Evolution in the Management of Postinfarct Ventricular Septal Defects From Surgical to Percutaneous Approach: A Single-Center Experience

Abstract: Background. Postinfarction ventricular septal defect (VSD) is an uncommon but serious complication of myocardial infarction associated with high mortality. While traditionally postinfarct VSDs were only closed surgically, percutaneous closure is a newer treatment strategy that has been introduced with success in recent years. We sought to assess trends in treatment choice at our center. Methods and Results. A single-center, retrospective study design included all patients treated for postinfarction VSDs, either surgically or percutaneously, from January 1992 to December 2012. Percutaneous closure was performed using the self-expandable, double-disc Amplatzer closure device. Over the 20-year study period, a total of 25 patients were treated for postinfarct VSDs, with 18 managed surgically and 7 managed percutaneously. Two patients with an initial surgical repair experienced patch dehiscence and were subsequently treated percutaneously, bringing the number in this group to 9. The use of surgical closure declined over time, with percutaneous closure being the only treatment strategy used from 2004 onward. Mortality rates were 44% and 75% for those with final percutaneous and surgical closure, respectively (P<.13). Mortality rates in patients presenting with and without cardiogenic shock were 80% and 46%, respectively (P<.05). Conclusion. Percutaneous closure has become the preferred treatment of postinfarct VSDs at our center. Percutaneous closure may be a viable and non-inferior treatment strategy compared to traditional surgical closure. 

J INVASIVE CARDIOL 2013;25(7):339-343

Key words: percutaneous VSD closure, surgical VSD closure

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Ventricular septal defect (VSD) is an infrequent complication following myocardial infarction, with an incidence that has reduced over time with the evolution of the treatment of acute myocardial infarction (AMI).^1-4 Despite a reducing incidence and an improved standard of care, mortality following postinfarct VSDs remains high. Medically managed patients with postinfarct VSDs have 30-day mortality rates as high as 94%.² Given this high mortality rate, surgical closure has traditionally been advocated as the preferred treatment strategy. However, even in surgically treated patients, mortality remains high, with reported rates ranging from 23%-81%.^5-8 

Percutaneous closure of postinfarct VSDs has emerged over the last decade as an alternative treatment strategy. This was first attempted in 1988 by Lock et al, but all 3 patients in this study with postinfarct VSDs died during their hospital stay.^3,9 However, with improvement in device technology, successful case reports and case series have subsequently been reported. Our own series of 5 patients showed that a percutaneous strategy could be used with success, with 3/5 patients surviving to 12 months.¹⁰ Another larger series described 29 percutaneously treated patients with a 30-day mortality rate of 65%.¹¹ 

While percutaneous closure has been shown to be a viable alternative to surgical repair, little is known about how widely this new strategy has been adopted into clinical practice. Therefore, we sought to assess trends in treatment choice for postinfarct VSDs with either percutaneous or surgical closure at our center. 

Methods

Study design. This is a single-center, retrospective case series study. In 2012, data were obtained from databases in the surgical department and cardiac catheterization laboratory by an independent analyst on patients treated between January 1, 1992 to December 31, 2012. Subsequent analysis of the data was performed in consultation with an independent statistician. 

Patients. Patients were eligible if they were admitted to the Green Lane Cardiovascular Service with postmyocardial infarction VSDs. Those patients with postinfarct VSD managed medically were excluded from analysis, leaving only those who received either surgical or percutaneous intervention for inclusion. The Green Lane Cardiovascular Service comprises two sites, Green Lane Hospital (until December 2003) and Auckland City Hospital (from 2003 to 2012). Patients were included if they had confirmed VSD on either transthoracic (TTE) or transesophageal echocardiogram (TEE). Clinical suspicion alone was not sufficient. Mortality outcomes were compared between surgical and percutaneous patients. If patients had both surgical and percutaneous closure of their VSD, they were allocated into the group based on the last definitive closure procedure. Therefore, those patients with patch dehiscence after surgery who underwent subsequent percutaneous closure were allocated to the percutaneous group for analysis. 

