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European Heart Journal Advance Access originally published online on October 19, 2006
European Heart Journal 2006 27(23):2889-2895; doi:10.1093/eurheartj/ehl340
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© The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Percutaneous closure of ventricular septal defects in children aged <12: early and mid-term results

Gianfranco Butera*, Mario Carminati, Massimo Chessa, Luciane Piazza, Raul Abella, Diana Gabriella Negura, Alessandro Giamberti, Bussadori Claudio, Angelo Micheletti, Youssef Tammam and Alessandro Frigiola

Department of Pediatric Cardiology and Cardiac Surgery, Istituto Policlinico San Donato, Via Morandi, 30, 20097 San Donato Milanese, Italy

Received 30 January 2006; revised 19 September 2006; accepted 5 October 2006; online publish-ahead-of-print 19 October 2006.

* Corresponding author. Tel: +39 2 52774328; fax: +39 2 52774459. E-mail address: gianfra.but{at}lycos.com


   Abstract
Top
 Abstract
Introduction
 Methods
 Statistical methods
 Results
 Discussion
 Clinical implications
 Study limitations
 Conclusions
 References
 
Aims The aim of the article is to study the safety, efficacy, and follow-up of percutaneous closure of muscular ventricular septal defect (mVSD) and perimembranous ventricular septal defect (pmVSD) in children.

Methods and results Between January 2000 and June 2005, among 140 patients who underwent percutaneous closure of an mVSD or a pmVSD, 88 were aged lt;12. Two different Amplatzer devices were used: the mVSD occluder and the pmVSD occluder. Mean age and weight at procedure were 4.5±3.3 years and 18.7±11.2 kg, respectively. Percutaneous closure was successfully achieved in 83 subjects (94%). No deaths occurred. Thirteen patients (14.7%) had early complications: device embolization (n=4), vascular complications (n=3), and rhythm abnormalities (n=6). These were transient complications in all but one case [1.1% complete atrioventricular block (cAVB) needing pacemaker implantation]. During a median follow-up of 24 months, three subjects treated for a pmVSD needed pacemaker implantation due to the occurrence of cAVB. Multivariable analysis using Cox's proportional hazard regression showed that age was the only risk factor associated with the occurrence of cAVB (P=0.028; relative risk: 0.25).

Conclusion Percutaneous closure of mVSD and pmVSD in children can be performed safely and successfully. The occurrence of cAVB is a major concern in young children with pmVSD.

Key Words: Septal defect • Children • Treatment • Percutaneous


   Introduction
Top
 Abstract
 Introduction
Methods
 Statistical methods
 Results
 Discussion
 Clinical implications
 Study limitations
 Conclusions
 References
 
Surgical closure of a ventricular septal defect (VSD) is now a routine procedure. The morbidity and mortality related to surgical procedures have been reported in the literature.1–8

In the last decade, percutaneous techniques to close cardiac defects have been developed. Closure of atrial septal defects and patent ductus arteriosus using transcatheter devices has been widely reported,9–12 and these techniques can now be used even in very young children.13,14 More recently percutaneous techniques and devices have been developed specifically for closure of muscular VSD (mVSD) and perimembranous VSD (pmVSD). The initial experience in humans appears encouraging,15–18 but there are no data from large series of children with an adequate follow-up.

Here, we report our early and mid-term follow-up results of percutaneous closure of mVSD and pmVSD in 88 subjects aged <12.


   Methods
Top
 Abstract
 Introduction
 Methods
Statistical methods
 Results
 Discussion
 Clinical implications
 Study limitations
 Conclusions
 References
 
Between January 2000 and June 2005, we prospectively collected data on 140 patients who underwent transcatheter closure of a VSD at our institution. Eighty-eight of these 140 subjects were children aged <12 (range 0.5–12 years). Patients were assessed by a standard echocardiographic protocol: all patients underwent transthoracic echocardiography (TTE) that was performed with a Vingmed 800 (Vingmed Sound, Horten, Norway) and a System Five performance ultrasound system (Vingmed Sound) using a transducer appropriate to each patient's size and body weight.

Inclusion and exclusion criteria
The criteria for inclusion in this study were clinical and/or echocardiographic evidence of a significant left-to-right shunt through an mVSD or a pmVSD in patients under 12 years of age.

