|Year : 2022 | Volume
| Issue : 2 | Page : 80-86
Postoperative outcomes in patients with post infarction ventricular septal defect – Institutional experience
Deepti Kakkar, Devvrat Desai
U. N. Mehta Institute of Cardiology and Research Centre, Civil Hospital Campus, Ahmedabad, Gujarat, India
|Date of Submission||12-Mar-2022|
|Date of Decision||28-Mar-2022|
|Date of Acceptance||23-Apr-2022|
|Date of Web Publication||12-Aug-2022|
Dr. Devvrat Desai
Department of Cardiovascular and Thoracic Surgery, U. N. Mehta Institute of Cardiology and Research Centre, Civil Hospital Campus, Asarva, Ahmedabad - 380 016, Gujarat
Source of Support: None, Conflict of Interest: None
Context: Postinfarction ventricular septal defect (VSD) is a rare but serious complication of myocardial infarction with a reported incidence of 1% to 3% in the pre thrombolytic era and <0.5% post thrombolytic therapy. Risk of death is greatest immediately after myocardial defect and then gradually declines. Early surgical treatment is recommended; however, surgical repair is associated with a high rate of mortality.
Aim: To investigate the immediate survival outcome and prognostic factors associated with surgical repair of postinfarction ventricular septal rupture at our institute over a 3-year period.
Materials and Methods: From April 2012 to April 2015, 32 patients underwent surgical repair of post-infarction ventricular septal rupture at our institute. Patients were identified from the electronic medical records database and preoperative, intraoperative, and postoperative variables were retrieved. Multiple perioperative variables such as anthropometric data, demography, and clinical history and preoperative details such as echocardiographic indices, coronary angiography, and intraoperative variables were analyzed. The outcomes were compared between the survivors and nonsurvivors.
Results: Overall, younger patients tolerated the disease and the surgery better than the older population (59.96 ± 10.67 vs. 69.11 ± 8.11; P = 0.02). Female sex, cardiogenic shock (n = 20, 86.95% vs. n = 2, 22.22%; P = 0.001), and emergency surgery were independently associated with higher risk of postoperative mortality. History of systemic hypertension was found to be significantly associated with poor postoperative outcomes (survivors n = 9, 39.1% vs. nonsurvivors n = 8, 88.9%; P = 0.017). In our series, the overall mortality was 28.1% (n = 9). Higher NYHA class at presentation, intra-aortic balloon pump requirement and low ejection fraction are all independently associated with poor outcomes. Longer interval between the myocardial infarct and surgical repair is associated with a lower risk of operative mortality. Preoperative renal dysfunction (61.77 ± 19.04 vs. 41.36 ± 21.15; P = 0.025) and postoperative renal dysfunction (65.26 ± 28.81 vs. 27.27 ± 9.04; P = 0.001) is one of the most important predictors of postoperative outcome. The duration of aortic cross-clamp and cardiopulmonary bypass was not associated with early mortality in this study (89.17 ± 42.70 vs. 97.11 ± 76.38; P = 0.775).
Conclusion: Postinfarction VSD still remains one of the most challenging conditions to treat surgically with considerable early mortality. Although percutaneous device closure and left ventricular assist devices may be used as a method to stabilize the patient preoperatively and improve the chances of survival after surgery, it is currently not advocated as a definitive treatment option. All efforts should be made to predict and prevent postoperative renal dysfunction as it is the single-most important factor affecting both short- and long-term survival outcomes.
Keywords: Cardiogenic shock, complications of myocardial infarction, coronary artery bypass grafting, early outcome, ventricular septal defect
|How to cite this article:|
Kakkar D, Desai D. Postoperative outcomes in patients with post infarction ventricular septal defect – Institutional experience. Heart India 2022;10:80-6
|How to cite this URL:|
Kakkar D, Desai D. Postoperative outcomes in patients with post infarction ventricular septal defect – Institutional experience. Heart India [serial online] 2022 [cited 2022 Sep 29];10:80-6. Available from: https://www.heartindia.net/text.asp?2022/10/2/80/353734
| Introduction|| |
Postinfarction ventricular septal defect (VSD) is an opening in the ventricular septum resulting from rupture of acutely infarcted myocardium. It is a rare but serious complication of myocardial infarction (MI) with a reported incidence of 1% to 3% in the pre thrombolytic era and <0.5% with thrombolysis.,, Usual time of occurrence is within 1 week in nonthrombolysed patients and within ≤24 h of thrombolysis.
