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Ann Thorac Surg 2008;85:1591-1596. doi:10.1016/j.athoracsur.2008.01.010
© 2008 The Society of Thoracic Surgeons

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Right arrow Myocardial infarction


Original Articles: Adult Cardiac

Ventricular Septal Rupture Complicating Acute Myocardial Infarction: Clinical Characteristics and Contemporary Outcome

Steen Hvitfeldt Poulsen, MD, DMScia, Michael Præstholm, MDa, Kim Munk, MDa,*, Per Wierup, MD, DMScib, Henrik Egeblad, MD, DMScia, Jens Erik Nielsen-Kudsk, MD, DMScia

a Department of Cardiology, Aarhus University Hospital, Skejby, Denmark
b Department of Cardiothoracic Surgery, Aarhus University Hospital, Skejby, Denmark

Accepted for publication January 2, 2008.

* Address correspondence to Dr Munk, Department of Cardiology, Aarhus University Hospital, Skejby, Brendstrupgaardsvej 100, 8200 Aarhus N, DK 8200, Denmark (Email: kim.munk{at}ki.au.dk).


    Abstract
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
Background: The objective of this paper was to study the patient characteristics and contemporary short- and long-term outcome in patients with postinfarct ventricular septal rupture.

Methods: Based on patient files and register data we performed a review of 64 consecutive patients with ventricular septal rupture complicating acute myocardial infarction, admitted to our tertiary center.

Results: The mean age of the patients was 70 ± 7. The median time was five days from onset of symptoms to the diagnosis of the ventricular septal rupture. The overall 30-day, one-, and five- year mortalities were 62%, 72%, and 95%, respectively. Medical treated patients (n = 19) had a 30-day mortality of 100%. Among surgically treated patients (n = 45) the survival at one month, one and five years was 71%, 48%, and 32%, respectively. History of hypertension, complicating congestive heart failure, and age were associated with poor outcome.

Conclusions: Despite improvements in medical and interventional techniques the early as well as the long-term prognosis remains poor in this contemporary series.


    Introduction
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
Ventricular septal rupture in acute myocardial infarction (AMI) is a well-recognized mechanical complication associated with a very high mortality [1–3]. The use of thrombolytic agents seems to have reduced the incidence from 1% to 2% in the prethromobolytic era to 0.2% [1, 2, 4]. In the prethrombolytic era septal rupture occurred most often in the first week of AMI, typically three to five days after onset of symptoms [1, 4, 5]. The outcome after septal rupture in the prethrombolytic era was extremely poor, with an in-hospital mortality rate of approximately 45% in surgically treated patients and 90% in medically managed patients [1–3]. Predictors of a poor late outcome in this population included cardiogenic shock, inferior infarction, and poor right ventricular function [4, 6–8]. After introduction of thrombolysis and primary percutaneous coronary intervention, the clinical characteristics and course in unselected postinfarction ventricular septal defect patients have mainly been examined in relatively small studies or in subgroup analysis. Data in larger selected postinfarction populations are available from the SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK? (SHOCK) registry trial and the Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries (GUSTO-I) trial [9, 10]. However, in the SHOCK trial only patients with manifest shock were included and data were far from complete in each and every patient. In the GUSTO-I trial, the patient profile was biased due to the particular enrolment criteria used in this study [9, 10]. Data from these selected populations indicate that the overall mortality rates remain high with 73.8% at 30 days in the GUSTO trial and 87% in the SHOCK trial [9, 10]. Hence, the aim of this paper was, in a contemporary group of consecutive patients with postinfarction ventricular septal defect referred to our tertiary center, to study the patient characteristics, the short and long-term outcomes, and the influence of different treatment strategies on outcome.


    Patients and Methods
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
We reviewed the medical records of 64 consecutive patients admitted to our tertiary cardiac center with ventricular septal rupture complicating AMI during the period from January 1993 to December 2002. Data were collected retrospectively. Individual consent for participation was therefore not obtained. This approach was approved by the local ethical committee. The diagnosis of AMI was based on typical clinical symptoms, electrocardiographic signs of infarction, and a documented elevation of cardiac enzymes (creatine kinase and creatine kinase MB fraction) to at least twice the upper normal limits. The ventricular septal rupture was diagnosed by echocardiography (disrupted ventricular septum with evidence of left-to-right shunt by color Doppler) in all cases.