A left-to-right shunt was considered significant when the following were found: (i) cardiomegaly on chest X-ray; (ii) left atrial enlargement, defined as a left atrial-to-aortic ratio >1.5; (iii) left ventricular enlargement (left ventricular volume overload), defined as a left ventricular end-diastolic diameter >+2 standard deviations (SD) above the mean for the patient's age; (iv) symptoms: frequent respiratory infections and/or failure to thrive. Frequent respiratory infections were defined as more than six events per year.19 Failure to thrive was defined according to Hamil et al.20

We intended that patients should weigh at least 5 kg to be eligible for percutaneous closure of a VSD, although we did treat some subjects weighing <5 kg, who had significant post-operative residual VSD.

We undertook a percutaneous procedure when we could use long sheaths of the following sizes according to weight: 6–8 Fr in subjects weighing from 3.5–6 kg, 7–9 Fr in subjects weighing from 6–8 kg, and 8–10 Fr in subjects weighing>8 kg. This enabled us to close mVSD of up to 8–12 mm in subjects weighing 3.5–6 kg, 12–14 mm in subjects weighing 6–8 kg, and>14 mm in subjects weighing>8 kg, whereas we could close pmVSD of up to 6–8 mm in subjects weighing 3.5–6 kg, 8–10 mm in subjects weighing 6–8 kg, and>12 mm in subjects weighing>8 kg.

A defect was defined too large to be closed percutaneously when a device and a long sheath larger than the one possible for body weight would have been needed.

Only subjects with a rim of at least 1 mm separating the aortic valve from the pmVSD were included. We excluded patients with an infundibular defect, patients with pmVSD and prolapse of an aortic cusp, and patients with mal-aligned VSD.

Parents gave their informed written consent to the procedure.

The general characteristics of the patients are reported in Table 1.


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  		Table 1 General characteristics

 
Devices and delivery systems used
Two different Amplatzer devices (AGA Medical Corp) were used: the mVSD occluder (MVSD-O) and the pmVSD occluder (pmVSD-O).15–18 These devices have a woven mesh of 72 nitinol wires with shape memory. They are made of a 0.004–0.005 in. nitinol wire with a polyester mesh inside. These devices and their delivery systems have been previously described.16

Procedures
Percutaneous closure of a VSD is performed under general anaesthesia with oro-tracheal intubation. Patients are given heparin 100 IU/kg and antibiotics intravenously. The procedure is performed under fluoroscopic and transoesophageal echocardiographic (TEE) control. Access is through the right internal jugular vein and right femoral artery for mid-muscular and apical VSD, whereas right femoral vein and left femoral artery accesses are used for high mVSD and pmVSD.

Standard right and left cardiac catheterization, standard left ventriculography to study mVSD and pmVSD and angiography of the ascending aorta are performed in all cases. The size of the VSD and its relation to the aorta are confirmed. The diameter of the VSD is calculated by integrating data from TEE and angiographic measurements. A device 1–2 mm larger than the measured VSD diameter is chosen.

The VSD is crossed from the left ventricle using a right coronary artery catheter (Cordis Corp., USA) or an Amplatzer right coronary catheter (Cordis Corp., USA), and an exchange floppy Terumo guide-wire (Terumo Corp., Japan) advanced into the pulmonary artery or the superior or inferior vena cava. The wire is then snared (EV3, MN, USA) to establish an arteriovenous circuit.

Procedures for mid-muscular (Figure 1), apical VSD, and high mVSD and pmVSD (Figures 2 and 3) have been previously reported in detail.16


Figure 3401
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  		Figure 1 Percutaneous closure of an mVSDs. Top right: the angiogram demonstrates a single mid-mVSD; top left: a cine angiogram demonstrating snaring of the guide-wire passed from the left ventricle up to the superior vena cava; low right: the long sheath is in the ascending aorta coming from the right ventricle through the VSD; low left: left ventriculography showing almost complete VSD closure.

 

Figure 3402
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  		Figure 2 Percutaneous closure of a pmVSD. Left: the angiogram demonstrates a single pmVSD and left ventricular overload; middle: snaring of the guide-wire passed from the left ventricle in the left pulmonary artery; right: cine image showing the position of the delivery sheath in the apex of the left ventricle.

 

Figure 3403
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  		Figure 3 Percutaneous closure of a pmVSD. Right: left ventricular angiogram after device release, showing good device position and no residual shunt. Note the platinum marker located in the left ventricular disk pointing towards the left ventricular apex; left: an ascending aortic angiogram demonstrating no aortic regurgitation.

