HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Dalrymple-Hay, M.J.R. Articles by Monro, J.L. Search for Related Content PubMed PubMed Citation Articles by Dalrymple-Hay, M.J.R. Articles by Monro, J.L.

Eur J Cardiothorac Surg 1998;13:286-292
© 1998 Elsevier Science NL

Should coronary artery bypass grafting be performed at the same time as repair of a post-infarct ventricular septal defect?¹

Wessex Cardiothoracic Centre, Southampton General Hospital, Tremona Road, Southampton S016 6YD, UK

Received 29 September 1997; received in revised form 2 January 1998; accepted 14 January 1998.

Corresponding author. Tel.: +44 1703 796124; fax: +44 1703 796614.

	Abstract

Top Abstract Introduction Patients and methods Statistical analysis Results Survival Discussion Conclusion Appendix A. Conference... References

 
Objective: The value of coronary artery bypass grafting (CABG) at the time of repair of a post-infarct ventricular septal defect (VSD) remains controversial. The aim of this study was to analyse the effect of CABG on early mortality and survival following repair of an acquired VSD. Methods: Over 23 years, 179 patients, 118 male, 61 female, mean age 66 years (range 43–80), have undergone repair of a post-related VSD in our unit. A total of 29 patients, who predominantly form the earlier part of the series, were operated on greater than 1 month after the infarct and are, therefore, excluded. Coronary angiography was performed in 98 (65.3%) of the remaining 150 patients. Of these, 41 had coronary artery disease (CAD) limited to the infarct-related vessel and 57 had additional significant CAD. Those with CAD limited to the infarct-related vessel were not grafted (Group A). Of those, 40 with significant CAD underwent CABG at the time of VSD repair (Group B) and 17 did not (Group C). In 52 patients the coronary anatomy was not documented (Group D). Risk factors for early mortality were evaluated using logistic regression. Actuarial survival was compared using log rank and Wilcoxon tests. Cox’s proportional hazards method was used to determine factors affecting survival. Results: Overall, 30 day mortality was 32%. CABG did not significantly decrease operative mortality (logistic regression). There was no statistically significant difference in early mortality or actuarial survival between the four groups. CABG was not associated with an increased survival (Cox’s method). Conclusions: Concomitant CABG at the time of VSD repair does not affect early mortality nor confer survival benefits. There seems to be no demonstrable benefit in revascularisation at the time of repair and, therefore, it may be unnecessary to perform CABG or coronary angiography in these patients.

Key Words: Ventricular septal defect • Coronary artery bypass grafting • Survival

	Introduction

Top Abstract Introduction Patients and methods Statistical analysis Results Survival Discussion Conclusion Appendix A. Conference... References

 
The incidence of ventricular septal rupture following a myocardial infarct is approximately 1% [1]. The timing of the rupture varies between several hours and several weeks following the infarct. The site of rupture depends on the coronary anatomy and the infarcted vessel.

There is general agreement that early surgical correction is the treatment of choice [2] [3] [4]. It remains less clear, however, as to the value of coronary artery bypass grafting (CABG) at the time of repair. If CABG is to be undertaken, there needs to be a proven benefit in either operative mortality, freedom from angina following repair or survival, which exceeds any additional risk that occurs as a result of the coronary angiography and CABG.

To date, no series has shown a positive relationship between operative mortality and CABG, indeed only one author [5] has shown a relationship between the number of diseased coronary vessels and operative mortality.

Authors who have addressed quality of life following repair of an infarct-related VSD have demonstrated no benefit from CABG at the time of repair [6].

Several series have found no relationship between CABG and survival [2] [3] [4] [6] [7]. Some authors, however, report improved survival associated with CABG, Anderson et al. [8] reported an improved survival associated with a right coronary graft, Muerchke et al. [9] found that CABG significantly increased survival but on univariate analysis only and Cox et al. [10] showed that incomplete revascularisation was found to be a significant risk factor for late death.

We examine the relationship between CABG at the same time as repair of a post-related VSD and operative mortality, survival and freedom from angina following repair.

	Patients and methods

Top Abstract Introduction Patients and methods Statistical analysis Results Survival Discussion Conclusion Appendix A. Conference... References

 
Between January 1972 and December 1995, 179 patients underwent correction of a post-infarct VSD in our unit. In the earlier parts of the series, surgery was sometimes deferred for greater than 1 month after the infarct. This was the case for 29 patients who are excluded from this study (the operative mortality for this group was zero.) The remaining 150 were operated on within 1 month of infarction, 73% on the day of septal rupture and 16% 1 day after septal rupture. There were 99 males and 51 females with a mean age 66 years (range 43–80).