Most of the successful operative cases were reported in patients with congestive heart failure weeks after the initial infarct; hence, it was believed that surgery should be delayed to allow scaring of the necrotic myocardium to provide for a more stable repair. With growing experience, improvement in surgical techniques and postoperative management, early repair is advocated, particularly in stable patients, before hemodynamic deterioration and associated multiorgan failure ensue.
Without surgical treatment, early death is common; <30% of patients survive 2 weeks, and only 10% to 20% survive more than 4 weeks.,,, Risk of death is greatest immediately after MI and then gradually declines. The diagnosis of postinfarction VSD in itself is an indication for operation because of the associated large left-to-right shunt and poor outcomes if left untreated.,, However, surgical repair is associated with high mortality. Hospital mortality after postinfarct VSD repair is approximately 30% to 40%. 5-year survival ranges from 44% to 57% and 10-year survival is about 29% to 36%.,,, The identification of risk factors for poor outcomes after traditional surgical repair may help identify the patients who are most likely to benefit from intervention.
Aim and objective
This study aims to investigate the immediate survival outcome and prognostic factors associated with surgical repair of postinfarction ventricular septal rupture at our institute over a 3-year period. Our objective is to identify preoperative clinical characteristics and their effects on the associated complications and immediate in hospital outcomes in our institute in all the patients who underwent surgical repair of postinfarction ventricular septal rupture from April 2012 to April 2015.
The perioperative risk factors such as time from infarct to development of VSD, time from the diagnosis of VSD to surgery, cardiogenic shock, preoperative renal function, intra-aortic balloon pump (IABP) and inotropic support, effect of concomitant coronary revascularization and their influence on the postoperative outcome were assessed.
The postoperative outcomes, including prolonged mechanical ventilation, stay in intensive care, the incidence of low cardiac output and multiorgan dysfunction, residual defect, and cerebrovascular accidents, were compared in the survivors and the nonsurvivors groups.
Cardiogenic shock is defined as (1) systolic blood pressure <80 mm Hg or cardiac index below 1.8 L/min/m2 despite maximal treatment, or (2) intravenous inotropes or IABP, or both, necessary to maintain systolic blood pressure above 80 mm Hg or cardiac index above 1.8 L/min/m2). Stroke is defined as documented (computed tomography/magnetic resonance imaging) anatomical insult resulting in irreversible cerebrovascular damage. Acute kidney injury is defined as oliguria, reduced eGFR, rising BUN, and serum potassium levels requiring renal replacement therapy as per the below-mentioned criteria. Deep vein thrombosis is defined by the Doppler assessment of the thrombus. Sepsis defined by TC ≥11,000/cu mm, fever ≥100o F, raised levels of C-reactive protein, procalcitonin, isolation of any organism on culture and sensitivity from either blood, urine, endotracheal secretions.
| Materials and methods|| |
From April 2012 to April 2015, 32 patients underwent surgical repair of postinfarction ventricular septal rupture at our institute. Patients were identified from the electronic medical records, and preoperative, intraoperative, and postoperative variables were retrieved. All the patients referred or diagnosed with known postinfarction ventricular septal rupture on the basis of clinical findings, echocardiography, and conventional angiography. Patients with severe preoperative cardiogenic shock, severe renal dysfunction, neurological obtundation, and cardiac index <1.5 L/min/m2 were considered inoperable and excluded from the study group. Patients undergoing redo surgeries and concomitant surgery for cardiac valve replacement or repair were excluded from the study group.
