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European Heart Journal Advance Access published online on November 25, 2008
European Heart Journal, doi:10.1093/eurheartj/ehn524
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Immediate primary transcatheter closure of postinfarction ventricular septal defects

Holger Thiele1,*, Carl Kaulfersch1, Ingo Daehnert2, Martin Schoenauer3, Ingo Eitel1, Michael Borger4 and Gerhard Schuler1

1 Department of Internal Medicine/Cardiology, University of Leipzig - Heart Center, Strümpellstr. 39, 04289 Leipzig, Germany
2 Department of Pediatric Cardiology, University of Leipzig - Heart Center, Leipzig, Germany
3 University of Leipzig, Internal Medicine, Leipzig, Germany
4 Department of Cardiothoracic Surgery, University of Leipzig - Heart Center, Leipzig, Germany

Received 31 March 2008; revised 10 September 2008; accepted 31 October 2008.

* Corresponding author. Tel: +49 341 865 1426, Fax: +49 341 865 1461, Email: thielh{at}medizin.uni-leipzig.de


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Funding
 References
 
Aims: Immediate surgical repair of ventricular septal defect (VSD) complicating acute myocardial infarction is associated with high mortality. Percutaneous device closure appears to be safe and effective in patients treated for a residual shunt after initial surgical closure, as well as in patients with a chronic post-infarct VSD. Primary transcatheter VSD closure in the acute setting may also offer advantages over surgery.

Methods and results: Between September 2003 and February 2008, 29 consecutive patients underwent primary transcatheter VSD closure. Clinical, procedural, and outcome data were collected. Patients were divided into those with and those without cardiogenic shock at presentation for risk stratification. The median follow-up time of surviving patients was 730 days. The median time between VSD occurrence and closure was 1 day [interquartile range (IQR) 1–3] and the initial procedural success rate was 86%. The shunt (Qp:Qs) could be reduced from 3.3 (IQR 2.3–3.8) to 1.4 (IQR 1.2–1.7; P < 0.001). Procedure-related complications such as major residual shunting, left ventricular rupture, and device embolization occurred in 41%. The overall 30-day survival rate was 35%. Mortality was higher for cardiogenic shock in comparison to non-shock patients (88 vs. 38%, P < 0.001).

Conclusion: Interventional acute VSD closure is a promising technique that can be performed with a high procedural success rate and may offer an alternative to surgery. Despite the less invasive technique, mortality of postinfarction VSD remains high, particularly in patients with cardiogenic shock. Further developments in devices and delivery techniques are required.

Key Words: Acute myocardial infarction • Ventricular septal defect • Interventional closure • Amplatzer occluder • Cardiogenic shock


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Funding
 References
 
Ventricular septal defect (VSD) complicating acute myocardial infarction (AMI) is an infrequent but hazardous event occurring in the first week after the index event.1 In the era of fibrinolytic reperfusion, the incidence of infarct-related VSD is described to be in the range of 0.2–0.34%.1 In the interventional era, however, there is a lack of reports available on the incidence of VSD occurrence. Surgical closure of postinfarction VSD is the treatment of choice for this serious complication since 90% of patients without defect closure will die within 2 months.2 After the first surgical description in 1957,3 mortality rates of surgical closure remain high at 20–87% in current series.4–7 Such high mortality rates are not unexpected given the advanced patient age, comorbidities, severity of coronary artery disease, haemodynamic instability, as well as technical challenges of the surgical procedure.4–7 Current guidelines recommend immediate surgical VSD closure irrespective of the patient's haemodynamic status to avoid further haemodynamic deterioration.8,9 Septal branches are exposed to shear stress and necrotic tissue removal processes early after VSD occurrence, which may result in subsequent abrupt VSD expansion and sudden haemodynamic collapse. However, many surgeons recommend surgical VSD closure after a 3–4 week delay to allow scarring of the surrounding tissue to occur, which allows for firmer anchoring of suture and patch material. Waiting several weeks after an initial VSD diagnosis, however, introduces a selection bias which may result in excessively positive results for some surgical series.10