Demographic data, medical history, electrocardiographic patterns, Killip class, hemodynamic data, and angiographic and echocardiographic findings were obtained for each patient. Medical treatment and scheduled timing of surgery were noted. Two-dimensional Doppler echocardiography was performed in all patients to assess left ventricular systolic function, location and character of the ventricular septal defect, Doppler pressure gradient, and systolic pulmonary artery pressure.

The overall strategy of the department throughout the study period was to delay surgical repair for at least 3 to 14 days according to each surgeon's preference, in the hope that the septal muscle would become sturdier over time. All patients were operated with a uniform technique, using a single Dacron patch (Bard Medical, Tempe, AZ).

A division between early (≤2 days from diagnosis of ventricular septal defect) and late (>2 days) surgery was used to distinguish those who needed acute-subacute operation because they were decompensated or were judged to be too unstable at the time of diagnosis from those who underwent scheduled surgery.

Mortality
Causes of death and survival information for the entire population were obtained from medical records and through the Danish Central Personnel Register, where all deaths in the country are recorded within two weeks. The survival information was obtained in February 2003.

Statistical Analysis
Continuous variables were summarized as mean ± SD and the rank sum test was used for comparisons. Categoric variables were compared by the {chi}2 test. Survival rates were plotted according to the Kaplan-Meier method and comparison of survival rates between subgroups were tested with the log-rank test. A multivariate Cox proportional hazard analysis was performed to identify independent predictors of cardiac death. Variables included were age, heart rate, a history of hypertension, diabetes mellitus, Killip class, infarct location, systolic blood pressure, ejection fraction, and previous myocardial infarction. A p value of less than 0.05 was considered significant. SPSS version 10.0 (SPSS Inc, Chicago, IL) was used for calculations.


    Results
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
Clinical Characteristics
Table 1 displays the baseline characteristics for the 64 patients. Median time from debut of AMI symptoms to diagnosis of the ventricular septal rupture was five days (range, 0 to 195 days). Twenty-seven percent and 64% of the cases were diagnosed within two days, respectively, one week after the reported onset of AMI symptoms (Fig 1).


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Table 1 Patient Characteristics
 

Figure 1
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Fig 1. The time course from onset of symptoms to diagnosis of the left ventricular septal rupture.

 
Based on electrocardiographic (ECG) findings, the index myocardial infarction was inferior in 29 patients, anterior in 30 patients, and combined anterior and inferior in 3. The index myocardial infarction was characterized by ST-segment elevation and (or) Q-waves in 97% of cases. Two patients presented with left bundle branch block. Based on echocardiography, the location of the septal rupture was equally distributed between an anterior and inferior-posterior location.

Angiographic and Hemodynamic Data
Coronary angiography was performed in 55 patients (86%). The majority had single-vessel or double-vessel coronary artery disease (51% and 31%, respectively) while the remaining 18% had triple-vessel disease. The left anterior descending artery was identified as the infarct-related artery in 23 patients (42%), the right coronary artery in 29 patients (53%), and the left circumflex artery in only 3 patients (5%).

Hemodynamic characteristics are shown in Table 2. At admission, 32% and 59% of the patients demonstrated a systolic blood pressure less than 90 mm Hg and less than 100 mm Hg, respectively. A heart rate greater than 100 beats per minute was noted in 41% of all cases. The mean left ventricular ejection fraction was mildly reduced (mean, 0.44 ± 0.1; range, 0.25 to 0.65) and was significantly higher in inferior infarcts compared with anterior infarcts (0.47 ± 0.09 vs 0.41 ± 0.09, p < 0.02). None of the patients demonstrated severe mitral valve regurgitation. Consistent with the presence of a left-to-right shunt, the pulmonary systolic pressure was elevated as assessed by Doppler measurements of tricuspid valve regurgitation jets (Table 2).


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Table 2 Hemodynamic Profile of Patients
 
Treatment
Thrombolytic therapy had been administrated in 28 patients (44%) while seven of the patients (11%) underwent primary angioplasty. Vasopressor therapy was given in 38 patients (59%) combined with intraaortic balloon counter pulsation therapy (IABP) in 35 patients (55%). Acute severe renal failure developed during the first 24 hours in 6 patients. They were treated with hemodialysis.

