Asian Cardiovasc Thorac Ann 2008;16:215-220
© 2008 Asia Publishing EXchange Ltd
Postinfarction Ventricular Septal Defect: Patch Repair with Infarct Exclusion
Lokeswara R Sajja, MCh,
Gopi C Mannam, FRCS,
Rama S Gutti, MCh,
Nagasaina R Goli, MCh,
Sriramulu Sompalli, MD1,
Raghava R Penumatsa, DM2
Division of Cardiothoracic Surgery
1 Division of Cardiac Anesthesiology
2 Division of Cardiology, CARE Hospital The Institute of Medical Sciences, Hyderabad, India
For reprint information contact: Gopi C Mannam, FRCS Tel: 91 40 3041 8888 Fax: 91 40 5562 5003 Email: gopi.mannam{at}gmail.com, CARE Hospital, The Institute of Medical Sciences, Road No: 1, Banjara Hills, Hyderabad 500 034, AP, India.
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ABSTRACT
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Postinfarction rupture of the interventricular septum is usually fatal without prompt surgical intervention. Repair of postinfarction ventricular septal rupture by an endocardial patch technique with infarct exclusion is associated with less morbidity and mortality. The results of this repair in 22 consecutive patients were analyzed retrospectively. After myocardial infarction, 16 patients were operated on within 7 days, 3 at 8–21 days, and 3 at 3–6 weeks. 2D-echocardiography, color Doppler studies and coronary angiography were performed in all patients prior to surgery. The mean age of the patients was 57.46 ± 5.31 years and 20 were male; 15 were in cardiogenic shock or congestive heart failure at the time of operation. There were 5 (22.7%) operative deaths. Postoperative complications included low cardiac output, renal failure and respiratory failure. Preoperative cardiogenic shock, severe right ventricular dysfunction, residual ventricular septal defect, and preoperative renal failure were predictors of operative mortality. There were 2 late deaths. A rapid diagnosis, aggressive medical management and prompt surgical intervention are required to optimize survival and recovery in patients who present with septal rupture complicating myocardial infarction
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INTRODUCTION
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Left ventricular (LV) wall rupture is the cause of death in approximately one third of patients who have a fatal acute myocardial infarction (MI).1,2 Most ventricular ruptures occur in the LV free wall, and these are usually fatal. In 15%–20% of cases, the rupture occurs in the interventricular septum, and this is also often fatal unless surgically treated.1–5 In the pre-thrombolytic therapy era, septal rupture complicated 1%–3% of cases of acute MI.6,7 Among 41,021 patients in the GUSTO-I trial, ventricular septal rupture was suspected in 140 (0.34%) and confirmed by retrospective review in 84 (0.2%).8 The first successful repair was reported by Cooley and colleagues9 in 1957, and the technique developed by Daggett and colleagues10 became the established surgical procedure. This consists of infarctectomy and reconstruction of the septum and ventricular wall with synthetic fabric patches, but it is associated with high operative mortality when performed during the acute phase of MI.10,11 In 1987, a new technique was introduced whereby no infarctectomy was performed and the infarcted myocardium was excluded from the LV cavity with a pericardial patch sutured to the LV endocardium, which decreased surgical mortality.12,13 We report early outcomes in 22 consecutive patients in whom the infarct exclusion technique was used to repair ventricular septal rupture following acute MI.
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PATIENTS AND METHODS
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Between January 2001 and October 2006, 25 consecutive patients were referred for repair of postinfarction ventricular septal rupture at CARE Hospital, a tertiary referral center for cardiovascular diseases. Three patients aged 68, 72 and 73 years did not consent to the high-risk operation, and were not included in the study. The data of 22 patients who underwent repair were retrospectively analyzed. Among these, 16 (72.7%) were operated on during the acute phase within 7 days after the onset of MI, 3 (13.6%) were operated on at 8–21 days and 3 had surgery 3–6 weeks after MI as they were referred late from other institutions. The septal rupture occurred 1–5 days (mean, 1.9 ± 1.6 days) after MI. All except 2 patients were male, with a mean age of 57.46 ± 5.31 years. Table 1
shows the preoperative clinical profile. All patients had a left-to-right shunt demonstrated by color Doppler. Intraaortic balloon pump support was initiated preoperatively in 15 patients with cardiogenic shock or congestive heart failure, and 4 of these also required assisted ventilation during preparation for surgical repair. The location of the ventricular septal defect (VSD) and LV and right ventricular (RV) function were assessed by 2D-echocardiography and color Doppler (Table 2, Figure 1). Postoperatively, 2D-echocardiography was carried out on all patients to assess ventricular function and residual or recurrent VSD (Figure 2). The variables tested as predictors of operative mortality were LV and RV dysfunction, preoperative renal failure, location of VSD and residual VSD.