 
Early in our experience, we closed some cases of high mVSD with a >5 mm rim towards the aortic valve using a retrograde aortic approach and an mVSD-O. In these cases, the VSD is crossed from the left ventricle and the wire is placed in the apex of the right ventricle. The long sheath is advanced from the aorta through the VSD into the right ventricular apex. The device is advanced in the long sheath, and then the distal disc is opened in the right ventricle and withdrawn to the septum. The proximal disc is then opened, taking care to avoid any entrapment of the aortic valve with the disc of the device. Finally, the correct position is confirmed and the device is released.

VSD analysis
The diameter of the VSD was measured by TTE and TEE, using two-dimensional imaging and colour flow Doppler on long- and short-axis views. The vertical diameter was measured during left ventricular angiography using the views described earlier.

The locations of the VSD are reported in Table 1. A ventricular septal aneurysm was present in 25 patients (28%). All subjects with an aneurysm had a pmVSD. Associated lesions were encountered in five subjects. Multiple defects were found in three patients.

Residual shunt and valve regurgitation
A residual shunt was considered to be present when colour Doppler flow mapping showed a left-to-right shunt across the interventricular septum. A shunt was defined trivial (<1 mm colour jet width), small (1–2 mm colour jet width), moderate (2–4 mm colour jet width), or large (>4 mm colour jet width). Valve regurgitation was evaluated by colour Doppler flow imaging in a standard way.

Ten subjects had trivial aortic regurgitation. Seven out of 10 patients had a pmVSD. Twenty patients had trivial to mild tricuspid regurgitation. Finally, eight subjects had trivial to mild mitral regurgitation related to mitral annulus dilatation due to volume overload of the left ventricle.

Follow-up
All subjects underwent clinical examination, electrocardiography, chest X-rays, 24 h EKG-Holter monitoring, and TTE before discharge and at 1, 6, and 12 months after the procedure and yearly thereafter. Before discharge, urinalysis was performed to exclude haemolysis. Platelet anti-aggregation therapy with aspirin 5 mg/kg per day p.o. and endocarditis prophylaxis were prescribed for 6 months.


   Statistical methods
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 Abstract
 Introduction
 Methods
 Statistical methods
Results
 Discussion
 Clinical implications
 Study limitations
 Conclusions
 References
 
Data are expressed as a frequency or percentage for nominal variables, as the median (range) for categorical variables and as the mean±SD for continuous variables. The STATISTIX package version 8 was used for the statistical computations.

The following dependent outcome variables were analyzed: total complications, complete atrioventricular block (cAVB), device embolization, and vascular complications. The following independent variables were included in the analysis: age, weight, gender, defect type (congenital, residual post-surgery), defect position (perimembranous, muscular), device type (muscular Amplatzer device, eccentric Amplatzer device), device diameter, complex procedures (yes/no), multiple defects (yes/no), ventricular septal aneurysm (yes/no), device diameter/defect diameter measured on TTE, and device diameter/patient weight.

Univariate analysis was performed using the {chi}2 test, Fisher's exact test, unpaired Student's t-test, Wilcoxon rank sum test, one-way ANOVA, the Kruskall–Wallis test, log-rank test, and Cox regression analysis, as appropriate.

Multivariable analysis to study risk factors for the occurrence of early complications was performed using multiple logistic regression analysis. The regression model diagnostic was performed by obtaining the standardized residuals and Cook's D-values and examining them using Wilk–Shapiro and rankit plot tests. Independent variables with a P-value <0.2 in the univariate analysis were included in the multivariable model. Odds ratios (OR) and their 95% confidence intervals were calculated for independent variables included in the multivariable model.

Multivariable analysis using Cox's proportional hazard regression analysis was performed to study the role of independent variables on the occurrence of cAVB in the early period and during the follow-up. Evaluation of proportional hazards assumption was performed by using the goodness of fit testing approach.

All tests were two sided. A probability value of P<0.05 was considered statistically significant.


   Results
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 Abstract
 Introduction
 Methods
 Statistical methods
 Results
Discussion
 Clinical implications
 Study limitations
 Conclusions
 References
 
Procedural data
During the period of the study, all subjects with the inclusion criteria were sent to the catheterization laboratory with the intention to treat the defect percutaneously (Table 2). In 83 of 88 patients, the defect was successfully closed (94%). In four subjects, the procedure was aborted (see section on Complications for details) and one subject was sent for surgery after device embolization (see section on Complications for details).


