;85:192-194.[Abstract/Free Full Text]
  12. Amin Z, Berry JM, Foker JE, Rocchini AP, Bass JL. Intraoperative closure of muscular ventricular septal defect in a canine model and application of the technique in a baby J Thorac Cardiovasc Surg 1998;115:1374-1376.[Free Full Text]
  13. Kern FH, Hickey PR. The effects of cardiopulmonary bypass on the brainIn: Jonas RA, editor. Cardiopulmonary bypass in neonates, infants and young children. 1st ed.. Boston: Blackwell Science; 1994. pp. 263-278.
  14. Visconti KJ, Bichell DP, Jonas RA, Newburger JW, Bellinger DC. Developmental outcome after surgical versus interventional closure of secundum atrial septal defect in children Circulation 1999;100(suppl 19):II145-II150.[Medline]
  15. Stocker CF, Shekerdemian LS. Recent developments in the perioperative management of the paediatric cardiac patient Curr Opin Anaesthesiol 2006;19:375-381.[Medline]
  16. Xunmin C, Shisen J, Jianbin G, Haidong W, Lijun W. Comparison of results and complications of surgical and Amplatzer device closure of perimembranous ventricular septal defects Int J Cardiol 2007;120:28-31.[Medline]

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