Ventricular septal rupture repair was performed in 45 patients (70%) and patients with more than one-vessel disease had concomitant coronary artery bypass grafting (42%). Patients treated medically were significantly older, and a history of hypertension and advanced heart failure were more frequently present compared with patients who underwent surgery (Table 3). The median time from the diagnosis of ventricular septal rupture to surgery was six days (interquartile range, 1.5 to 12 days). Surgery was performed within 48 hours in 14 patients. Five patients who were scheduled for surgery after two to three days had to be operated on an earlier basis due to worsening of the clinical and hemodynamic status. Baseline characteristics in patients who had early surgery were comparable to patients with late surgery except from a significantly lower blood pressure (Table 4).


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Table 3 Profile of Medical or Surgically Treated Patients
 

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Table 4 Comparison of Patients Managed With Early or Late Surgical Repair
 
Short- and Long-Term Outcome
The overall 30-day, 1-, and 5-year mortality rates were 62%, 72%, and 95%, respectively. The median survival time was 32 days (interquartile range, 6 to 649 days). None of the medically treated patients survived 30 days while patients treated surgically had a 30-day survival rate of 71% (Fig 2). The long-term survival rate in the surgically treated group was 48% after one year and 32% after five years. In the surgically treated patients with an age 75 years or greater (n = 7) the one-year survival rate was 0% compared with 52% in patients with an age less than 75 years. The highest one-year survival rate among the surgically treated group was found in patients with an age less than 65 years (n = 12) as compared with patients with an age of 65 to 74 years (n = 26) (83% and 38%, respectively, p < 0.05) (Fig 4). Patients who underwent late (>2 days) or early (≤2 days) surgical repair had one-year survival rates of 64% and 38%, respectively (p < 0.05) (Fig 3). In patients who underwent late surgery (>2 days after the diagnosis), no statistical difference between the AMI treatment strategies (fast revascularization, conservative treatment) and mortality were found (p = 0.62). However, there was a tendency toward better one-year survival among patients treated with percutaneous angioplasty or thrombolysis (71%) compared with patients without revascularization (59%).


Figure 2
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Fig 2. Short-term cumulative survival in medically and surgically treated patients.

 

Figure 4
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Fig 4. Long-term survival in surgically treated patients according to age.

 

Figure 3
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Fig 3. Long-term survival in patients treated with early (≤2 days) or late surgery (>2 days).

 
A multivariate regression analysis was performed to identify factors associated with one-year mortality (Table 5). History of hypertension, high Killip class at admission, and heart rate were identified as independent predictors of mortality.


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Table 5 Multivariate Cox Regression Analysis for Predictors of All Cause Mortality After One Year
 

    Comment
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
In a relatively large consecutive and contemporary series of patients with AMI complicated with ventricular septal rupture, the present study demonstrates that the overall short- and long-term mortality remains high in the reperfusion era. It is notable that, due to the Danish socialized medicine practice, this material represents unselected patients from a defined geographic area within a defined time period.

Patient Characteristics
The average age in our study was 70 years, which appears consistent with the GUSTO-I trial and SHOCK trial but higher than observed in the prethrombolytic studies [6–10]. The increased age seems to be consistent with the increased age of the general population but may also reflect enhanced confidence to surgical treatment in the referring hospitals, even in elderly patients. The majority of our patients were men. This is in accordance with earlier studies but in contrast to the findings in the GUSTO-I and SHOCK trials, where a predominance of females was noted [9–13]. The median time from debut of AMI to ventricular septal rupture diagnosis was five days in our study and more than one-fourth of the patients developed the rupture within two days. This observation and data from the GUSTO-I trial may indicate that rupture might occur sooner than described in prethrombolytic studies [1, 5, 9, 13]. Although thrombolytic therapy reduces infarct size, reperfusion may potentially promote hemorrhage and dissection in the myocardium, thus accelerating the risk of rupture. Rupture was also seen within one to two days in the smaller group of patients treated with primary angioplasty. It should be noted, however, that the early recognition of septal rupture merely may reflect that access to echocardiography in the primary hospitals is facilitated nowadays.

As shown by others we found a predominance of one-vessel disease with a total occlusion of the infarct-related coronary artery in approximately 50% of patients. Anterior infarcts have in some studies been associated with a more frequent development of septal rupture than inferior-posterior infarcts [5, 13–15]. In the present study, the ECG location of the AMI and the location of the septal rupture by echocardiography were equally distributed between anterior and inferior-posterior locations in accordance with other patient series [16].