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  		Table 2 Procedural data and devices used

 
An internal jugular venous approach was used in 23 subjects, whereas a venous femoral access was used in 65.

Complex procedures
Complex procedures (combined procedures, hybrid procedures, closure of multiple VSD, post-surgical residual VSD) were performed in 17 children (19%). Five subjects underwent combined procedures: pulmonary valve dilatation in two subjects, atrial septal defect closure in one, patent ductus arteriosus in one, and atrial septal defect and small patent ductus arteriosus closure in one. Hybrid procedures were performed in three patients. Two subjects underwent VSD closure before surgical debanding of the pulmonary artery and one before repair of aortic coarctation. One of these subjects had multiple defects that were closed using two devices. Two more subjects were treated for multiple VSD. Finally, seven patients underwent percutaneous closure of a post-surgical residual VSD. Two of these were treated in an ‘acute setting’ since they could not be weaned from mechanical support. Five more subjects were treated electively. These patients had undergone surgery, a median of 1.5 years (range: 7 months–4.5 years), before the percutaneous procedure.

Complications
Early post-procedural complications
No deaths occurred. In five subjects, the procedure was aborted. In two patients (two 8-year-old girls with mal-aligned pmVSD), it was impossible to obtain a stable position of the device, which was retrieved before unscrewing it. One 6-month-old girl was sent for surgery after device embolization to the pulmonary artery; this baby had previously undergone an operation to correct aortic coarctation. These subjects were treated very early in our experience and it is possible that there was an error in their selection or a lack in operator's experience. In two patients with pmVSD (a 3.5-year-old female and a 6-year-old boy), cAVB developed during manoeuvres of the catheter or Terumo guide-wire. The procedure was stopped in both subjects, and they both recovered sinus rhythm within 1–2 h.

A total of 13 significant complications occurred (14.7%). These were device embolization (n=4), vascular complications (n=3), and rhythm abnormalities (n=6). However, in all but one child (1.1%) who needed pacemaker implantation, these were transient complications and the patients had no sequelae.

Univariate analysis showed that no variable predicted the occurrence of early complications. Only two variables showed a trend towards significance (device diameter/patient weight: no complication 0.52±0.35 vs. complication 0.71±0.37; P=0.06; device measure: no complication 8.4±2.3 mm vs. complication 9.2±2.2; P=0.09). In the multivariable model, defect position (P=0.15) was also included. However, no risk factors were found.

Device embolization
This complication occurred in four patients (4.5%). In one already described case with a large mVSD, the patient was sent to surgery. In three other cases, the device was recaptured in the right pulmonary artery (two cases) or in the descending aorta (one case) using a goose-neck snare and a Mullins long sheath. In these cases, a larger device was chosen and successfully implanted. The occurrence of device embolization was not related to any of the independent variables studied.

Vascular complications
Femoral arterial thrombosis occurred in three patients (3.4%). In a 4-year-old girl (18 kg), vascular surgery of the femoral artery was needed for safe removal of a 10 Fr arterial sheath used to recapture an 8 mm PMVSD-O device that had embolized in the descending aorta. In two 1-year-old girls (7.5 and 7 kg), thrombolysis with r-tPA was successful. The occurrence of vascular complications was not related to any of the independent variables studied.

Arrhythmic complications
Significant arrhythmias occurred in six patients with a pmVSD (6.8%). cAVB occurred during the procedure in two subjects in whom the procedure was aborted (described in the section on Early post-procedural complications). cAVB occurred soon after device release in two subjects with a pmVSD. In one child (a 2-year-old boy, 10 mm PMVSD-O), it was a transient event, whereas in the second (a 3.4-year-old girl), it persisted for some hours after implantation of a 10 mm PMVSD-O. The girl was sent for surgery and recovered stable sinus rhythm after surgical closure and device removal. cAVB developed 24 h after implantation of a 12 mm PMVSD-O in a 2-year-old boy. A permanent pacemaker was implanted into this child who has recovered stable sinus rhythm during follow-up. Finally, a 3.4-year-old boy treated with an 8 mm PMVSD-O developed cAVB 5 days after the procedure. He had a heart rate of 50 b.p.m. and was asymptomatic. We decided to treat him with corticoid therapy (1 mg/kg) for 2 weeks. The cAVB disappeared completely, and he is still in stable sinus rhythm 8 months after the procedure.