An interventional approach is a less invasive option and might allow for immediate complete VSD closure or initial haemodynamic stabilization. Immediate reduction of the left-to-right shunt, even if the VSD is not completely closed, may stabilize the patient enough to function as a bridge to surgery.11 Current interventional reports are mainly restricted to VSD closure in the chronic and subacute setting, or for residual shunts after initial surgical closure.12 This prospective study reports the results of primary interventional closure of acute postinfarction VSD.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Funding
 References
 
Between September 2003 and February 2008, 29 consecutive patients with VSD complicating AMI were admitted to the cardiology intensive care unit and underwent percutaneous interventional VSD closure. Inclusion criteria were the presence of a VSD as a result of preceding AMI without prior surgical closure attempt. Device closure was considered for all patients as the preferred treatment option, if technically feasible. Exclusion criteria were determined by echocardiography and consisted of a large VSD (>35 mm), an apical VSD without a suitable rim, and a basal VSD that was situated too close to the mitral, tricuspid and/or aortic valvular apparatus. During the study period, however, no patients were excluded due to the criteria defined above.

For risk assessment, patients were divided into those with and without cardiogenic shock at presentation. Cardiogenic shock was defined as (i) persistent systolic blood pressure <90 mmHg or vasopressors required to maintain blood pressure >90 mmHg; (ii) evidence of end organ failure (e.g. urine output <30 mL/h, cold skin and extremities, serum lactate >2 mmol/L); (iii) evidence of elevated left ventricular filling pressures with clinical signs of pulmonary congestion.13,14

Clinical and haemodynamic data, procedure and device details, as well as assessment and occurrence of complications or death were collected prospectively on all patients. For those patients surviving the hospital course, follow-up was performed by a structured telephone interview to assess the vital status. In addition, the clinical functional status was assessed by the New York Heart Association classification.

Interventional closure procedure
The procedure was performed under fluoroscopic and echocardiographic guidance. All patients received peri-interventional antibiotic prophylaxis with a single dose of Cefazolin (2 g), as well as aspirin (500 mg) and heparin (60 U/kg bodyweight) intravenously. If stenting of coronary arteries was performed, clopidogrel (600 mg orally during percutaneous coronary intervention (PCI), followed by 75 mg per day for at least 9 months) was administered in addition to long-standing aspirin.

The standard technique of transcatheter VSD closure has been described in detail previously.15,16 In brief, the femoral artery was punctured and a 6–8 French sheath was inserted. The VSD was then crossed from the left ventricle using a diagnostic right Judkins or a multipurpose catheter and a soft long guidewire, which was advanced into the pulmonary artery or the superior vena cava. The guide wire was then snared using an Amplatzer Gooseneck snare (Microvena Corporation, White Bear Lake, MN, USA) and exteriorized out of the right internal jugular vein, thereby establishing an arterial-venous circuit (Figure 1A–D). The delivery sheath was advanced through the jugular vein into the left ventricle where the tip of the sheath was placed. After removal of the delivery sheath dilator and wire, the loaded flexible double-umbrella device was advanced through the delivery sheath across the septal rupture into the left ventricle. The umbrella device was pushed partially out of its catheter sheath until release of the first umbrella. The delivery catheter was drawn back into the right ventricle until the left-sided umbrella was positioned against the left ventricular septum. Finally, the right-sided umbrella was released covering the rupture from the right side. During VSD occlusion, echocardiographic control was performed for device guidance and VSD visualization and assessment. No sizing balloons were used.


Figure 1
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  		Figure 1 Schematic drawing of different steps for ventricular septal defect occlusion. (A) Step 1 (left upper panel): ventricular septal defect crossing with a catheter; (B) Step 2 (right upper panel): ventricular septal defect crossing with a soft guide wire and advancement of the wire into the superior vena cava or pulmonary artery; (C) Step 3 (left lower panel): after establishment of arterial-venous circuit, advancement of delivery sheath from the right internal jugular vein through the ventricular septal defect and guidewire removal; (D) step 4 (right lower level): release of the closure device in the ventricular septal defect.