Treatment and Prognosis
Congestive heart failure was noted in 61% of the patients on admission with approximately one-third being in cardiogenic shock. Nearly two-thirds received inotropic support and diuretics and preoperative IABP was used in 55% of cases, which is in accordance with other reports [9, 15]. Although no definite documentation exists that IABP improves survival the use is widely accepted as a favorable support in the treatment of myocardial septal rupture. The IABP decreases left ventricular afterload, reduces the magnitude of the left-to-right shunt, and increases the coronary perfusion. Thus, IABP may stabilize and improve the clinical and hemodynamic condition in a number of patients. Severe hemodynamic deterioration developed in five initially stable patients. In these patients, who were scheduled for later operation, urgent need for surgical closure of the defect suddenly occurred. Deterioration before surgery and cardiogenic shock at admission are known strong predictors of early mortality and in accordance with these observations none of the five patients survived for 30 days [9, 15]. In accordance with previous reports we have demonstrated that clinical signs of heart failure, such as increased Killip class and increased heart rate, were independent predictors of long-term mortality [9, 12, 15].

Hospital survival in the United Kingdom during the period 1988 to 1999 was 31% to 47% in patients with ventricular septal rupture and for surgically treated patients in the SHOCK trial and GUSTO-I trial it was 19% and 53%, respectively. In the present study, the 30-day survival in surgically treated patients was as high as 76%. For patients who survive surgery, the long-term prognosis is relatively good. In the GUSTO-I trial, one-year survival was 47% in surgically treated patients. Similar to these results, we found a one-year survival of 48%. Furthermore, the five-year survival was 32% in our study, which is reasonably comparable with the 41% found by Deja and colleagues [15]. However, the mean age was only 65 years in the study by Deja and colleagues compared with a mean age in the present study of 70 years. This difference might indeed affect survival with younger patients displaying a more favorable prognosis than elderly as also illustrated in the present study. As in the prethrombolytic era, the prognosis in medically treated patients remains extremely poor with an in-hospital mortality of 94% in the GUSTO-I trial, 96% in the SHOCK Registry, and 100% in the present study [9, 10]. In the present report, the medically treated patients were significantly older compared with the surgically treated patients, otherwise they seemed comparable. As shown previously and emphasized by the present study, advanced age is associated with poor outcome. In this regard, it is also noteworthy that none of our surgically treated patients with an age of 75 years or more survived the first four months after surgery. However, the strongest predictor of long-term outcome was a history of hypertension. Hypertension is a recognized predictor for septal rupture in AMI but has not previously been associated with long-term prognosis [17, 18].

Strategy for Management
Besides a surgical strategy, the predominant medical strategy prior to surgery is to reduce left ventricular (LV) filling pressures and afterload. This involves the following: (1) IABP treatment- inotropics (or both in combination) in cases with signs of heart failure or cardiogenic shock (blood pressure below 90 mm Hg); (2) diuretics; and (3) dialysis in cases with an oliguria. After surgery, the medical strategy is based on standard cardiac care involving diuretics to decrease LV filling pressures, angiotensin-converting enzyme inhibitors, and beta blockers to diminish LV wall stress and afterload. The treatment strategy in this study has provided results comparable with the majority of previously published papers. Still, our 30-day mortality is 24%! How can we improve outcome? In accordance with our expectations we found in the present study that patients who were operated early (<2 days after diagnosis) had a more adverse outcome compared with patients who underwent late surgery. This observation is likely to be explained by selection bias with more advanced stages of heart failure with significant lower baseline blood pressures (Table 4). The fragile necrotic myocardium is a major concern while operating on an urgent basis. Therefore, from a technical perspective the best time to perform surgery is after fibrotic healing of the necrotic muscle. However, in a histologic study it was demonstrated that proliferation of connective tissue was not present until the third week after infarction [19]. Furthermore, in a large proportion of patients it is not possible to postpone surgery because they develop severe heart failure and multiorgan dysfunction. A sudden hemodynamic deterioration between admission and scheduled later operation carried 100% mortality in our population, a result similar to findings of other reports [15]. A logical measure to avoid further hemodynamic deterioration should be to operate upon the patients immediately after establishment of the diagnosis when a coronary angiography has been performed. A surgical technique with infarct exclusion by means of a large endocardial patch has permitted early operation. This technique was described by Deja and colleagues [15] and by David and colleagues [20] who reported a 30-day mortality of 14%. Their strategy was to operate all patients expeditiously. Presently, we have adopted this technique and are operating the vast majority emergently.

