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Ann Thorac Surg 2009;87:687-692. doi:10.1016/j.athoracsur.2008.11.052
© 2009 The Society of Thoracic Surgeons
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Original Articles: Adult Cardiac

Postinfarction Ventricular Septal Defects: Towards a New Treatment Algorithm?

Simon Maltais, MD, MSa, Reda Ibrahim, MDb, Arsène-Joseph Basmadjian, MDb, Michel Carrier, MDa, Denis Bouchard, MDa, Raymond Cartier, MDa, Philippe Demers, MDa, Martin Ladouceur, MSc, Michel Pellerin, MDa, Louis P. Perrault, MD, PhDa,*

a Cardiac Surgery, Montreal Heart Institute and Université de Montréal, Montreal, Quebec, Canada
b Cardiology Department, Montreal Heart Institute and Université de Montréal, Montreal, Quebec, Canada
c Biostatistics Department, McGill University Health Centre, Montreal, Quebec, Canada

Accepted for publication November 20, 2008.

* Address correspondence to Dr Perrault, Institut de Cardiologie de Montréal, 5000 rue Bélanger, Montreal, Quebec, H1T 1C8, Canada (Email: louis.perrault{at}icm-mhi.org).


Adult cardiac surgery: The Annals of Thoracic Surgery CME Program is located online at http://cme.ctsnetjournals.org. To take the CME activity related to this article, you must have either an STS member or an individual non-member subscription to the journal.

 

   Abstract
Top
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 References
 
Background: We reviewed our experience at the Montreal Heart Institute with early surgical and percutaneous closure of postinfarction ventricular septal defects (VSD).

Methods: Between May 1995 and November 2007, 51 patients with postinfarction VSD were treated. Thirty-nine patients underwent operations, and 12 were treated with percutaneous closure of the VSD.

Results: Half of the patients were in systemic shock, and 88% were supported with an intraaortic balloon pump before the procedure. Before the procedure, 14% of patients underwent primary percutaneous transluminal coronary angioplasty. The mean left ventricular ejection fraction was 0.44 ± 0.11, and mean Qp/Qs was 2.3 ± 1. Time from acute myocardial infarction to VSD diagnosis was 5.4 ± 5.1 days, and the mean delay from VSD diagnosis to treatment was 4.0 ± 4.0 days. A moderate to large residual VSD was present in 10% of patients after correction. Early overall mortality was 33%. Residual VSD, time from myocardial infarction to VSD diagnosis, and time from VSD diagnosis to treatment were the strongest predictor of mortality. Twelve patients were treated with a percutaneous occluder device, and the hospital or 30-day mortality in this group was 42%.

Conclusion: Small or medium VSDs can be treated definitively with a ventricular septal occluder or initially to stabilize patients and allow myocardial fibrosis, thus facilitating delayed subsequent surgical correction.

Ventricular septal rupture is a rare but deadly complication after acute myocardial infarction (MI) [1]. Before the reperfusion era, postinfarction ventricular septal defects (VSD) complicated 1% to 2% of acute MI [1, 2]. However, introduction of early reperfusion therapy such as thrombolysis and more recently primary percutaneous coronary intervention (PCI) has significantly reduced the incidence of this complication. In the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I) study, postinfarction VSD was confirmed by echocardiography in only 84 of 41,021 patients (0.2%) [3]. Absence of angina has been associated with increased incidence of postinfarction VSD [4], possibly because angina leads to myocardial preconditioning and collateral formation, which protect the myocardium from septal rupture.

Ventricular septal rupture generally occurs during the first week after acute MI [2, 5–7]. This complication has a bimodal presentation, however, with a high incidence in the first day and 3 to 5 days after acute MI. In the GUSTO-I trial, 94% of cases happened during the first day after the MI, and the median time for VSD presentation was 16 hours in the Should We Emergently Revascularize Occluded Coronaries in Cardiogenic Shock (SHOCK) trial [3, 8].