 
Devices
Amplatzer® ASD and VSD occluders depending on VSD size and morphology, were used. The Amplatzer® atrial septal defect (ASD) and VSD occluders (AGA Medical Corporation, Plymouth, MN, USA) are self-expanding devices made of nitinol. These occluders consist of two umbrellas and a middle part or ‘waist’. Polyester fabric inserts help close the holes and provide a foundation for tissue growth over the occluder after deployment. Depending on the fabrication, the maximum left umbrella size is 54 mm for the 38 mm ASD occluder and 32 mm for the recently released 24 mm Amplatzer® muscular VSD occluder postinfarction (PI). The waist ranges from 4 mm for ASD, 7 mm for muscular VSD, and 10 mm for muscular PI VSD occluders. All devices are secured to a delivery cable and inserted into a delivery sheath ranging from 6 to 10 French in size. The device size and type were chosen according to echocardiographic VSD measurements.

Statistical analysis
There was no formal sample size calculation. Categorical variables are expressed as number and percentage of patients. Continuous parameters are expressed as median with interquartile range (IQR). Differences between patients with and without cardiogenic shock were assessed by Fisher's exact or Chi-square test for categorical variables, and by the Student t-test or Wilcoxon rank-sum test for continuous data as appropriate. Long-term survival was assessed by the methods of Kaplan–Meier and differences between patients with and without cardiogenic shock were assessed by the log-rank test. Significance in all statistical tests was assumed at P < 0.001 because of adjustments for multiple testing.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Funding
 References
 
The median patient age was 72 years (IQR 67–79; range: 48–84 years) and 55% were female. The AMI preceding the VSD was anterior in 14 and inferior/posterior in 15 patients. At the time of presentation, cardiogenic shock was present in 16 (55%) patients. Coronary angiography was performed prior to VSD closure in all patients with 51%, 28%, and 21% having single, double, and triple vessel disease. PCI of the infarct-related artery was attempted in 16 (55%) patients. In the remaining 13 patients, PCI was not performed because of non-significant stenosis and/or non-viable myocardium several days after the index event. The median left ventricular ejection fraction was 45% (IQR 35–55). All patients were supported by intra-aortic balloon counterpulsation.11 The median length of time from infarction to VSD occurrence was 2 days (IQR 1–4.5) and the time from VSD occurrence to percutaneous device closure was 1 day (IQR 1–3). Demographic and clinical findings of patients with and without cardiogenic shock are summarized in Table 1.


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  		Table 1 Patient characteristics

 
Interventional ventricular septal defect closure procedure and periprocedural complications
Individual patient data, procedural characteristics, complications, and vital status at follow-up are summarized in Table 2. The median fluoroscopy and procedure times were 24 min (IQR 17.8–34) and 75 min (IQR 57.8–85), respectively. A median of 115 mL (IQR 80–155) contrast dye was required. Successful device deployment was performed in 25 of the 29 patients (86%). Deployment was not possible for a variety of reasons. In the first patient, third degree AV-block occurred after crossing the VSD with the delivery sheath. Before pacing could be instituted, the patient expired despite cardiopulmonary resuscitation and before the device could be delivered. In the second patient, the VSD was too large and each device dislocated into the right ventricle and therefore had to be withdrawn. This patient underwent successful surgical VSD closure 5 days later with an otherwise uneventful outcome. In the third patient, the device dislocated into the right ventricle. The patient presented with cardiogenic shock and died due to haemodynamic deterioration before another closure attempt could be started. The fourth patient had left ventricular rupture related to manipulation of the VSD during device positioning, resulting in sudden cardiac death.


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  		Table 2 Individual patient and procedure characteristics, complications, and functional status at follow-up

 
Despite initial successful device implantation, two additional cardiogenic shock patients died in the catheterization laboratory as a result of left ventricular rupture. Altogether, five patients (17%) died due to procedure related complications in the catheterization laboratory.

After transfer to the intensive care unit, three patients developed partial or total dislocation of the closure device into the right ventricle. In one, surgery with device removal and VSD patch closure was performed with an otherwise uneventful clinical course. Another patient was not deemed a suitable surgical candidate and subsequently died. One patient with partial device dislocation had only mild left-to-right-shunting and therefore no further intervention was required. Six weeks after discharge, however, this patient was readmitted for infective endocarditis of the device requiring surgery. The patient died postoperatively (Figure 2).