Transient minor complications
Transient atrial fibrillation occurred in one 5-year-old boy: no treatment was needed. A transient right bundle branch block occurred in three subjects, whereas a transient left bundle branch block occurred in two other patients. Three subjects developed moderate groin haematoma. Transient, mild haemolysis was recorded in two subjects, but resolved spontaneously within 48 h after the procedure.

Valve regurgitation and residual shunts
Pre-operative aortic, tricuspid or mitral valve regurgitation remained unchanged after the procedure. No significant new regurgitation of valves occurred. A trivial intraprosthetic residual shunt was present in 28 subjects (33%) at the end of the procedure. At discharge, 12 patients (14%) showed a tiny residual shunt and none had signs of haemolysis. TTE at 1, 6 and 12 months showed a trivial residual shunt in one patient (1.2%) due to a small fenestration within the aneurysm.

Hospital stay
All subjects in whom the percutaneous procedure was uneventful stayed in hospital for 2 days after the procedure. In cases with minor arrhythmic abnormalities, even transient bundle branch blocks, the hospital stay was prolonged to 72 h. The mean hospital stay was 4.2±1.2 days.

Follow-up
Follow-up data were obtained from all patients. The median duration of follow-up was 24 months (range 3–66 months). No deaths or cases of endocarditis occurred. Patients with failure to thrive had complete recovery of growth (from the 10th percentile up to the 50th percentile during the follow-up). Subjects with frequent respiratory infections had no significant recurrences. Left ventricular dimensions returned to normal in all subjects but one.

During the entire follow-up period, three subjects developed cAVB. Two of these three experienced syncope (a 4-year-old boy and a 1.2-year-old girl both treated with an 8 mm PMVSD-O) due to paroxysmal cAVB, 4 and 20 months after procedure, respectively. Another patient (a 2.7-year-old boy treated with a 12 mm PMVSD-O) developed asymptomatic cAVB with a heart rate of 40 b.p.m. 12 months after defect closure. An endocardial ventricular pacemaker was implanted into all these subjects.

Analysis of risk factors for the occurrence of cAVB
A total of nine patients experienced cAVB during the period of the study. All of them had a pmVSD. This rhythm abnormality occurred early in six patients, whereas in three it was a late event. Pacemaker implantation was needed in 17% of the cases of early cAVB (1/6) and in 100% of the cases of late cAVB (3/3).

Univariate analysis showed that the following variables were significantly associated with the occurrence of cAVB: VSD location (pmVSD: 9/56 vs. mVSD: 0/32; P=0.02) and age (Cox regression analysis: P=0.033; relative risk: 0.62).

In patients with pmVSD, the occurrence of cAVB was not associated with either the ratio of the device measure to VSD diameter measured on TTE (Cox regression analysis: P=0.9) or the presence of aneurysm of the ventricular septum (Log-rank test: P=0.9).

In multivariable analysis, other than age, patient's weight was included. However, only age was statistically correlated to the occurrence of cAVB during follow-up (P=0.028; relative risk: 0.25). The site of the VSD was not entered into this model because cAVB did not occur in any patients with an mVSD.


   Discussion
Top
 Abstract
 Introduction
 Methods
 Statistical methods
 Results
 Discussion
Clinical implications
 Study limitations
 Conclusions
 References
 
VSDs account for ~20% of all forms of congenital hearts defects.21 The majority of VSD (~60%) is perimembranous or membranous. mVSDs account for ~15% of VSD.

Children with volume overload of the left chamber due to a VSD require closure of the defect in order to prevent ventricular dilatation and dysfunction, arrhythmias, aortic regurgitation, pulmonary arterial hypertension, endocarditis, or a double-chambered right ventricle.22

Surgery is the gold standard for VSD closure, and there is a large body of data about surgical VSD closure in children. Although this is generally a safe procedure, it does have some potential risks, including cAVB in 1–5%,1,2,6,8 significant residual VSD in 1–10%,1,3–5 the necessity for re-operation in 2%,1 and even death in 0.6–5%.1,4–7 Furthermore, infections, tachy-arrhythmias, and neurological complications may occur.1

In the last decade, percutaneous approaches to the closure of VSD have been developed.23–24 However, only the recent introduction of Amplatzer mVSD-O and pmVSD-O has increased the number of subjects in whom percutaneous closure is feasible.15–17 Although there are various reports about percutaneous closure of VSD,15–18 there is a lack of data on the safety, feasibility, and efficacy of percutaneous VSD closure in children. Literature data about percutaneous VSD closure are reported in Table 3.22–31


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  		Table 3 Literature on percutaneous VSD closure

 
In our series of 88 children, the percutaneous procedure was achieved successfully in 94%. Early complications occurred in 13 subjects (14.7%). However, in all but one case (1.1%), the complications were transient and the patients had no sequelae. Multivariable analysis showed that no variable predicted the occurrence of early complications. There were no serious complications related to the closure of mVSDs either early or late after the procedure.