Outcomes after acute post-MI VSD in the era before thrombolysis were poor, with mortalities of about 45% in surgically treated patients and 90% in medically treated patients [9, 10]. Cardiogenic shock is associated with an extremely poor prognosis, with an 87% mortality compared with 59% in the SHOCK trial [8]. Pretre and colleagues [11] reported an early mortality rate of 26% in 54 patients who underwent surgical closure of a postinfarction VSD. In the GUSTO-I trial, the 8 patients with septal rupture, who were in Killip III or IV at presentation, died [3].

Current guidelines of the American College of Cardiology-American Heart Association for the treatment of postinfarction VSD recommend immediate surgical repair, regardless of clinical status (class I recommendation) [12]. Multiple series emphasized the importance of early surgical repair, but the ideal timing of the intervention is still a matter of debate [13]. Thus, the treatment and the correct management of patients presenting with VSD after acute MI is still a subject of interest, especially in the era of evolving technologies such as percutaneous transseptal occluders.

This study evaluated our outcomes in today's era of percutaneous advances of postinfarction VSD closure. Secondary purpose included an analysis of multivariate predictors of in-hospital or 30-day mortality in this high-risk population. We reviewed our 12-year experience at the Montreal Heart Institute with the treatment of postinfarction VSD rupture. A new treatment algorithm is proposed for this complex and morbid pathology.


   Material and Methods
Top
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 References
 
Patient Selection
Between May 1995 and November 2007, 51 patients with a diagnosis of postinfarction VSD were treated at the Montreal Heart Institute. Of these, 39 patients underwent operations, and 12 were considered for primary or residual percutaneous closure. The protocol was reviewed and approved by the Montreal Heart Institute Research Center Ethical Committee. Written informed consent was obtained from all patients.

A preoperative transthoracic echocardiography study was done in all patients. Patients were brought promptly for hemodynamic catheterization after the initial MI or after VSD rupture and hemodynamic deterioration. No patients received intravenous thrombolysis before VSD correction, and besides counterpulsation with an intraaortic balloon pump (IABP), no other mechanical assist devices were used. From 2001, all patients were considered for percutaneous closure after acute MI.

The treatment modality was decided by a consensus between the cardiac surgeon and the interventional cardiologist. Patients with a medium to large diameter (> 15 mm) VSD were considered for immediate operation, and patients with small to moderate VSD were evaluated for percutaneous closure. When anatomically possible, unstable patients with a high operative risk (right ventricular failure, age > 75 years, preoperative shock) were considered, on an individual basis, for primary percutaneous closure with the Amplatzer (AGA Medical Corp, Plymouth, MN) device (Fig 1). The optimal diameter of the device using the Amplatzer (pi-mVSD) was twice the size of the VSD or at least 10 mm larger than the measured VSD. Because the largest occluder available has a 24-mm diameter, we defined 15 mm as the largest VSD amenable for percutaneous closure.


Figure 1
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  		Fig 1. Percutaneous closure of a septal rupture with the catheter-based ventricular septal Amplatzer device. This figure shows how percutaneous closure could be an alternative or a bridge to surgical repair in selected patients.

 
Statistical Analysis
Continuous variables were tested for statistical significance using the t test. Categoric variables were compared using the {chi}2 test and the Fisher exact test, as appropriate. Patient characteristic variables were expressed as means ± standard deviation and percentages. We performed univariate and multivariate logistic regression analyses to identify significant predictors of hospital or 30-day mortality. Logistic regression was used to obtain adjusted and unadjusted odds ratios (OR) and their 95% confidence intervals (CI) of predictors of early mortality. Statistical significance was set at p < 0.05. Statistical analysis was performed with SAS 9 software (SAS Institute Inc, Cary, NC).