Figure 2
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  		Figure 2 Study profile, success rate, and outcome.

 
The left-to-right shunt (Qp:Qs) could be reduced from 3.3 (IQR 2.3–3.8; measurements available in all patients) to 1.4 (IQR 1.2–1.7; P < 0.001; measurements available in 24 patients) post-device deployment. In four patients, however, there was a residual Qp:Qs of more than 1.5:1. Of these, two were not considered surgical candidates. Despite intra-aortic balloon pumping, these patients succumbed to multiorgan failure 7 and 9 days after interventional VSD closure. The other two patients could be initially stabilized and underwent successful surgical patch closure 3 and 4 months after the index event.

Patients were further divided into the first and second half of our experience to assess for a possible ‘learning curve’ effect. There was no difference in fluoroscopy time (median 30.3 min; IQR 19.7–37.5 vs. 21.1; IQR 16.4–29, P = 0.14), procedure time (median 76 min; IQR 58.3–84.3 vs. 72; IQR 56–85, P = 0.58), or contrast dye use (median 90 mL; IQR 65–165 vs. 120 mL; IQR 90–150; P = 0.64) for patients undergoing interventional closure in the first or second half of the study group. There was also no difference in any of clinical outcomes between the two time periods. Furthermore, we did not find any difference in procedural success rate according to the type of device implanted (i.e. ASD vs. muscular or PI VSD occluder) (Figure 2).

Mid-term follow-up
At 30-day follow-up, a total of 19 patients had died leading to an overall survival rate of 35%. The earliest deaths occurred during the procedure itself. The latest death occurred 18 days after transcatheter closure in a male patient due to cerebral infarction. Most of the cardiogenic shock patients (12 of 14 patients, 86%) had a grave postprocedural course and died within the first 18 days after the procedure. The 30-day cumulative survival curves for cardiogenic shock vs. no cardiogenic shock patients are shown in Figure 3A.


Figure 3
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  		Figure 3 (A) Kaplan–Meier curves for patients with and without cardiogenic shock at 30-day follow-up. The log-rank test was used to calculate the difference in survival. (B) Kaplan–Meier curve indicating the overall cumulative survival at long-term follow-up.

 
Long-term follow-up
At long-term follow-up, one additional patient died from infective endocarditis at the site of the VSD closure device despite surgical intervention. The overall survival rate was 31% (Figure 3B). Nine patients at a median follow-up of 730 days (IQR 459–1160) are alive and well. Their functional capacity has improved to New York Heart Association class II for six and class III for three patients. There has been no noted incidence of device or thrombus embolization.


   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Funding
 References
 
The current study represents, to the best of our knowledge, the largest experience to date of primary transcatheter closure of a postinfarction VSD in the acute setting. Similar to the studies of surgical closure, the overall mortality rate for such patients remains very high, in particular for those presenting with cardiogenic shock. The elevated mortality rate is mainly attributed to disease severity and comorbidities, but may also be related to the current suboptimal interventional closure technique and available devices.

Interventional closure
Since the introduction of interventional VSD closure by Lock et al.,17 several case reports and some smaller series have been reported of transcatheter closure of postinfarction VSD.18–24 The overall published number of interventional postinfarction VSD procedures is <100 patients and the majority of such patients underwent VSD closure in the chronic/subacute phase, or were restricted to patients with residual shunting after surgical patch closure.12 Consequently, these published series have an inherent selection bias since the highest risk patients would have died before reaching the chronic/subacute phase of the disease process. In contrast, we herein report a prospective series of all consecutive patients with VSD admitted to our cardiology intensive care unit. Despite the fact that in some cases, patients were in severe cardiogenic shock and the chance of a successful outcome was considered to be unlikely, interventional closure was nonetheless attempted to determine if we could improve the grim prognosis of such patients. Our selection of ‘all-comers’ with acute postinfarction VSD is probably responsible for our observed elevated mortality rate. It is important to note, however, that mortality rates of 87–100% were reported for postinfarction VSD patients with cardiogenic shock in the multicentre, prospective GUSTO-I trial, and the SHOCK-registry.1,7 The results from these two studies probably represent most closely the true mortality rate of VSD patients without the selection bias that exists in most surgical or interventional based reports.