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Figure 1. Thinned-out posterior basal interventricular septum with a ventricular septal defect (VSD) jet, in modified short-axis view. LV = left ventricle, RV = right ventricle.
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Figure 2. Intact endocardial patch with no residual shunt. LV = left ventricle, RV = right ventricle, VSD = ventricular septal defect.
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A transesophageal echocardiography probe was placed in all patients soon after induction of anesthesia. The heart was exposed through a standard median sternotomy. The left internal mammary artery was dissected at this stage if concomitant coronary artery bypass grafting was contemplated. Cardiopulmonary bypass was instituted using double-venous and ascending aortic cannulation after systemic heparinization. Myocardial protection was achieved with intermittent antegrade cold blood cardioplegia. Myocardial revascularization was performed first, followed by VSD repair. All significantly diseased coronary arteries were grafted when they supplied a non-infarcted area. The surgical technique used for repair of VSD was described by David and colleagues.13 In patients with anterior VSD, an incision was started near the LV apex 1–2 cm from, and parallel to, the left anterior descending coronary artery, and carried right through the infarcted muscle. The VSD was located, and the margins of the infarcted muscle were identified. A polytetrafluoroethylene patch was tailored according to the LV infarction and sutured to the lower part of the non-infarcted endocardium of the interventricular septum with a continuous 3/0 polypropylene suture. The patch was also sutured to the non-infarcted endocardium of the anterolateral ventricular wall. Once the patch was completely secured to the LV endocardium, the infarcted myocardium became largely excluded from the LV cavity. The ventriculotomy was simply closed over 2 strips of Teflon felt (Impra, Inc., Tempe, AZ, USA). In patients with posterior VSD, the incision was made in the LV inferior wall 1–2 mm from the posterior descending artery. The incision was started at the mid portion of the inferior wall and extended proximally towards the mitral annulus and distally towards the apex of the ventricle. The VSD margins were located in the proximal half of the posterior septum in 14 patients, and the posteromedial papillary muscle was involved in 5. A patch was tailored to a triangular shape of appropriate size. The base of the triangle was sutured to the annulus of the mitral valve with a continuous 3/0 polypropylene suture, starting at a point corresponding to the level of the posteromedial papillary muscle, and moving medially toward the septum until non-infarcted healthy endocardium was reached. The medial margin of the triangular patch was sutured to the healthy septal endocardium with a continuous suture. The side of the patch was sutured to the posterior LV wall, along a line corresponding to the medial margin of the base of the posteromedial papillary muscle. The infarcted RV wall was left undisturbed.
Data were summarized by frequencies and percentages for categorical factors, and means and standard deviations for continuous factors. Univariate odds ratios and 95% confidence intervals were calculated for different variables to determine their independent effect on operative mortality.
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RESULTS
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There were 5 operative deaths (22.7%): one patient could not be weaned off cardiopulmonary bypass, 2 died of low cardiac output, 1 died of septicemia leading to multiorgan failure, and another died of acute renal failure. The survivors required inotropic and intraaortic balloon pump support for 3.11 ± 0.76 days postoperatively. Four of the 5 patients who died had residual VSD. Three of 4 patients who were operated on within 24 hours of ventricular septal rupture died. Four of the survivors required assisted ventilation for more than 48 hours postoperatively. The intensive care unit stay for survivors was 4.11 ± 0.78 days; for non-survivors, it was 7.0 ± 1.0 days. The mean hospital stay for survivors was 12.56 ± 2.96 days. Six patients who presented in cardiogenic shock had serum creatinine > 2.0 mg·dL–1; 3 of them died, all of whom had a posterior ventricular septal rupture. All patients had complete revascularization at the time of VSD repair.
Univariate analysis showed cardiogenic shock, severe RV dysfunction, residual VSD and preoperative renal failure to be predictors of operative mortality. Table 3 shows the operative mortality in various subgroups of patients. Table 4 shows the univariate odds ratios and 95% confidence intervals calculated for different variables to determine their independent predictive value for operative mortality. Of 5 patients in whom the posteromedial papillary muscle was involved, 2 died in the immediate postoperative period, another died during follow-up 6 months after surgery, and 2 developed mild mitral regurgitation (regurgitant jet area 
3.0 cm2).