   Results
Top
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 References
 
Patient Characteristics and Hemodynamic Data
Characteristics for the 51 patients (66% men) in the study are presented in Table 1. Mean age was 68 ± 9 years old. A history of coronary artery disease was present in 16%. Standard comorbidities were hypertension in 52%, diabetes mellitus in 18%, hypercholesterolemia in 38%, obesity (body mass index > 35 kg/m2) in 12%, active smoking in 54%, and family history of coronary artery disease in 33%. In this group, 12 patients (23%) underwent percutaneous closure of a post-MI VSD. From this group, 2 patients were bridged to surgical correction of a residual VSD, 4 had a primary definitive percutaneous treatment of a post-MI VSD, 1 had off-pump coronary artery bypass grafting 11 months after percutaneous closure, and 3 underwent correction of a significant residual VSD. Unfortunately, 2 patients died promptly during or shortly after the percutaneous procedure.


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  		Table 1 Patient Characteristics
 
Table 2 presents the characteristics of the acute MIs and preoperative hemodynamic variables for all patients. Left anterior MI was the initial anatomic location of the MI in 42% of patients and inferior MI in the remaining patients. The left anterior descending (LAD) and the right coronary arteries (RCA) were almost equally involved, with the LAD being the culprit lesion in 47% and the RCA in 53% of patients. A single coronary artery lesion was involved in 45%. Preoperative cardiogenic shock (< 80/40 mm Hg) was present in 43% of patients, and 88% of these required preoperative insertion of a IABP. Preoperative percutaneous coronary intervention of the culprit lesion was performed in 14% of patients. Mean preoperative left ventricular ejection fraction (LVEF) documented by echocardiography was 0.44 ± 0.11, and the mean cardiac index was 2.5 ± 0.7 L/min/m2. The average Qp/Qs ratio, a calculated indicator of the left to right shunt across the VSD, was 2.3 ± 1.0.


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  		Table 2 Hemodynamic and Myocardial Infarction Characteristics
 
VSD Closure
The VSD diameter in the 51 study patients averaged 11.7 ± 4.1 mm (range, 5 mm to 21 mm; Table 3). The average time between MI and VSD diagnosis was 5.4 ± 5.1 days, and the average time between the VSD diagnosis and definitive treatment was 4.0 ± 4.0 days. An elevated serum creatinine level was found in 27% of patients before VSD repair. Intubation was required in 12%. In 76% of patients, the surgical procedure performed for the VSD was the endomyocardial pericardial exclusion patch proposed by David in 1995 [14]. In all other patients, the VSD was closed using the Daggett technique [15]. The David endomyocardial closure was the standard technique used shortly after its publication in 1995.


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  		Table 3 Description of Ventricular Septal Defect Characteristics
 
On the basis of preoperative hemodynamic characteristics and anatomic considerations, the culprit artery was addressed in 62% of patients in the surgical group. Significant (> 70%) partially occluded vessels were also addressed when appropriate. Mean extracorporal bypass circulation time was 166 ± 63 minutes, with a mean aortic cross-clamping time of 110 ± 51 minutes. In 10 patients (25%) in the surgical group, intraoperative trivial nonsignificant residual ventricular septal ruptures were observed by transesophageal echocardiography but were not detectable when evaluated at transthoracic echocardiography before discharge. After correction, 5 patients (13%) had significant moderate (1 patient) to large (4 patients) residual ventricular septal ruptures.

The overall early in-hospital and 30-day mortality was 33%. The most frequent cause of death was multiorgan failure. Mean hospital length of stay averaged 16 days for the patients in the study.

Surgery vs Percutaneous Closure
Table 4 presents the comparison of both groups according to the two treatment modalities used (surgical or percutaneous repair). As presented, no significant differences were noted between groups when compared for age, hypertension, preoperative shock, preoperative IABP, LVEF, time between MI and VSD diagnosis, time between VSD diagnosis and treatment, posterior VSD, residual VSD, and early death. As expected by patient selection, only VSD diameter was statistically different between groups. The VSDs in patients referred for percutaneous closure were smaller than those in the surgical group.