The statistical analysis was performed using Statistical Package for Social Sciences ver 22.0, IBM, USA. Continuous variables are described as mean ± standard deviation. Categorical variables are described as frequency and percentage. Demographic variables of age, gender, height, weight, BSA, DM, HTN, history of smoking, angina and infraction, and location of infarct were collected. Clinical variables like vitals, the timing of surgery, preoperative and postoperative renal function, serum creatinine, inotropic support, pre- and postoperativeventilation, pre- and postoperative IABP were collected. Postoperativeoccurrence of stroke, DVT, infection, arrhythmia, and mortality was analyzed.
Shapiro–Wilk test was used to find the normality. Student's paired t-test or Mann–Whitney was used to find the significance difference between the pre and post comparisons of serum creatinine, BUN, IABP, and inotropes. Independent t-test was used here to compare the means between two unrelated groups (survivors vs. nonsurvivors) on the same continuous variables. Chi-square or Fisher's exact test was used to measure the association between the gender, Preoperative angina, smoking, diabetes, hypertension with complications. P < 0.05 was considered statistically significant.
During the study period, the patients who were diagnosed with postinfarction VSD and planned for surgical repair underwent initial workup, including basic hematological investigation, chest X-ray, electrocardiogram and trans-thoracic Echocardiography. They were hemodynamically stabilized with IABP, inotropic support, and mechanical ventilation as and when required. Transesophageal Echocardiography was performed immediately after the induction of general anesthesia for all the patients.
All patients had a midline sternotomy approach, if concomitant coronary artery revascularization was planned, conduits either left internal mammary artery (LIMA) or Saphenous vein graft (RSVG) or both were prepared as per individual patient requirement., Cardiopulmonary bypass was established using aortic and selective Bicaval cannulation technique. Aortic cross-clamp applied. The patient was cooled to 28°C, and myocardial protection was achieved with cold blood cardioplegia (St. Thomas Solution) at 4°C via antegrade route. Cavae snared. Left heart vented via the Right superior pulmonary vein.
The VSD was approached through the left ventricle, the advantages being a clear view not encumbered by trabeculae carnae and placement of the patch on the high-pressure side of the defect, ensuring a more secure closure. In the case of an anterior infarct, ventriculotomy was done in the area between viable and infarcted myocardium 1–2 cm from and parallel to the anterior descending artery [Figure 1]. The location of VSR, the margins of the infarcted muscle, anatomy of the Mitral valve are inspected.
|Figure 1: Ventriculotomy incision in presence of anterior ventricular septal defect. Repair using pledgetted sutures on the polytetrafluoroethylene patch and noninfarcted myocardium. LV: Left ventricular, RV: Right ventricular|
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The defect is repaired using 0.6 mm thickness polytetrafluoroethylene (PTFE) patch (GORE-TEX), which is sutured on the LV side of the septum with pledgetted sutures securing it to the noninfarcted myocardium on the ventricular septum. Infarcted myocardium is not excised. Ventriculotomy is closed with interrupted polyester sutures buttressed on either side between PTFE felt strips and further reinforced with 2-0 polypropylene continuous sutures.
In the case of posterior VSD, the heart is lifted out of the pericardium and stabilized with a wet sponge underneath. The defect is approached through a vertical incision on the LV along the occluded posterior descending artery. PTFE patch is used to close the VSD; the posterior ventricular wall is repaired with the second patch using mattress sutures. Occasionally, depending on the size and quality of free wall myocardium, the free edges can be approximated and closed primarily (and reinforced with a pericardial or felt strip) rather than using a second patch.