The only serious concern of percutaneous VSD closure is the occurrence of cAVB. This complication required pacemaker implantation in four subjects (4.5%) with pmVSD in our series. The cAVB rates reported in the literature are very low, but it should be noted that only early post-procedural results have been published. In our series, the median follow-up was 24 months and cAVB was a late event in three out of the four subjects requiring pacemaker implantation. In multivariable analysis, the only variable associated with the occurrence of cAVB was age at procedure. In particular, the relative risk was 0.25, showing that younger subjects were at higher risk for the occurrence of cAVB.

Although, some authors have underlined that an over-sized device is a risk factor for the occurrence of cAVB, in particular, in subjects with pmVSD, this was not confirmed by our data. Finally, some authors32 have suggested that a course of steroids should be used in an effort to avoid pacemaker implantation. We used this approach successfully in one subject. However, although this therapy may be useful in an acute setting, we believe it is unlikely to be useful for late events occurring during the follow-up.

It should be appreciated that cAVB block can also occur after surgical closure of a VSD; indeed, this complication develops in about 1–5% of subjects so treated.1,2,6,8 However, compared with surgery in which cAVB usually appears early after the operation, in patients treated percutaneously, the occurrence of cAVB is quite unpredictable and it is usually a late problem. This complication is related to the proximity of the conduction system to the margins of the pmVSD. Therefore, both surgery and device implantation may interfere with atrioventricular conduction. Various mechanisms may be considered as causative. It is possible that the presence of the device may disturb atrioventricular conduction by direct traumatic compression. Furthermore, the device may give rise to an inflammatory reaction or scar formation in the conduction tissue. However, there are no direct data about the mechanisms involved in the occurrence of cAVB after percutaneous closure of a pmVSD. Large studies are needed to clarify the real impact of arrhythmic problems in these patients and the mechanism of the events.


   Clinical implications
Top
 Abstract
 Introduction
 Methods
 Statistical methods
 Results
 Discussion
 Clinical implications
Study limitations
 Conclusions
 References
 
The percutaneous technique of VSD closure is widely appreciated by patients and their parents because it has less psychological impact (given the absence of a skin scar), the time spent in hospital is shorter, the procedure causes less pain and discomfort, and there is no need for admission to an intensive care unit. In the current era, percutaneous VSD closure provides a valuable alternative to surgery even in cases with complex morphology and in very young children.

However, the decision to perform percutaneous closure of pmVSD in young subjects must be carefully weighed, given the challenging nature of this technique and the risk of cAVB. Finally, due to the late occurrence of cAVB, careful monitoring of rhythm and atrioventricular conduction is mandatory during the follow-up.


   Study limitations
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 Abstract
 Introduction
 Methods
 Statistical methods
 Results
 Discussion
 Clinical implications
 Study limitations
Conclusions
 References
 
First of all, only in very experienced hands can these techniques be carried out safely and complications managed in the proper way. Furthermore, highly specialized surgical back-up must always be available. Secondly, although the techniques of percutaneous closure appear to be safe in the medium-term follow-up, it is not known whether they are safe in the very long-term, whereas the long-term safety and efficacy of surgery are well documented.


   Conclusions
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 Abstract
 Introduction
 Methods
 Statistical methods
 Results
 Discussion
 Clinical implications
 Study limitations
 Conclusions
References
 
The percutaneous technique of closing VSD in children, even very young and symptomatic ones, is associated with excellent success and closure rates, no mortality, and low morbidity. In current day practice, percutaneous closure of muscular and perimembranous defects is a valuable alternative to surgery. Longer follow-up data and improvements in device characteristics are needed to reduce the risk of cAVB.

Conflict of interest: none declared.