Preoperative and operative variables recorded included age, sex, a history of pre-existing coronary artery disease (CAD) (history of angina, MI or CABG), time from MI to operation, time from MI to detection of murmur, time from detection of murmur to operation, presence of preoperative arrhythmia, preoperative systolic blood pressure, preoperative NYHA status, preoperative serum urea and site of myocardial infarction (anterior or inferior). The number of coronary arteries with significant stenosis (>50% decrease in diameter vessel on angiography was deemed significant), aortic cross clamp time, cardiopulmonary bypass time and performance of CABG (including number of grafts) was also recorded. Operative mortality was defined as death within 30 days of surgery.

To clarify the analysis, patients were divided into four groups. Group A had a significant coronary stenosis in the infarct-related vessel only, this vessel was not grafted. Group B had significant coronary stenosis in the non infarct-related coronary vessels and underwent CABG at the time of VSD repair and group C had a significant stenosis in the non infarct-related coronary arteries but did not undergo CABG at the time of repair. Group D had no documentation of the coronary anatomy and were not grafted.

Repair technique
The repair technique has remained essentially unchanged over the last 10 years. Bovine pericardium is used to cover the defect and the area of septal infarction. This is fixed with sutures through viable muscle. The bovine pericardium is deliberately large and lies loosely over the defect. LV pressure is relied upon to hold the pericardium over the VSD during systole. It is brought out through the infarctotomy and the ventricle closed with teflon strips and two layers of sutures.

	Statistical analysis

Top Abstract Introduction Patients and methods Statistical analysis Results Survival Discussion Conclusion Appendix A. Conference... References

 
Statistical analysis were performed according to standard statistical protocols incorporated in the SAS statistical package JMP (SAS Institute, Cary, NC). Risk factors for operative mortality were analysed using logistic regression. Survival information was obtained from general practitioners. When the patients general practitioner could not be traced data was obtained from the Office for National Statistics (National Health Service Branch). Survival was analysed using Kaplan–Meier curves. Survival between groups was compared using Log rank and Wilcoxon tests. Cox’s proportional hazard method was used to relate variables to survival.

	Results

Top Abstract Introduction Patients and methods Statistical analysis Results Survival Discussion Conclusion Appendix A. Conference... References

 
Patient data
Group D consisting of 52 patients did not undergo coronary angiography preoperatively, in 49 of these the diagnosis was confirmed using echo-doppler and in 3 using ventriculography alone. Coronary angiography was, therefore, performed in 98 patients.

A total of 41 patients had a significant coronary stenosis in the infarct-related vessel only which was not grafted (group A), 57 had significant coronary stenosis in the non-infarct coronary vessels; 40 (group B) and 17 (group C) underwent CABG at the time of VSD repair. The demographics and variables recorded in each group can be seen in Table 1. There were significantly more anterior than inferior infarcts in group D compared to group A, B and C. Cardiopulmonary bypass and aortic cross clamp time was significantly longer in group B than any other group. There was no significant difference between any of the other variables in the different groups.

The only variable significant on multiple logistic regression was cardiopulmonary bypass time (P=0.03). Cardiopulmonary bypass remained significant when patients who had to undergo more than one repair were excluded (P=0.05).

	Survival

Top Abstract Introduction Patients and methods Statistical analysis Results Survival Discussion Conclusion Appendix A. Conference... References

 
Follow-up is 98% complete and ranged from 2–226 months (mean 72 months). Survival including in-hospital mortality at 1, 2, 5 and 10 years is 60±4 (n=83), 58±4 (n=77), 49±4 (n=52) and 31±5% (n=13), respectively ( Fig. 1 ). The relationship between preoperative and operative variables and survival is shown in Table 3.

View larger version (13K): [in this window] [in a new window]   Fig. 1. Survival following repair of an infarct-related VSD (including in hospital mortality).

Survival for groups A, B, C and D are shown in Fig. 2 . There was no significant difference in survival between all the groups (Log rank P=0.59, Wilcoxon P=0.52) or between groups B and C ( Fig. 3 ) (Log rank P=0.57, Wilcoxon P=0.34).

View larger version (18K): [in this window] [in a new window]   Fig. 2. Survival following repair of an infarct-related VSD (including 30 day mortality). Group A: CAD limited to the infarct-related vessel. Group B: additional significant CAD and underwent CABG. Group C: additional significant CAD but did not undergo CABG. Group D: coronary anatomy unknown, no CABG.