In three patients, the VSD was closed directly using pledgetted sutures and the same number underwent additional left ventricular remodeling surgery using the Dor technique. Twelve patients underwent concomitant coronary artery bypass grafting using either LIMA or RSVG or both as per the requirement following the standard practice.
| Observations and results|| |
Out of total of 32 patients, 62.5% patients were male.(n = 20). This correlates well with reports by Radford et al. l of a male preponderance (male: female = 3:2) The mean age of the sample population was 62.53 ± 10.83 years.(n = 32) For further analysis, we divided the study population into survivors (n = 23, 71.9%) and nonsurvivor (n = 9, 28.1%) subgroups. The overall mean age in the survivor group was significantly younger than the age of the nonsurvivors (59.96 ± 10.67 vs. 69.11 ± 8.11; P = 0.02). Mean height was 160.55 ± 8.07 cm (range-142–175 cm). The weight distribution was in the range of (45–90 kg) with a mean of 60.63 ± 12.15 kg and mean BSA of 1.63 ± 0.17 m2 (range 1.33–2.00 m2).
Past history of systemic hypertension (n = 17, 53.1%), diabetes mellitus (n = 20, 62.5%), smoking (n = 12, 37.5%) were included. All the patients had a positive history of coronary artery disease. One patient had a history of cerebrovascular accident without any residual neurological deficit. Two patients were known cases of chronic kidney disease not requiring dialysis. At the time of admission to our institution, 18.7% of patients were found to be in NYHA Functional Class II, 43.8% of patients were in NYHA Class III, and 37.5% presented in NYHA Class III and 37.5% presented in NYHA Class IV [Figure 2].
Anterior wall MI (n = 22, 68.8%) was the most common among all, explaining Apico-anterior VSD to be most frequent due to involvement of LAD. Antro-septal and Inferior wall MI were present in small proportion. Six out of 32 patients were thrombolysed (18.8%) using Streptokinase at a peripheral center. The duration from Acute MI to thrombolysis varied between 6 and 8 h. Thrombolytic therapy appears to reduce the overall incidence of cardiac rupture, probably by restoring vessel patency, salvaging myocardium, and preventing ongoing infarct expansion, resulting in a decreased incidence of late myocardial rupture.,,
The most common clinical presentation was acute pulmonary edema with highly unstable hemodynamics (n = 10, 31.25%) requiring supportive measures for stabilization, including mechanical ventilator support, IABP support and/or inotropic support. The mean preoperative intensive care stay was 35.5 ± 60.57 h, with seven patients (21.87%) requiring mechanical ventilator support. The mean duration for preoperative mechanical ventilator requirement was 5.13 ± 15.38 h. 19 patients (59.37%) required inotropic support and 21 patients (65.62%) needed IABP insertion, the mean duration for IABP requirement was 29.09 ± 31.3 h. The mean S. Creatinine level was 1.74 ± 0.64 mg/dl in patients with known renal dysfunction. Glomerular filtration rate was significantly low, with a mean of 41.30 ± 12.59 ml/min/1.73 m2. The preoperative BUN level was 26.99 ± 11.35 mg/dl. Preoperative ejection fraction for all the patients was on the lower side with a mean of 40.56% ±8.0. The most common location for ventricular septal rupture was Apical VSD.(n = 23, 71.9%) Others being mid-muscular (n = 7, 21.9%) and posterobasal.(n = 2, 6.3%). The size of the VSD and the compliance of the ventricles determines the amount of the shunt. In our case series, the largest VSD was 15 mm apical VSD with a gradient of 35 mm Hg across it. The smallest VSD was found in the mid-muscular region, 2 mm in size. The mean size of the ventricular defect was 7.27 ± 2.82 mm.
Preoperative transthoracic echocardiography revealed increased pulmonary artery systolic pressure in all patients, with a mean pulmonary artery systolic pressure of 45.09 ± 9.83 mm Hg. Increased PA pressure has a significant impact on the immediate postoperative outcomes for the patients [Table 1].
Conventional coronary angiography was done in all patients, and left anterior descending artery had total or subtotal occlusion in almost all the patients. Right coronary artery (n = 25, 78.12%) and left circumflex (n = 20, 62.5%) were also involved. The involvement of all three coronary arteries was found more commonly associated with massive myocardial infarct and VSD (n = 19, 59.37%) Some patients with double-vessel disease (n = 6, 18.75%) and single-vessel disease (n = 6, 18.75%) also had significant MI, followed by ventricular septal rupture.