   References
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 Abstract
 Introduction
 Methods
 Statistical methods
 Results
 Discussion
 Clinical implications
 Study limitations
 Conclusions
 References
 

  1. Mavroudis C, Backer CL, Jacobs JP. (2003) Ventricular septal defect. Pediatric Cardiac Surgery 3 rd Mosby, Inc pp. 298–320.
  2. Ross-Hesselink JW, Mejiboom FJ, Spitaels SEC, Van Domberg R, Van Rijen EH, Utens EM, Bogers AJ, Simons ML. (2004) Outcome of patients after surgical closure of ventricular septal defect at young age: longitudinal follow-up of 22–34 years. Eur Heart J 24:1057–1062.
  3. Kitagawa T, Durham LA, Mosca RS, Bove EL. (1998) Techniques and results in the management of multiple ventricular septal defects. J Thorac Cardiovasc Surg 115:848–856.[Abstract/Free Full Text]
  4. Wollenek G, Wyse R, Sullivan I, Elliot M, de Leval M, Stark J. (1996) Closure of muscular ventricular septal defects through a left ventriculotomy. Eur J Cardiothorac Surg 10:595–598.[Abstract]
  5. Serraf A, Lacour-Gayet F, Bruniaux J, Ouaknine R, Losay J, Petit J, Binet JP, Planche C. (1992) Surgical management of isolated multiple ventricular septal defects: logical approach in 130 cases. J Thorac Cardiovasc Surg 103:347–342.[Abstract]
  6. Hobbins SM, Izukawa T, Radford DJ, Williams WG, Trusler GA. (1979) Conduction disturbances after surgical correction of ventricular septal defect by the atrial approach. Br Heart J 41:289–293.[Abstract/Free Full Text]
  7. Backer CL, Winters RC, Zales VR, Takami H, Muster AJ, Benson DW, Mavroudis C. (1993) The restrictive muscular ventricular septal defect: how small is too small to close? Ann Thorac Surg 56:1014.[Abstract]
  8. Bol-Raap G, Weerheim J, Kappetein AP, Witsenburg M, Bogers AJ. (2003) Follow-up after surgical closure of congenital ventricular septal defects. Eur J Cardiothorac Surg 24:511–515.[Abstract/Free Full Text]
  9. Chessa M, Carminati M, Butera G, Bini RM, Drago M, Rosti L, Giamberti A, Pomè G, Bossone E, Carminati M. (2002) Early and late complications associated with transcatheter occlusion of secundum atrial septal defect. JACC 39:1061–1065.[Abstract/Free Full Text]
  10. Du Zhong-Dong, Hijazi Z, Kleinman CS, Silverman NH, Lamtz K. for the Amplatzer Investigators. (2002) Comparison between transcatheter and surgical closure of secundum atrial septal defect in children and adults. JACC 39:1836–1844.[Abstract/Free Full Text]
  11. Faella HJ and Hijazi Z. (2000) Closure of the patent ductus arteriosus with the Amplatzer PDA device: immediate results of the international clinical trial. Cathet Cardiovasc Intervent 51:50–54.[CrossRef][ISI][Medline]
  12. Pass RH, Hijazi Z, Hsu DT, Lewis V, Hellenbrand WE. (2004) Multicenter USA Amplatzer patent ductus arteriosus occlusion device trial. JACC 44:513–519.[Abstract/Free Full Text]
  13. Butera G, De Rosa G, Chessa M, Rosti L, Negura G, Piazza L, Giamberti A, Bossone E, Carminati M. (2003) Transcatheter closure of atrial septal defect in young children. Results follow-up JACC 42:241–245.
  14. Butera G, De Rosa G, Chessa M, Piazza L, Delogu A, Frigiola A, Carminati M. (2004) Transcatheter closure of persistent ductus arteriosus with the Amplatzer duct occluder in very young symptomatic children. Heart 90:1467–1470.[Abstract/Free Full Text]
  15. Bass JL, Kalra GS, Arora R, Masura J, Gavora P, Thanoupoulos B, Torres W, Sievert H, Carminati M, Fisher G, Ewert P. (2003) Initial human experience with the Amplatzer perimembranous ventricular septal occluder device. Cathet Cardiovasc Intervent 58:238–245.[CrossRef][ISI][Medline]
  16. Hijazi Z. (2003) Device closure of ventricular septal defects. Cathet Cardiovasc Intervent 60:107–114.[CrossRef][ISI][Medline]