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  		Table 4 Surgically Treated Patients Compared With Patients Treated With the Amplatzer Device
 
Univariate and Multivariate Regression Analyses
Table 5 identifies univariate factors associated with hospital or 30-day mortality for the overall group. Residual VSD after procedure (OR, 0.077; 95% CI, 0.008 to 0.733), time between MI and VSD diagnosis (OR, 0.778; 95% CI, 0.605 to 1.001), and delay between VSD diagnosis and treatment (OR, 0.800; 95% CI, 0.631 to 1.014) were the strongest univariate predictors of hospital or 30-day mortality. In contrast, age, hypertension, preoperative shock, posterior VSD, VSD diameter, and treatment modality (either percutaneous or surgical) were not univariate predictors for this early outcome. When the most significant factors were placed into a multivariate regression model, residual VSD (OR, 0.071; 95% CI, 0.007 to 0.690), time from MI to VSD diagnosis (OR, 0.757; 95% CI, 0.058 to 0.988), and time delay between VSD diagnosis and treatment (OR, 0.758; 95% CI, 0.580 to 0.992) were statistically significant (Table 6).


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  		Table 5 Univariate Analysis for Factors Associated With Hospital or 30-Day Mortality
 

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  		Table 6 Multivariate Analysis for Factors Associated With Hospital or 30-Day Mortality
 

   Comment
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
References
 
This retrospective analysis study described the experience of the Montreal Heart Institute with a rare but lethal complication after acute MI. The primary objective was to perform a descriptive analysis of our population and identify significant predictors of hospital or 30-day mortality. We reported our experience with the percutaneous treatment of postinfarction VSD using the Amplatzer occluder device. Early in-hospital mortality for the overall group was 33%, and the mean hospital length of stay was 16 days. These results are concordant with data already published from other groups reporting a 30% in-hospital mortality rate [11].

Crenshaw and colleagues [3] also reported that patients who survived the operation had a good long-term prognosis. They described a long-term mortality rate of only 6% among patients who survived the first 30 days postoperatively [3]. In another series of 60 patients, Davies and colleagues [10] reported good late survival for patients who survived the surgical repair of 69% at 5 years, 50% at 10 years, and 37% at 14 years [10]. All patients were in New York Heart Association functional class I or II at last follow-up. We could therefore hypothesize that our group of patients can expect a good outcome if they survive the first 30 days after surgical repair or percutaneous treatment.

Predictors of Poor Outcome
There is some evidence and some belief that the myocardium is too fragile for a safe repair after an acute post-MI septal rupture. A short waiting period after the diagnosis might be expected to allow the margins of the infarcted muscle to develop a firmer scar, thus facilitating surgical repair and decreasing the risks of recurrent VSD [6]. More recent studies, however, have reported an increased survival rate with rapid intervention after the diagnosis [13, 15].

Current guidelines of the American College of Cardiology-American Heart Association recommend immediate operative intervention in patients with acute septal rupture, regardless of their clinical status [12]. This recommendation is confirmed in the present study because the time between VSD diagnosis and treatment with surgical correction or percutaneous closure was the most significant predictor of hospital or 30-day mortality (OR, 0.758; 95% CI, 0.580 to 0.992). Residual VSD and time from MI to VSD diagnosis were also significant predictors of death. None of the other factors included in the analysis were significant.

When univariate and multivariate logistic regression analyses were used to identify predictors of residual VSD, no significant factors were associated with this outcome (data not shown). Attempts to stabilize the patient's condition with medical therapy often fail because most patients have a rapid deterioration and die. Patients need immediate surgical or percutaneous intervention.