The mean duration for symptoms to surgery was 94.76 ± 85.59 h. The selection of techniques for the surgery was completely individualized. The most common technique used was the modified two patch infarct exclusion technique (n = 29, 90.62%) the other being direct closure of defect (n = 3, 9.37%). The additional surgical left ventricular restoration was done in three patients using Dor's technique (n = 3, 9.37%). Twelve patients (37.5%) underwent concomitant coronary bypass grafting, the rest were not amenable to coronary revascularization in view of poor target coronary vessels. The mean cardiopulmonary bypass time was 137.91 ± 68.76 min and mean aortic cross-clamp time was 91.41 ± 53.03 min [Table 2].
The overall mean postoperative mechanical ventilation required was 66.41 ± 51.10 h, with mean postoperative intensive care stay 179.55 ± 147.11 h. The mean total postoperative hospital stay was 16.56 ± 9.21 days.
During immediate postoperative intensive care stay, almost all patients required prolonged inotropic support. The mean duration for the inotropic support requirement was 131.06 ± 98.99 h. Patients who needed high inotropic support or the intra-aortic balloon pump support were considered to have unstable hemodynamics.(n = 9, 28.1%). The mean duration for intra-aortic balloon pump support was 69.88 ± 49.01 h. In view of poor hemodynamics, continuous cardiac output was monitored using CCO catheter (Swan-Ganz), which helped in titrating the inotropic support better. The mean duration for cardiac output monitoring was 84.81 ± 46.05 h [Table 3].
All the patients prophylactically received anti-arrhythmic agent, amiodarone as intravenous infusion as post ventriculotomy patients are prone for arrhythmia in immediate postoperative period. In spite of being on amiodarone, total 12.5% patients experienced ventricular arrhythmia (n = 4).
Survivors versus nonsurvivors
For better understanding, we divided our study sample in further subgroups: Survivors (n = 23, 71.9%) and non survivors (n = 9, 28.1%) All the peri-operative variable were compared for these subgroups. The mean age of the nonsurvivor group was higher than the survivor group (59.96 ± 10.67 vs. 69.11 ± 8.59; P = 0.021), implying older age to be a significant risk factor. Height, weight, and body surface area were found to be nonsignificant. Females were at higher risk compared to male with significant P = 0.049.
History of systemic hypertension (n = 9, 39.1% vs. n = 8, 88.9%; P = 0.017) was associated with poor outcomes. Role for thrombolysis (n = 3, 13% vs. n = 3, 33.3%; P = 0.314) and urgent percutanesous revascularization (n = 2, 8.7% vs. none; P = 1) was found controversial with nonsignificant P values.
The nonsurvivors had unstable hemodynamics (n = 7, 77.77% vs. n = 2, 8.69%; P = 0.001) as compared to the survivor group. Similarly, the patients with stable hemodynamics at time of presentation preoperatively had better survival compared to unstable patients (n = 20, 86.95% vs. n = 2, 22.22%; P = 0.001), concluding that any hemodynamic instability pre or postoperatively is a predictor for poor outcome.
In the survivor group, mean time of preoperative intensive care stay was higher than the nonsurvivor group (44.65 ± 65.37 vs. 27.33 ± 52.07; P = 0.443). Furthermore, the mean duration for intra aortic balloon support was higher in the survivor group (26.17 ± 33.53 vs. 8.55 ± 10.22; P = 0.135). Although it was not significant statistically, it helped in decision-making. In nonsurvivor group, the requirement for mechanical ventilation support (4.00 ± 16.75 vs. 7.44 ± 10.41; P = 0.491) and inotropic support (20.48 ± 23.67 vs. 29.44 ± 51.76; P = 0.629) were higher. In nonsurvivors, the renal dysfunction was already established with significantly low glomerular filtration rate (61.77 ± 19.04 vs. 41.36 ± 21.15; P = 0.025), higher levels of mean serum creatinine (1.32 ± 0.58 vs. 1.7 ± 0.59; P = 0.119) and BUN levels.