  17. Holzer R, Balzer D, Qi-Ling C, Lock K, Hijazi Z. for the Amplatzer Muscular Ventricular Septal Defect Investigators. (2004) Device closure of muscular ventricular septal defects using the Amplatzer muscular ventricular septal defect occluder. JACC 43:1257–1263.[Abstract/Free Full Text]
  18. Chessa M, Carminati M, Cao QL, Butera G, Giusti S, Bini RM, Hijazi Z. (2002) Transcatheter closure of congenital and acquired ventricular septal defects using the Amplatzer occluder. J Invasive Cardiol 14:322–327.[Medline]
  19. Burgio GR. (1998) Il bambino con infezioni ricorrenti. In Plebani A (Ed.). Immunologia PediatricaMc Graw Hill Libri Italia Milano pp. 17.
  20. Hamil PV, Drizd TA, Johnson CL, Reed RB, Roche AF, Moore WM. (1979) Physical growth: National Center for Health Statistics percentiles. Am J Clin Nutr 32:607–629.[Abstract/Free Full Text]
  21. Rudolph AM. (2002) Ventricular septal defect. In Rudolph AM (Ed.). Congenital Diseases of the Heart: Clinical-Physiological Considerations 2nd ed. (Futura Publishing Company, Armonk, NY) pp. 197–244.
  22. Kidd L, Discroll DJ, Gersony WH, Hayes CJ, Keane JF, O'Follon WM, Pieroni DR, Wolfe RR, Weidman WH. (1993) Second natural history study of congenital heart defects: results of treatment of patients with ventricular septal defects. Circulation 87:Suppl. I, 138–151.
  23. Lock JE, Block PC, McKay RG, Baim DS, Keane JF. (1988) Transcatheter closure of ventricular septal defects. Circulation 78:361–368.
  24. Kalra GS, Verma PK, Dhall A, Singh S, Arora R. (1999) Transcatheter device closure of ventricular septal defects: immediate results and intermediate-term follow-up. Am Heart J 138:339–344.[CrossRef][ISI][Medline]
  25. Hijazi Z, Hakim F, Haweleh AA, Madani A, Tarawna H, Hiari A, Cao QL. (2002) Catheter closure of perimembranous ventricular septal defects using the new Amplatzer membranous VSD occluder: initial clinical experience. Cathet Cardiovasc Interv 56:508–515.[CrossRef][ISI][Medline]
  26. Thanopoulos BD, Tsaousis GS, Karanasios E, Eleftherakis NG, Paphitis C. (2003) Transcatheter closure of perimembranous ventricular septal defects with the Amplatzer asymmetric ventricular septal defect occluder: preliminary experience in children. Heart 89:918–922.[Abstract/Free Full Text]
  27. Thanopoulos BD, Tsaousis GS, Konstadopoulou GN, Zarayelyan AG. (1999) Transcatheter closure of muscular ventricular septal defects with the Amplatzer ventricular septal defect occluder: preliminary experience in children. J Am Coll Cardiol 33:1395–1399.[Abstract/Free Full Text]
  28. Arora R, Trehna V, Kumar A, Kalra GS, Nigam M. (2003) Transcatheter closure of congenital ventricular septal defects: experience with various devices. J Interv Cardiol 16:83–91.[CrossRef][Medline]
  29. Masura J, Gao W, Gavora P, Sun K, Zhan AO, Jiang S, Tiang-Liang C, Wang Y. (2005) Percutaneous closure of perimembranous ventricular septal defects with the eccentric Amplatzer device: multicenter follow-up study. Pediatr Cardiol 26:216–219.[CrossRef][ISI][Medline]
  30. Hijazi ZM, Hakim F, Al Fadley F, Abdelhamid J, Cao QL. (2000) Transcatheter closure of single muscular ventricular septal defects using the Amplatzer muscular VSD occluder: initial results and technical considerations. Cathet Cardiovasc Interv 49:167–172.[CrossRef][ISI][Medline]
  31. Pedra AC, Pedra SRF, Esteves CA, Pontes SC, Braga SL, Arrieta SR, Santana MV, Fontes VF, Masura J. (2004) Percutaneous closure of perimembranous ventricular septal defects with the Amplatzer device: technical and morphological considerations. Cathet Cardiovasc Interv 61:403–410.[CrossRef][ISI][Medline]
  32. Yip WC and Zimmermann F Hijazi ZM. (2005) Heart block and empirical therapy after transcatheter closure of perimembranous ventricular septal defect. Catheter Cardiovasc Interv 66:436–441.[CrossRef][ISI][Medline]

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