Current device and implantation procedure limitations
There are currently several limitations regarding the available technique and devices for percutaneous VSD closure: (i) the rigid delivery sheath that has to cross the VSD and needs to be advanced into the direction of the left ventricular outflow tract might tear the borders of the VSD, resulting in an increased VSD size or, in the worst case, left ventricular rupture; (ii) the requirement of guidewire removal after insertion of the delivery sheath also has disadvantages, in particular, if the primarily chosen left ventricular umbrella dislocates into the right ventricle. Such a complication requires new establishment of an arterial-venous conduit exposing the patient to additional risk. Newer device designs with the guidewire in place and with less rigid delivery sheaths might overcome this limitation;25 (iii) the currently available device sizes of the muscular VSD occluders are frequently not sufficient to fully close the VSD, which can be large and complex. As a consequence, ASD occluders with larger left-sided discs have to be used which can lead to suboptimal device deployment of the right ventricular disc due to the length of the waist. This often results in the so-called ‘cobra-phenomenon’ with persistent shunting.12 Furthermore, healing of the infarcted myocardium over time may increase the size of the VSD leading to device malapposition and embolization, as observed in three of our patients. This requires the use of devices that are larger than the measured VSD size at the time of implantation; (iv) the device design is also suboptimal in that immediate, complete closure of the VSD is not possible in many patients. The polyester fabric covering the holes in the nitinol mesh is too permeable in the early stages after device implantation. In contrast to ASD closure with lower transatrial pressure, the higher transventricular pressure for a VSD leads to persistent shunting until thrombus formation and endothelialization of the device has occurred. Left ventricular unloading with a percutaneous assist device might be an option to reduce the interventricular pressure gradient. These devices, however, are associated with additional complications.26 A denser fabric could overcome this limitation but is not yet available.

Surgical closure
The outcomes of interventional device closure are difficult to compare with those of published surgical series given the small patient numbers and the inherent selection bias present in nearly all such studies. Predictors of increased surgical mortality include haemodynamic instability, ventricular dysfunction, inferior VSD location, and early surgery.27–30 In contrast to surgical VSD closure, inferior and basal VSDs are more easily closed with an interventional technique due to the more favourable access from the upper jugular vein. Current mortality rates of surgical postinfarction VSD closure remains high at 20–87%, depending on patient acuity and length of follow-up.4–7,31,32 As a result of patient selection, those considered not to be surgical candidates are usually not included in these registries. Furthermore, in some studies, surgical correction is performed late (4–6 weeks) after VSD occurrence to allow scarring of the surrounding rim. Such a practice will certainly lead to partially biased results, as longer waiting periods will lead to survival of the fittest.10 In the current study, which did not exclude any patient, more than 50% of patients were in cardiogenic shock that is higher than in surgical series. In addition, the median time between VSD occurrence and closure was only 1 day which is in stark contrast to most surgical series.

Limitations
The major limitation of this trial is the relatively small patient number which is a reflection of the infrequent observance of postinfarction VSD in the current era of thrombolytic and interventional treatment of AMI. To the best of our knowledge, however, the current study represents the largest patient series reported so far. Another important consideration is the limited number of centres with sufficient expertise in performing these challenging procedures. The infrequent occurrence of postinfarction VSD results in only a few patients being treated annually even in large centres, thus rendering large studies impossible without multicentre involvement. A randomized comparison with surgery would also need to be addressed in such a multicentre trial.

In conclusion, primary percutaneous postinfarction VSD closure is a promising technique that might offer an alternative or an adjunctive treatment to surgery. Percutaneous VSD treatment allows immediate closure after the diagnosis is made, which might lead to stabilization or prevention of further deterioration. Despite the less invasive technique, mortality of postinfarction VSD remains high in particular for patients with cardiogenic shock. Further developments in devices and delivery techniques are required in order to optimize interventional outcomes. Additionally, future multicentre studies are required to identify patients best suited for surgical or interventional closure.


   Funding
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Funding
References
 
Study design and analysis were performed by Universität Leipzig–Herzzentrum, and funding was completely industry independent.

Conflict of interest: none declared.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Funding
 References
 

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