In patients who are severely hemodynamically compromised, it may be considered to use a ventricular assist device to bridge the patient to surgery with closure of the septal defect or to heart transplantation. The latter strategy has recently been reported with excellent outcome [21].

In this study, medically treated patients showed 100% mortality after 30 days. Therefore, the overall strategy is to correct the ventricular septal defect. In the elderly patients (>75 years), the prognosis with surgery is extremely grave and surgical treatment should probably only be offered in selected cases. In this particular group it may also be appropriate to consider the use of a transcatheter closure device; particularly if the patient is not considered for concomitant coronary artery bypass surgery, if the ventricular septal defect has a simple structure (predominantly anterior located), and if it is not located close to the mitral valve apparatus. Only case reports and small series have documented the yield of these devices that may change into significant future treatment options [22–24]. In this context, an 83-year-old patient with septal rupture was recently treated in our department with an Amplatz occluder and the outcome was successful.

Another controversial question is the need for concomitant coronary bypass surgery. Some series indicate that concomitant revascularization may improve late survival [25, 26], whereas others have failed to show any definitive benefit of concomitant bypass surgery [27, 28]. In the present study coronary grafting was only performed in patients with multivessel disease to ensure optimal conditions for the left and right ventricular performance in the postoperative phase.

In summary, the mean age of the patient with ventricular septal defects is higher than described in prethrombolytic series. Clinical signs of congestive heart failure on admission, advanced age, and a history of hypertension were associated with poor long-term outcome. Despite improvements in medical and interventional techniques the early as well as the long-term overall prognosis remained poor in this contemporary series. However, a more favorable prognosis was found in surgically treated patients who were younger than 75 years. The potential benefit of early transcatheter intervention in selected patients or by modified surgical techniques needs further exploration.