On preoperative echocardiography, the ejection fraction (41.52 ± 6.77 vs. 38.11 ± 10.59; P = 0.389) was on lower side for nonsurvivor group. The VSD morphology significantly affected the outcomes. The small restricted VSDs (8.00 ± 2.45 vs. 5.50 ± 3.02; P = 0.05) with higher gradient across the VSD (51.48 ± 14.28 vs. 68.44 ± 22.15; P = 0.015) and high systolic pulmonary artery pressure (42.96 ± 7.96 vs. 50.55 ± 12.37; P = 0.047) were found more in nonsurvival group. Intraoperative variables, such as cardiopulmonary bypass time (131.04 ± 62.43 vs. 155.44 ± 84.38; P = 0.447) and aortic cross-clamp time (89.17 ± 42.70 vs. 97.11 ± 76.38; P = 0.775), were not significantly different; however, both were higher in nonsurvivor group. Concomitant revascularization had no statistical significance in survival. The mean length of stay in intensive care was 201.48 ± 151.45 h [Table 4].
Immediate postoperative bleeding requiring the re-exploration was seen significantly higher in the nonsurvivor group (n = 1, 4.3% vs. n = 3, 33.3%; P = 0.057) which added to the morbidity and poor outcome. Only one patient had cerebrovascular accident in the survivor group. Sepsis was diagnosed more in nonsurvival group but not statistically important (21.7% vs. 55.6%; P = 0.096).
Some of the patients experienced multiorgan dysfunction (n = 11, 34.4%) which included acute kidney injury (n = 11, 34.4%), of which 5 (15.6%) had to undergo dialysis. The kidney function tests done in the postoperative period showed a significantly deranged profile in nonsurvivor group. In the nonsurvivor group, almost all patients had multiorgan dysfunction and ended up in low cardiac output state, which explains the cause for higher morbidity and mortality.
Limitations of the study
Ours being a single center retrospective study, we are unable to certify that all the potential confounders have been examined. This study is further limited by the lack of an ideal control group of patients with similar disease entities but managed conservatively. The relatively short postoperative follow-up period does not provide information about the long-term outcomes and the factors affecting it in the survivor group. Furthermore, we were not able to compare all the variables in the patients who underwent surgery but had a very early postoperative death which adds to the confounding factors. The lack of data about the patients who died while waiting for surgery or electively opted out from the high-risk procedure due to financial limitations is an added limitation of this study. For a better understanding of the disease, associated risk factors and outcomes, a multicenter prospective study is required.
| Conclusion|| |
Postinfarction VSD still remains one of the most challenging conditions to treat surgically with considerable early mortality. Although percutaneous device closure and left ventricular assist devices may be used as a method to stabilize the patient preoperatively and improve the chances of survival after surgery,,, it is currently not advocated as a definitive treatment option. All efforts should be made to predict and prevent postoperative renal dysfunction as it is the single most important factor affecting both short- and long-term survival outcomes.
Institutional Ethics Committee approval was taken for this study.
Both the authors have contributed equally in designing the analysis, data collection, data analysis, manuscript writing.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Crenshaw BS, Granger CB, Birnbaum Y, Pieper KS, Morris DC, Kleiman NS, et al.
Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. GUSTO-I (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) Trial Investigators. Circulation 2000;101:27-32.
Sá MP, Sá MV, Barbosa CH, Silva NP, Escobar RR, Rueda FG, et al.
Clinical and surgical profile of patients operated for postinfarction interventricular septal rupture. Rev Bras Cir Cardiovasc 2010;25:341-9.
Birnbaum Y, Fishbein MC, Blanche C, Siegel RJ. Ventricular septal rupture after acute myocardial infarction. N Engl J Med 2002;347:1426-32.