Endpoints. The primary study endpoint was to assess trends in treatment choice over time of either surgical or percutaneous approaches for postinfarct VSDs. Secondary endpoints were in-hospital and long-term mortality in both percutaneous and surgically treated patients. Mortality in patients presenting with and without cardiogenic shock (CS) was also determined. 

Surgical procedure. All surgical VSD closures were undertaken via a median sternotomy with cardiopulmonary bypass and hypothermia at 33 ˚C. Cardiopulmonary bypass was established using aortic and bicaval cannulation and caval snares. To access the interventricular septum, the left ventricle was opened with an incision through the area of infarct. Once the VSD was identified, it was closed without tension with a patch. Depending on surgeon preference, either a Dacron or Teflon patch was used. Continuous sutures, interrupted sutures, or both were used to secure the graft. Glue was also applied to secure the patch repair. The ventriculotomy was then closed without tension, with some patients needing a second patch applied to secure the closure. In addition to VSD repair, a proportion of patients also had coronary artery bypass grafting. Sternal closure was with wire and vicryl over pleural and mediastinal drains. 

Percutaneous procedure. Percutaneous closure was undertaken using the Amplatzer postinfarction muscular VSD closure device or an atrial septal defect (ASD) occluder, which are self-expandable, double-disc devices made from nitinol wire mesh filled with polyester patches. Various sizes are available, ranging from 12-30 mm. Each procedure was performed under general anesthesia, with both TEE and fluoroscopic guidance. A left ventricular angiogram was first performed to establish landmarks with access via the right femoral artery. A right internal jugular (RIJ) sheath was then inserted and intravenous heparin and 1 gram cephazolin administered. A JR4 catheter was then advanced into the left ventricle (LV) and manipulated into the mouth of the VSD, allowing a Glidewire to be passed through the VSD into the right ventricle (RV) and a catheter advanced over the wire. The Glidewire was then removed and a 260 or 400 cm Wholey wire was advanced into the pulmonary artery and captured using a snare advanced from the RIJ vein. The wire was then exteriorized to form a complete arteriovenous loop. The RIJ sheath was then exchanged for a 12 Fr AGA delivery sheath that was advanced across the VSD. The chosen device was then advanced through the delivery system. The LV disk was deployed and pulled back under TEE guidance and the RV disk was deployed under fluoroscopic guidance. Before device release, the final position was confirmed by both TEE and fluoroscopy. 

Statistical analysis. The number and percentage of patients describe categorical variables. Continuous variables were described as medians with interquartile ranges. To assess differences between patients, the Fisher’s exact, Chi-square, and Student’s t-test were used. Kaplan-Meier method was used to assess long-term survival. Log-rank test was used to assess differences between surgical and percutaneous patients and those presenting with and without CS. 

Results

Patients. A total of 25 patients were treated for postmyocardial infarction VSDs between January 1, 1992 and December 31, 2012. Eighteen patients (72%) were initially treated with surgical repair and 7 patients (28%) were treated percutaneously. Of the 18 surgically treated patients, 2 suffered significant patch dehiscence and underwent percutaneous closure, bringing the number treated percutaneously to 9. Baseline characteristics were similar between the two groups; however, surgical patients had more use of intraaortic balloon counterpulsation (IABP) and also a shorter time frame between VSD diagnosis and repair (Table 1). 

Primary and secondary endpoints. The use of percutaneous closure as primary therapy has increased over time, and has become the only first-line therapy used over recent years. The first 2 percutaneous cases in 2003 and 2004 were performed following unsuccessful surgical repair. After these initial two cases, all subsequent patients presenting with postinfarction VSDs were managed with percutaneous closure as first-line therapy. The last surgical repair to be attempted in our center was in 2004 (Figure 1). The individual patients, with patient characteristics, type of repair, and long-term mortality are presented in Table 2. 

Ten out of 25 patients died in-hospital, 3 in the percutaneous group and 7 in the surgical group. After discharge from hospital, 6 further patients died (1 in the percutaneous and 5 in the surgical group). The long-term survival curves for both percutaneous and surgically treated patients are presented in Figure 2. Overall, 75% of patients died after surgical closure and 44% died after percutaneous closure. There was no difference between percutaneous and surgical repair for both in-hospital (P<.66) and long-term mortality (P<.33). The long-term survival curves for patients presenting with and without CS are shown in Figure 3. Patients presenting in CS (10/25) and those without CS (15/25) had a mortality of 80% and 46%, respectively, with a trend toward significance (P=.05). 