View larger version (17K): [in this window] [in a new window]   Fig. 3. Survival following repair of an infarct-related VSD (including 30 day mortality). Group B: additional significant CAD and underwent CABG. Group C: additional significant CAD but did not undergo CABG.

	Discussion

Top Abstract Introduction Patients and methods Statistical analysis Results Survival Discussion Conclusion Appendix A. Conference... References

A total of 52 patients (34.6%) did not undergo coronary angiography. Over the 25 years of the study changes in cardiac catheterisation equipment and clinical experience have altered cardiologists willingness to perform coronary angiography. The risk associated with coronary angiography in a patient with a post-infarct VSD has changed since 1972, hence the reasons for withholding coronary angiography have changed over this time period. Furthermore, the use of echocardiography to confirm the diagnosis, has removed the requirement for contrast ventriculography which in itself altered individual cardiologists perception of the need for contrast studies.

In this series we found predominantly three reasons for not performing coronary angiography.

It was withheld from the more unstable patients because a delay in surgical correction was thought to increase operative risk. In this series, 32 patients who did not undergo coronary angiography were in cardiogenic shock. We accept, however, that in most units today angiography can be performed rapidly prior to surgical correction and should not unnecessarily delay the operative procedure.

Angiography was also sometimes not performed because it can lead to a deterioration in haemodynamic status and, therefore, increase operative risk. Several authors have discussed patients being destabilised by angiography [11] [12]. Cox et al. [10] recently reported that 5/104 (4%) patients with a post-infarct VSD became compromised during angiography.

We have previously found that patients with anterior infarction are less likely to have significant coronary stenoses than those with inferior infarcts. This has also been reported in some [9] but not all other series [10] and has lead to some cardiologists not choosing to perform coronary angiography in patients with anterior infarction.

It is impossible to categorise the reason why certain patients did not undergo coronary angiography. In some instances it was a combination of reasons e.g. an unstable patient with an anterior infarct.

We accept that having not performed angiography on all patients there is the theoretical chance that this may have lead to a bias in patient selection when comparing group D to A, B and C. This is not the case when comparing groups A, B and C. Data concerning group D was, therefore, not entered into operative mortality or survival models when the affect of CAD and CABG was tested.

It is also accepted that there are potential differences in the coronary angiography of patients in groups B and C. For instance, a patient with an anterior defect, a high grade discrete proximal right coronary lesion and a large distal artery is treated on coronary angiographic terms the same as a patient with a small right coronary artery with severe distal disease. The former is more likely to be grafted than the latter. There are, however, a limited number of ways the coronary angioigraphic findings can be grouped to leave a reasonable number of patients in each group and the system used in this paper is routinely applied in clinical practice and has been used in other comparisons of CAD and the effect of CABG.

Operative mortality
We can demonstrate no significant benefit with respect to operative mortality from concomitant CABG at the time of repair. This is also the experience of other authors [3] [4] [7] [9] [10]. Komeda et al. [5] showed that three-vessel disease was predictive of operative mortality on univariate analysis alone. No data concerning the value of CABG was presented in this series. They also admitted, however, that "because the numbers were small and the overall operative mortality relatively low, the results of this analysis may not be valid".

There was no difference in operative mortality between the two most crucial groups, B and C. Of the variables associated with operative mortality (Table 2), only cross clamp and cardiopulmonary bypass times were significantly different in groups B and C (group B longer). It may be that these longer times associated with CABG explain the increased operative mortality in group B, though we feel this is unlikely.

In our experience, only longer cardiopulmonary bypass time was significantly associated with an increase in operative mortality using multiple logistic regression. This probably reflects the time when the myocardium is rested because it has been impossible to discontinue cardiopulmonary bypass rather than a true effect of the longer cardiopulmonary bypass time. The fact that aortic cross clamp time is not significant on multiple logistic regression supports this explanation.

In summary, therefore, we have no data to show CABG either increases or decreases operative mortality, but accept this is not a reason to elect not to perform CABG.

Freedom from angina
We have not formally assessed our late functional results since 1993 [6]. At this time, however, only 5 patients in the series had angina. All of these had a preoperative angiogram and had not required CABG. Of these patients, 82% were in NYHA functional class I or II.

It has not been our policy to catheterise patients following repair of a post-infarct VSD routinely, so it is impossible to delineate the progression of significant CAD. No patients in group D have developed angina and, therefore, these have also not been catheterised.