    References
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 

  1. Topaz O, Taylor AL. Interventricular septal rupture complicating acute myocardial infarction: from pathophysiologic features to the role of invasive and noninvasive diagnostic modalities in current management Am J Med 1992;93:683-688.[Medline]
  2. Heitmiller R, Jacobs ML, Daggett WM. Surgical management of postinfarction ventricular septal rupture Ann Thorac Surg 1986;41:683-691.[Abstract]
  3. Davies RH, Dawkins KD, Skillington PD, et al. Late functional results after surgical closure of acquired ventricular septal defect J Thorac Cardiovasc Surg 1993;106:592-598.[Abstract]
  4. Moore CA, Nygaard TW, Kaiser DL, Cooper AA, Gibson RS. Postinfarction ventricular septal rupture: the importance of location of infarction and right ventricular function in determining survival Circulation 1986;74:45-55.[Abstract/Free Full Text]
  5. Edwards BS, Edwards WD, Edwards JE. Ventricular septal rupture complicating acute myocardial infarction: identification of simple and complex types in 53 autopsied hearts Am J Cardiol 1984;54:1201-1205.[Medline]
  6. Cummings RG, Califf R, Jones RN, Reimer KA, Kong YH, Lowe JE. Correlates of survival in patients with postinfarction ventricular septal defect Ann Thorac Surg 1989;47:824-830.[Abstract]
  7. Held AC, Cole PL, Lipton B, et al. Rupture of the interventricular septum complicating acute myocardial infarction: a multicenter analysis of clinical findings and outcome Am Heart J 1988;116:1330-1336.[Medline]
  8. Feneley MP, Chang VP, O'Rourke MF. Myocardial rupture after acute myocardial infarction. Ten year review. Br Heart J 1983;49:550-556.[Abstract/Free Full Text]
  9. Crenshaw BS, Granger CB, Birnbaum Y, et al. Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction Circulation 2000;101:27-32.[Abstract/Free Full Text]
  10. Menon V, Webb JG, Hillis LD, et al. Outcome and profile of ventricular septal rupture with cardiogenic shock after myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries in cardiogenic shocK?. J Am Coll Cardiol 2000;36:1110-1116.[Abstract/Free Full Text]
  11. Radford MJ, Johnson RA, Daggett Jr WM, et al. Ventricular septal rupture: a review of clinical and physiologic features and an analysis of survival Circulation 1981;64:545-553.[Abstract/Free Full Text]
  12. Deville C, Fontan F, Chevalier JM, Madonna F, Ebner A, Besse P. Surgery of post-infarction ventricular septal defect: risk factors for hospital death and long-term results Eur J Cardiothorac Surg 1991;5:167-175.[Abstract]
  13. Lemery R, Smith HC, Giuliani ER, Gersh BJ. Prognosis in rupture of the ventricular septum after acute myocardial infarction and role of early surgical intervention Am J Cardiol 1992;70:147-151.[Medline]
  14. Skehan JD, Carey C, Norrell MS, de Belder M, Balcon R, Mills PG. Patterns of coronary artery disease in post-infarction ventricular septal rupture Br Heart J 1989;62:268-272.[Abstract/Free Full Text]
  15. Deja MA, Szostek J, Widenka K, et al. Post infarction ventricular septal defect - can we do better? Eur J Cardiothorac Surg 2000;18:194-201.[Abstract/Free Full Text]
  16. Di Summa M, Actis Dato GM, Centofanti P, et al. Ventricular septal rupture after a myocardial infarction: clinical features and long term survival J Cardiovasc Surg (Torino) 1997;38:589-593.[Medline]
  17. Shapira I, Isakov A, Burke M, et al. Cardiac rupture in patients with acute myocardial infarction Chest 1987;92:219-223.[Medline]
  18. Oskoui R, Van Voorhees LB, DiBianco R, Kiernan JM, Lee F, Lindsay Jr J. Timing of ventricular septal rupture after acute myocardial infarction and its relation to thrombolytic therapy Am J Cardiol 1996;78:953-955.[Medline]
  19. Fishbein MC, Maclean D, Maroko PR. The histopathologic evolution of myocardial infarction Chest 1978;73:843-849.[Medline]
  20. David TE, Dale L, Sun Z. Postinfarction ventricular septal rupture: repair by endocardial patch with infarct exclusion J Thorac Cardiovasc Surg 1995;110:1315-1322.[Abstract/Free Full Text]
  21. Faber C, McCarthy PM, Smedira NG, Young JB, Starling RC, Hoercher KJ. Implantable left ventricular assist device for patients with postinfarction ventricular septal defect J Thorac Cardiovasc Surg 2002;124:400-401.[Free Full Text]
  22. Lee EM, Roberts DH, Walsh KP. Transcatheter closure of a residual postmyocardial infarction ventricular septal defect with the Amplatzer septal occluder Heart 1998;80:522-524.[Abstract/Free Full Text]
  23. Benton JP, Barker KS. Transcatheter closure of ventricular septal defect: a nonsurgical approach to the care of the patient with acute ventricular septal rupture Heart Lung 1992;21:356-364.[Medline]
  24. Szkutnik M, Bialkowski J, Kusa J, et al. Postinfarction ventricular septal defect closure with Amplatzer occluders Eur J Cardiothorac Surg 2003;23:323-327.[Abstract/Free Full Text]
  25. Muehrcke DD, Daggett Jr WM, Buckley MJ, Akins CW, Hilgenberg AD, Austen WG. Postinfarct ventricular septal defect repair: effect of coronary artery bypass grafting Ann Thorac Surg 1992;54:876-883.[Abstract]
  26. Cox FF, Plokker HW, Morshuis WJ, Kelder JC, Vermeulen FE. Importance of coronary revascularization for late survival after postinfarction ventricular septal rupture. A reason to perform coronary angiography prior to surgery. Eur Heart J 1996;17:1841-1845.[Abstract/Free Full Text]
  27. Dalrymple-Hay MJ, Monro JL, Livesey SA, Lamb RK. Postinfarction ventricular septal rupture: the Wessex experience Semin Thorac Cardiovasc Surg 1998;10:111-116.[Medline]
  28. Loisance DY, Lordez JM, Deleuze PH, Dubois-Rande JL, Lellouche D, Cachera JP. Acute postinfarction septal rupture: long-term results Ann Thorac Surg 1991;52:474-478.[Abstract]



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