Seventeen patients who survived the operation were followed-up: 13 were in New York Heart Association class I and 2 were in class II at a mean follow-up of 19.2 ± 20.36 months. Patients with mild LV dysfunction operated on more than 3 weeks after MI were on antifailure treatment in the form of digoxin and diuretic therapy for 4 weeks. Antifailure treatment was continued for 6–12 weeks in all survivors with moderate to severe LV dysfunction. None of the patients needed any further revascularization procedure during follow-up. There were 2 late deaths at 6 and 8 months after repair, due to congestive heart failure. Both of these patients had a posterior VSD and there was no residual VSD during follow-up, but they developed moderate mitral regurgitation. The quality of life of the survivors was good. The Kaplan-Meier survival curve after early repair of postinfarction VSD is presented in Figure 3. Short-term survival (excluding hospital deaths) at 0, 6 and 9 months was 77.3%, 72.7% and 67.5% respectively.
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Figure 3. Kaplan-Meier survival curve for the patients undergoing repair of postinfarction ventricular septal defect. CUM Survival = cumulative survival.
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DISCUSSION
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Coronary artery disease occurs at a young age in the Indian population, and so does acute MI and its complications, such as septal rupture. The large GUSTO database showed a lower incidence of post-MI VSD (0.2%) and a shorter time interval between MI and ventricular septal rupture (median, 1 day) than in the pre-thrombolytic era.8 Despite advances in surgical care, operative mortality is still considerable, approaching 50%, with the major risk factors being cardiogenic shock, renal failure, RV and/or LV failure, posterior/inferior location and residual VSD.14 The management consists of VSD closure, myocardial revascularization and aggressive end-organ support.
Residual shunts are found up to 40% of patients after repair.15 It was recommended that most patients with post-MI VSD presenting in cardiogenic shock or congestive heart failure should be operated on urgently if they are in a hemodynamically stable condition, and immediately if they are in cardiogenic shock.13,15 The operative risk increases if multiorgan dysfunction is allowed to develop, particularly renal failure5. Cardiogenic shock has been identified as the single most important determinant of operative mortality in many series as well as in our study.12,16 Cardiogenic shock in patients with postinfarction VSD is caused by various factors, but RV dysfunction is the most important, particularly in patients with posterior VSD who often have extensive RV dysfunction.17 The need for urgent repair after diagnosis is a consistent risk factor for early mortality.18
The traditional operative techniques for patients with post-MI VSD consisted of infarctectomy and reconstruction of the LV and RV walls with a Dacron fabric graft.10 These procedures were associated with increased LV and RV dysfunction, and consequently high operative mortality19. A double-patch and glue technique using left and right ventriculotomies was introduced, with a lower incidence of recurrent VSD.14 The operative mortality rate in most series ranged from 35% to 50%, with the exception of the study by Skillington and colleagues16 in which the overall mortality rate was 20.8%. The technique of endocardial patch with infarct exclusion is physiologically sound and should enhance operative survival because it leaves the right ventricle undisturbed and restores LV geometry; reported operative mortality is 13.5%.13 Although cardiogenic shock is an important determinant of operative mortality, it does not alter the long-term outcome of survivors. Factors such as LV function, renal failure and extent of coronary artery disease are important, and patients in cardiogenic shock should be aggressively treated with intraaortic balloon pump support, vasodilators, inotropes and assisted ventilation if necessary prior to coronary angiography; the operation should follow soon after angiography.12 Patients with postinfarction VSD require considerable hospital resources when they are admitted in cardiogenic shock. In our series, 15 of 22 patients were in cardiogenic shock or congestive heart failure, and the operative mortality was 23% which is comparable to recent reports.15,16 Intensive care unit stay was prolonged for patients in cardiogenic shock compared to those not in shock.
The repair of acute postinfarction VSD by endocardial patch with infarct exclusion probably avoids additional damage to the right ventricle. Cardiogenic shock, renal dysfunction, RV dysfunction on admission^ and residual VSD are important predictor of hospital mortality.
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ACKNOWLEDGMENTS
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We sincerely thank Dr. Bhogaraju Anand, MBBS, DNB (Psy), BPM, OYPC of Care Foundation, for the statistical analysis of this study.
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REFERENCES
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ABSTRACT
INTRODUCTION