Percutaneous Closure of Postinfarction Septal Rupture
In today's era of percutaneous interventions, some patients may benefit from percutaneous closure of the septal rupture with catheter-based devices. Few studies have reported this new technique as an alternative to the surgical repair [16–19]. In the percutaneous group, 5 patients died, for a hospital or 30-day mortality of 42%. One patient with a 14-mm VSD died of device embolization into the pulmonary artery 3 days after the procedure. This patient had the largest VSD attempted for percutaneous closure in this series. One patient died of acute iatrogenic right ventricle perforation and tamponade during the procedure before device implantation. The other 3 patients died of multiple organ failure.

It is important to stress that as the site of the septal rupture in patients with acute MI becomes surrounded by necrotic tissue, attempts to pass the closure device through the VSD may increase the size of the rupture and tear residual fragile tissue. One patient in this group with a large residual VSD underwent elective surgical correction of the residual defect 8 months after the initial stabilization of the acute post-MI VSD with the percutaneous procedure. Another patient underwent successful triple-vessel off-pump coronary artery bypass grafting 11 months after the device implantation for residual incapacitating angina.

Proposed New Treatment Algorithm
The new device occluder can allow transcatheter closure of VSD in the acute setting. This procedure has been used for the residual closure of a septal defect after patch closure [16]. Others suggested that the device could bring hemodynamic relief after acute MI to allow surgical correction of the VSD after the myocardium has had time to fibrose [20]. We further propose a new algorithm where acute small or medium VSDs can be treated initially with a ventricular septal occluder. In this study, there was no statistical difference in in-hospital or 30-day mortality between patients treated initially surgically or with the percutaneous device (p = 0.56). The Amplatzer device can therefore allow myocardial fibrosis to form, facilitating delayed subsequent surgical correction if a significant residual VSD persists (Fig 2).


Figure 2
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  		Fig 2. Proposed algorithm to treat postinfarction ventricular septal defects (VSDs). We propose a new multidisciplinary algorithm where acute small or medium VSD could be treated initially with a ventricular septal occluder. (CABG = coronary artery bypass graft; MI = myocardial infarction; PCI = percutaneous coronary intervention; TTE = transthoracic echocardiography.)

 
When large (≥ 15 mm) VSDs are encountered, patients should undergo immediate operation, because large myocardial deficits are more prone to device embolization or residual VSD after device implantation. In the present study, the patient with the largest VSD who underwent percutaneous closure died of early device embolization. In our experience, the optimal diameter of the device using the Amplatzer post-MI occluder (pi-mVSD) should be twice the size of the VSD or at least 10-mm larger than the measured VSD. This is partially because the largest occluder available has a 24-mm diameter.

Limitations
This study is a retrospective cohort analysis. Although techniques of multivariate analysis may adequately control for measurable biases, unmeasured bias may still exist and influence the presented results. The nonblinded single-center nature of the study may influence the results and, hence, the technique for initial approach of patients with postinfarction VSD.

Conclusion
The timing of surgical or percutaneous intervention is critical in the approach of patients with a diagnosis of postinfarction VSD. Patients should undergo emergency surgical or percutaneous intervention to prevent hemodynamic deterioration and multiorgan failure. Many studies have shown that the patient's preoperative hemodynamic status is a major determinant of the postoperative outcome, rather than the ejection fraction or the size of intracardiac shunt [15]. In selected patients, percutaneous closure can be an alternative or a bridge to surgical repair, such as in patients with uncertain neurologic status or multiorgan failure at presentation.

New combined techniques are also currently evolving where small congenital VSD are closed on the beating heart with the VSD occluder through a lower ministernotomy incision [20]. However, a team of interventionalists and surgeons should carefully approach large VSDs because the risk of device embolization from poor quality of necrotic myocardial tissues is expected. In the future, development of new techniques and devices may improve the surgical results of the treatment of postinfarction VSD.


   References
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 References
 

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Related Article

Invited Commentary
Francis Pagani
Ann. Thorac. Surg. 2009 87: 693. [Extract] [Full Text] [PDF]



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Ann. Thorac. Surg., March 1, 2009; 87(3): 693 - 693.
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