Survival
We found no benefit in survival from concomitant CABG at the time of repair (Cox’s proportional hazards method). Furthermore, there was no difference in survival between patients in the three groups A, B, C and D or between the two crucial groups, B and C. This is a common finding in both single [2] [7] and multicentre [3] [4] series.

Conclusions from survival data in any series become increasingly powerful as the survival time and number of patients in the series increases. It is an unfortunate consequence of any rare pathology, such as post-infarct VSD, that the number of patients in any one series is small. In addition, the statistical power of any analysis is further decreased by the association with a high operative mortality and procedure performed in an elderly population. The average age at operation was 66 years and, therefore, truly ‘long term’ survival is likely to be limited. Conclusions from the survival data must, therefore, be interpreted with caution, however, the understanding of the role of CABG in patients with a post-infarct VSD has been based on series of 68, [8] 92 [10] and 75 [9] patients, respectively, a similar size to this series.

These have demonstrated a relationship between CABG at the time of repair and survival and merit further discussion.

Anderson et al. [8] showed that a right coronary artery graft improved survival. In this series, however, a right coronary artery graft was performed only in patients with an anterior VSD. Patients with an anterior VSD had significantly better survival (64% at 1 year) compared to inferior defects (11% at 1 year). The perceived benefit of this graft is, therefore, probably a reflection of the increased survival of patients with anterior defects and not the true effect of CABG.

Muehrcke et al. [9] showed a benefit from CABG in patients with significant associated coronary artery disease on univariate analysis alone. This benefit was greater in patients with anterior compared to inferior infarcts.

There are two points in Muehrcke’s paper which require attention. If changes in survival are to be ascribed to the effect of CABG then a decrease in death directly due to myocardial ischaemia or secondary to the complications of myocardial ischaemia must be shown. This was not the case for this series. In addition, the mean time to operation from infarction was prolonged in comparison to the majority of series (19 vs. 7 days in our experience). Patients who have been stabilised medically present a very different surgical challenge and may benefit from CABG. These have been excluded from this analysis (>90% patients operated on within 2 days of septal rupture) and this may account for the difference. It may be, however, that in Muehrcke’s series a few patients were treated conservatively for prolonged periods of time and have, therefore, disproportionately increased this mean time.

Cox et al. [10] reported that incomplete myocardial revascularisation was a significant predictor of late mortality. A more powerful predictor in this series, however, was post-operative cardiac failure. It would be interesting to delineate the relationship between post-operative cardiac failure and CABG at the time of repair. Unfortunately, the precise causes of late death of which >75% were cardiac causes were not listed. Hence, again it is impossible to delineate those due to myocardial ischaemia that may have been prevented by CABG. It is interesting to note that longer aortic cross clamp times were also a predictor of late mortality.

There is also one possible bias in patient selection in Cox’s series [10]. In the group who underwent complete revascularisation they included 10 patients in whom a branch of the infarcted vessel was grafted. It is unclear whether these patients had other significant coronary artery disease which was bypassed or whether they had CAD in the infarct-related vessel only. If the latter is true inclusion in the same group as those with double or triple vessel disease in which significant lesions were bypassed is not valid.

We are unable in our series to report precisely the causes of death. This is because in many instances no autopsy was performed and although a copy of the death certificate is obtained it is not always possible to determine this information. For example, when the cause of death is listed as heart failure, it is impossible to clarify if this is due to myocardial ischaemia. Of note, however, there was no difference in the proportion of cardiac causes of death between the groups.

	Conclusion

Top Abstract Introduction Patients and methods Statistical analysis Results Survival Discussion Conclusion Appendix A. Conference... References

 
Our data does not support the hypothesis that CABG at the time of repair improves operative mortality, alters freedom from angina following repair or confers any survival benefit.

This is not a reason to abandon CABG at the time of repair. We believe, however, that until a decrease in causes of death due to myocardial infarction or the complications of myocardial ischaemia is clearly shown, with no additional increased operative risk from CABG, questions exist as to the benefit of CABG at the same time as repair. At present there is incomplete evidence in the literature to support routine CABG.

	Footnotes

 
Presented at the 11th Annual Meeting of The European Association for Cardio-Thoracic Surgery, Copenhagen, Denmark, September 28–October 1, 1998.