Brunn F. On the diagnosis of acquired rupture of the ventricular septum of the heart. Wien Arch Inn Med 1923;6:533.
Cooley DA, Belmonte BA, Zeis LB, Schnur S. Surgical repair of ruptured interventricular septum following acute myocardial infarction. Surgery 1957;41:930-7.
Fukushima S, Tesar PJ, Jalali H, Clarke AJ, Sharma H, Choudhary J, et al.
Determinants of in-hospital and long-term surgical outcomes after repair of postinfarction ventricular septal rupture. J Thorac Cardiovasc Surg 2010;140:59-65.
Jeppsson A, Liden H, Johnsson P, Hartford M, Rådegran K. Surgical repair of post infarction ventricular septal defects: A national experience. Eur J Cardiothorac Surg 2005;27:216-21.
Heitmiller R, Jacobs ML, Daggett WM. Surgical management of postinfarction ventricular septal rupture. Ann Thoracic Surg 1986;41:683-91.
Ryan TJ, Anderson JL, Antman EM, Braniff BA, Brooks NH, Califf RM, et al
. ACC/AHA guidelines for the management of patients with acute myocardial infarction: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Acute Myocardial Infarction). J Am Coll Cardiol 1996;28:1328-419.
O'Gara PT, Kushner FG, Ascheim DD, Casey DE, Chung MK, De Lemos JA, et al
. ACCF/AHA guideline for the management of ST-elevation myocardial infarction: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2013;61:e78-140.
Mehta RL, Kellum JA, Shah SV, Molitoris BA, Ronco C, Warnock DG, et al.
Acute Kidney Injury Network: Report of an initiative to improve outcomes in acute kidney injury. Crit Care 2007;11:R31.
Stone GW, Ohman EM, Miller MF, Joseph DL, Christenson JT, Cohen M, et al.
Contemporary utilization and outcomes of intra-aortic balloon counterpulsation in acute myocardial infarction: The benchmark registry. J Am Coll Cardiol 2003;41:1940-5.
Barker TA, Ramnarine IR, Woo EB, Grayson AD, Au J, Fabri BM, et al.
Repair of post-infarct ventricular septal defect with or without coronary artery bypass grafting in the northwest of England: A 5-year multi-institutional experience. Eur J Cardiothorac Surg 2003;24:940-6.
Perrotta S, Lentini S. In patients undergoing surgical repair of post-infarction ventricular septal defect, does concomitant revascularization improve prognosis? Interact Cardiovasc Thorac Surg 2009;9:879-87.
Radford MJ, Johnson RA, Daggett WM Jr, Fallon JT, Buckley MJ, Gold HK, et al.
Ventricular septal rupture: A review of clinical and physiologic features and an analysis of survival. Circulation 1981;64:545-53.
Peuhkurinen KJ, Risteli L, Melkko JT, Linnaluoto M, Jounela A, Risteli J. Thrombolytic therapy with streptokinase stimulates collagen breakdown. Circulation 1991;83:1969-75.
Hillis LD, Firth BG, Winniford MD. Variability of right-sided cardiac oxygen saturations in adults with and without left-to-right intracardiac shunting. Am J Cardiol 1986;58:129-32.
Sai-Sudhakar CB, Firstenberg MS, Sun B. Biventricular mechanical assist for complex, acute post-infarction ventricular septal defect. J Thorac Cardiovasc Surg 2006;132:1238-9.
Samuels LE, Entwistle JC 3rd
, Holmes EC, Parris T, Wechsler AS. Mechanical support of the unrepaired postinfarction ventricular septal defect with the Abiomed BVS 5000 ventricular assist device. J Thorac Cardiovasc Surg 2003;126:2100-1.
Thiele H, Kaulfersch C, Daehnert I, Schoenauer M, Eitel I, Borger M, et al.
Immediate primary transcatheter closure of postinfarction ventricular septal defects. Eur Heart J 2009;30:81-8.
[Figure 1], [Figure 2]
[Table 1], [Table 2], [Table 3], [Table 4]