The defects were closed percutaneously using the Amplatzer muscular VSD occluder, with device sizes ranging from 12-24 mm in all but 1 patient in whom a 30 mm Amplatzer ASD septal occluder was used. Following percutaneous closure, 6 patients retained a small residual shunt, and 1 patient had a mild-moderate shunt. The degree of residual shunt was not determined for 2 patients. 

Discussion

There has been little published information on trends in treatment choice for postinfarct VSDs. Percutaneous closure of postinfarct VSDs was introduced in our center when it was performed after failed surgical closure as “rescue” therapy for 2 cases in 2003 and 2004. Since the encouraging results from these initial cases, our study demonstrates a change in practice to an exclusively primary percutaneous approach for managing postinfarct VSDs. 

We found no difference between surgical and percutaneous repair for either in-hospital or long-term mortality, although there did appear to be a trend favoring percutaneous closure. There is a suggestion that surgical repair has higher late mortality after discharge. All but 1 percutaneous patient who survived to discharge were still living at the time of follow-up. Late mortality may appear to be higher in the surgical group, as it likely reflects the early mortality of those presenting with CS. While there was no difference between the proportion of patients in CS between the two cohorts, the surgical cohort had higher use of IABP, suggesting treating clinicians felt they were more unstable or possibly reflecting more common use of IABP in the cardiac surgical environment. Patients presenting with VSD in CS have been shown to have worse mortality. The SHOCK trial registry showed patients presenting with VSD and CS had in-hospital mortality of 87%.⁵ In Thiele et al’s percutaneous series, patients with CS who had a technically successful closure still had a 30-day mortality of 86%.¹¹ Our own series showed that patients in CS had a trend toward higher mortality, consistent with the finding of previous studies. 

The surgical cohort had a shorter duration between VSD diagnosis and repair, with the percutaneous cohort more likely to have delayed closure of the VSD after diagnosis. The most likely explanation for this difference is that since this was not a randomized study, the treatment strategy for each patient was selected based on clinical grounds. It appears that over time, there has been a reluctance to take on patients for early surgery and those who survive the acute phase of presentation ultimately proceed to percutaneous repair. For both surgical and percutaneous approaches, there has been considerable debate regarding the optimum timing of closure. The current guidelines recommend urgent surgical repair after VSD diagnosis. Some surgical centers have opted for delayed surgical closure to allow myocardial healing.³ A surgical series reported by Jeppsson et al demonstrated an inverse relationship between 30-day mortality and time between diagnosis and repair, with urgent repair being an independent risk factor of mortality. This does not necessarily advocate delaying surgical intervention, but simply reflects that patients who have delayed intervention tend to be the “survivors.” Patients presenting with CS or requiring IABP were unlikely to survive to undergo delayed repair.⁷ 

Study limitations. The main limitation of this study is the small number of patients, but with numbers similar to other studies in this area. It is difficult to make direct comparisons between surgical and percutaneous repair; given the study’s retrospective design, it was not possible to control for confounders. Patients in this study were not treated based on a study protocol, but treatment was guided by expert clinical opinion; therefore, it was not possible to control for treatment variables. However, despite these limitations, since percutaneous closure has been used as first-line therapy in our center, in-hospital and long-term mortality rates have appeared to improve. With careful patient selection, percutaneous closure performed by experienced operators may be a viable and non-inferior treatment strategy compared to traditional surgical closure. 

References

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From the Green Lane Cardiovascular Service, Auckland City Hospital, Auckland, New Zealand. 

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.

Manuscript submitted February 4, 2013, provisional acceptance given March 4, 2013, final version accepted March 22, 2013.

Address for correspondence: Dr Janarthanan Sathananthan, 45 Magma Crescent, Stonefields, Auckland, New Zealand 1072. Email: janar.s@hotmail.com