	Appendix A. Conference discussions

Top Abstract Introduction Patients and methods Statistical analysis Results Survival Discussion Conclusion Appendix A. Conference... References

 
Dr T. Pezzella (Worcester, MA): My associate, Dr Bill Daggett, would not forgive me if I didn’t make at least one comment. It’s clear that in the Massachusetts General Hospital experience and others, that coronary artery bypass grafting concomitantly does improve the mortality and survival. I would ask, in a particular subset of patients, particularly inferior infarct in a dominant right coronary artery with proximal obstruction, would you not bypass the right coronary artery hoping to improve marginal flow, given the fact that right ventricular dysfunction is a clear morbid factor in this particular group of patients?

Also, do you have any substantial data regarding morbidity in the various groups in terms of ICU stay, intra aortic balloon use and total hospital stay?

Dr M.J.R. Dalrymple-Hay: I’ll deal with the second question first. There is no difference between the groups in terms of preoperative risk, length of hospital stay, ICU stay or balloon use.

With regards to your first question, at present we have no data to support the hypothesis that we should graft that vessel.

Dr C. Alhan (Istanbul, Turkey): We, in our center, also carry on the same strategy for post-MRI VSDs. Furthermore, we don’t use angiography in those seriously ill patients. My question is, does myocardial protection technique have an impact on outcome in these patients? As I see, you have been performing this operation since 1972, and I believe there have been some changes in your myocardial protection, myocaridal management.

Dr M.J.R. Dalrymple-Hay: Inadequately protected myocardium will obviously increase the operative risk. We have routinely used antegrade cold crystalloid cardioplegia and to date haven’t changed from using that.

Dr C. Alhan: No blood cardioplegia?

Dr M.J.R. Dalrymple-Hay: We would now use blood cardioplegia but not in this series no.

Dr C. Knott-Craig (Oklahoma, OK): I enjoyed this rather controversial paper very much. How many of those patients that demonstrated ischemia after the repair died before being offered revascularization? And how do you think that would influence your conclusions if you could demonstrate that there were patients that died while awaiting coronary bypass surgery after surviving a successful repair?

Dr M.J.R. Dalrymple-Hay: We formerly analyzed the quality of life and the angina status of patients postoperatively in 1993. I haven’t done that in this analysis. I can tell you that in 1993, when there were 60 patients alive, 5 of them had angina. Of those 5, 2 were receiving treatment. And all of them had preoperative angiography that had no significant coronary lesion on it. So, none of those patients would have been grafted at the time anyway.

Dr M. Schmuziger (Meyrin-Geneve, Switzerland): I was very intrigued by your paper because it concerns an ever on-going discussion, that started years ago. I would like to ask you about the patency rate achieved in patients with triple-vessel disease who underwent myocardial revascularization (Group B in your study). What was the patency rate at 5 and 10 years in patients revascularized who presented with infarction and triple-vessel disease and what was the proof of ischemia in these patients? I believe this is a crucial question, because if all bypasses were found occluded, there would be no differences between the groups.

Dr M.J.R. Dalrymple-Hay: We haven’t performed angiography in that group of patients postoperatively, so I can’t answer that question accurately.

Dr D. Muehrcke (Jacksonville, FL): I had an opportunity of looking up our experience at the Massachusetts General Hospital, and I presented it to the Society of Thoracic Surgeons about 6 years ago. We came up with a different conclusion than you’ve come up with today. We found that bypass grafting was helpful at the time of VSD repair. We also found that it makes logical sense because people who are bypassed tend to live longer than people who are not bypassed who have severe 3-vessel disease. How would you reconcile your results today given the fact that usually patients who are bypassed tend to live longer if they have 3-vessel disease than if they’re not?

Dr M.J.R. Dalrymple-Hay: I think there are two essential differences. Firstly, you operated on people in that series significantly later than we have done in our series. And the operation becomes safer as time proceeds from ventricular septal rupture, and therefore, the risk of a longer bypass run and the grafting is less.

Secondly, I don’t think you actually showed a decrease in the incidence of death from myocardial ischemia or the complications of myocardial ischemia, because you couldn’t list the causes of death, or at least in the paper I saw you didn’t. I think until you clearly show that, it’s difficult to say that the conferred benefit from coronary artery bypass grafting is due to the bypass grafting alone.

Dr S. Mattila (Helsinki, Finland): We did a similar study retrospectively 10 years ago. We took a series of patients who had undergone coronary bypass surgery in association with a septal repair and those who didn’t have the revascularization. We came to the same conclusion. There was no statistical significant difference between those groups in operative mortality or later outcome.

I don’t recommend not to revascularize the patients because I don’t think the groups were equal. Because when you have a patient with a septal rupture, this means sudden occlusion of a major vessel and damage of a large area of the septal tissue. That is the major lesion in that heart. That cannot occur if there are collaterals.

Nowadays we, of course, seldom see these patients anymore because of the beta blockers. But, if the patients have stenosis in other areas of the heart, I would like to recommend to revascularize those. For that part which is already gone, you can’t get any benefit by revascularization. I think that is the major factor which influences the later outcome of those patients and that is why it overcomes the other minor lesions which could benefit from the bypass surgery. So, they are not actually equal, the groups, when you do this type of surgery.

Dr Aberg: So, the question is really what are your views as the selection of the patients into the various groups? Do you have any differences there?

Dr M.J.R. Dalrymple-Hay: What, in the preoperative risk factors for each group?

Dr Aberg: Well, in the discernible risk factors, but also in your policymaking and so forth, because it’s not always that you can catch the risk factors and put them on paper.

Dr M.J.R. Dalrymple-Hay: I mean an error of that sort is possible in any study. All I would say is I agree with the gentleman from Helsinki that repair of the defect is obviously critical. There will be difference in the coronary anatomy between, in our case, group B and group C, but in a study such as this we have to identify a reference point to which angiograms can be compared which does not subdivide the data into too many small groups. This has never been perfect and is the same for all studies of this nature.

	References

Top Abstract Introduction Patients and methods Statistical analysis Results Survival Discussion Conclusion Appendix A. Conference... References

 

1. Feneley M, Chang V, O'Rourke M. Myocardial rupture after acute myocardial infarction: 10 year review. Br Heart J 1983;49:550-556.[Abstract/Free Full Text]
2. Skillington P, Davies R, Luff A, Williams J, Dawkins K, Conway N, Lamb R, Shore D, Monro J, Ross J. Surgical treatment for infarct-related ventricular septal defects. Improved early results combined with analysis of late functional status. J Thorac Cardiovasc Surg 1990;99:798-808.[Abstract]
3. Hill J, Stiles Q. Acute ischaemic ventricular septal defect. Circulation 1989;89(Suppl I):112-114.
4. Held A, Cole A, Lipton B Rupture of the interventricular septum complicating acute myocardial infarction: a multicentre analysis of clinical findings and outcome. Am Heart J 1988;116:1330-1336.[Medline]
5. Komeda M, David T, Fremes S. Surgical repair of postinfarction ventricular septal defect. Circulation 1990;82(Suppl IV):243-247.
6. Davies R, Dawkins K, Skillington P, Lewington V, Monro J, Lamd R, Gray H, Conway N, Ross J, Whitaker L. Late functional results after surgical closure of acquired ventricular septal defect. J Thorac Cardiovasc Surg 1993;106:592-598.[Abstract]
7. Deville C, Fontan F, Chevalier J, Madonna F, Ebner A, Besse P. Surgery for postinfarction ventricular septal defect: risk factors for hospital death and long-term results. Eur J Cardiothorac Surg 1991;5:167-175.[Abstract]
8. Anderson D, Adams S, Bhat A, Pepper J Post-infarction ventricular septal defect: the importance of site of infarction and cardiogenic shock on outcome. Eur J Cardiothorac Surg 1989;3:554-557.[Abstract]
9. Muehrcke D, Daggett W, Buckley M, Akins C, Hilgenberg A, Austen W Postinfarct ventricular septal defect repair: effect of coronary artery bypass grafting. Ann Thorac Surg 1992;54:876-883.[Abstract]
10. Cox F, Morshius W, Thijs Plokker H, Kelder J, Vermeulen F. 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]
11. Selzer A, Gerbode F, Kerth W. Clinical haemodynamic and surgical considerations of rupture of the ventricular septum after myocardial infarction. Am Heart J 1969;78:598-607.[Medline]
12. Piwnica A, Menasche P, Beaufils P, Julliard J-M. Long term results of emergency surgery for post-infarction ventricular septal defect. Ann Thorac Surg 1987;44:274-276.[Abstract]

This article has been cited by other articles:

				A. Jeppsson and P. Johnsson Reply to Ramnarine and Grayson Eur. J. Cardiothorac. Surg., July 1, 2005; 28(1): 186 - 187. [Full Text] [PDF]

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Dalrymple-Hay, M.J.R. Articles by Monro, J.L. Search for Related Content PubMed PubMed Citation Articles by Dalrymple-Hay, M.J.R. Articles by Monro, J.L.