Surgery for post infarction ventricular septal defect (VSD): risk factors for hospital death and long term results q

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1 European Journal of Cardio-thoracic Surgery 21 (2002) Surgery for post infarction ventricular septal defect (VSD): risk factors for hospital death and long term results q L. Labrousse a, *, E. Choukroun a, J.M. Chevalier b, F. Madonna a, F. Robertie a, F. Merlico a, P. Coste c, C. Deville a a Department of Cardio-Vascular Surgery, Hopital Haut-Lévêque, Avenue de Magellan, Bordeaux-Pessac, France b Hopital d Instruction des Armées Robert Picqué, Villenave d Ornon, France c Department of Intensive Care of Cardiology, Bordeaux Heart University Hospital, Bordeaux-Pessac, France Received 20 September 2001; received in revised form 3 January 2002; accepted 16 January 2002 Abstract Objective: Repair of post infarction ventricular septal defect (VSD) is still a challenging procedure with a high risk of recurrence of the VSD and subsequent mortality. The aim of this retrospective study was to assess if technical change in the surgical procedure was followed by an improvement in recurrence of the VSD and operative results. Method: This retrospective study from 1971 to 2001 included 85 patients operated on early (,15 days) after the occurrence of a post infarction VSD. Double patch technique was introduced in A total of 44 variables were studied by a uni- and multivariate analysis. Results: Hospital death occurred in 36 patients. Significant factors for hospital mortality included: preoperative and evolution of the clinical status, right ventricular function and type of repair (one or two patches). Moreover, no recurrence was observed in patients repaired with the double patch technique (P ¼ 0:09). None of the studied variables were significant for long term survival. Concomitant CABG was not associated with higher hospital mortality and long-term survival rate was similar in patients with or without concomitant CABG. Conclusion: The use of the double patch technique and glue by avoiding recurrence of the VSD played a role in the reduction of the hospital mortality. This technique has to be recommended in the early repair of post infarction VSD. Concomitant CABG can be done safely to control the added risk of an associated coronary artery lesion. q 2002 Elsevier Science B.V. All rights reserved. Keywords: Myocardial infarction; Ventricular septal defect; Coronary disease; Cardiac surgery 1. Introduction Post infarction ventricular septal defect (VSD) is a rare but serious complication of myocardial infarction [1], usually quickly followed by low cardiac output and multi organ failure. Medical treatment is known no to be efficient in these case [1], and early surgical treatment (closure of the VSD) is recommended to reverse the hemodynamic deterioration [2 6]. However surgical repair is associated to a high rate of mortality (20 40%) even in the more recent reports [1 6]. We have previously reported risk factors for early mortality in our institution [7] to try to identify patients with preoperative high risk of mortality, and for whom some alternative procedures could have been q Presented at the joint 15th Annual Meeting of the European Association for Cardio-thoracic Surgery and the 9th Annual Meeting of the European Society of Thoracic Surgeons, Lisbon, Portugal, September 16 19, * Corresponding author. Tel.: ; fax: address: louis.labrousse@chu-bordeaux.fr (L. Labrousse). proposed. Unfortunately, heart transplantation is too dependant of an available graft, and circulatory assist devices as a bridge to heart transplantation can not be proposed especially because of the age of these patients. So, only an improvement in the operative technique can improve results and make this complication less dramatic. In front of this pathology, because of necrotic muscle and friable endocardial tissue, the suture of the Dacron patch is difficult with a high risk of recurrence of the VSD and subsequent mortality [2]. So to deal with this complication, we introduced in 1986 the use of double patch technique and glue, which became systematic after The aim of this retrospective study was to assess if technical changes in the surgical procedure were followed by an improvement in recurrence of the VSD and operative results /02/$ - see front matter q 2002 Elsevier Science B.V. All rights reserved. PII: S (02)

2 726 L. Labrousse et al. / European Journal of Cardio-thoracic Surgery 21 (2002) Patients and methods 2.1. Clinical status One hundred and one consecutive patients with post infarction VSD were operated on in our institution between December 1971 and December One patient who underwent heart transplantation will not be considered in this study. The fifteen patients who were operated on more than 15 days after the occurrence of the VSD were excluded. So, 85 post infarction VSD operated on at less than 15 days (mean: 3.4 days; median 3 days) after its occurrence composed the basic patient population. There were 51 males and 34 females, with a mean age of 69 years 6 months ranging from 52 to 82 years. The site of the infarction and of the perforation was anterior in 50 patients (59%) and posterior in 35 patients (41%). The medical history revealed hypertension in 35 patients (41%), nicotinism in 28 (32%), previous myocardial infarction in nine (11%), angina in 23 (27%) and diabetes mellitus in 12 (14%). The patients were retrospectively divided into four groups according to their clinical status at initial evaluation. Group 1: 16 patients (19%) presented with cardiogenic shock, defined as a systolic pressure below 70 mmhg with evidence of inadequate organ (oliguria) and peripheral perfusion; group 2: 28 patients (33%) had low cardiac output and severe congestive heart failure; group 3: 40 patients (47%) were stable with mild congestive heart failure; and group 4: one patient without congestive heart failure. All except the one of the group 4 were under inotropic support (dobutamin and/or adrenalin). Preoperative intra-aortic balloon pump (IABP) support, available in our institution since 1974, was used in 81 patients (95%). Before 1980, it was only use in patients with cardiogenic shock or severe congestive heart failure (groups 1 and 2). Since 1980 it was routinely used in all patients except for patients in whom peripheral vascular arterial disease prevented its use Cineangiography and coronarography All available preoperative cineangiograms were blindly reviewed. Left ventriculography was available in 65 patients and right ventriculography in 57. The right ventricular function was estimated from the percentage of reduction of the right ventricular mid cavity diameter as proposed by Fananapazir [9] and Jones [10]. From the left anterior oblique projection, the right ventricular mild cavity diameter was measured at end systole and end diastole, and the percentage of reduction in right ventricle diameter calculated as follows: RV diastolic diameter 2 RV systolic diameter 100% : RV diastolic diameter Coronary angiograms available in 72 patients, were analyzes in order to establish a preoperative coronary score. The method used has been previously described in our previous study [7]. The postoperative score derived from the preoperative score remained the same unless a lesion was treated by coronary bypass graft. In that case the lesion was quantified 0 in the postoperative score. The main cardiac catheterization data studied were: pulmonary arterial pressure (systolic, diastolic and mean), right and left atrial pressure, right ventricular pressure, left ventricular end diastolic pressure, cardiac index and pulmonary to systemic flow ratio Surgical management All patients were operated on through a median sternotomy with extracorporeal circulation and moderate hypothermia (28 338C). Cardiopulmonary bypass was established between both caval veins with caval tapes and ascending aorta. A bubble oxygenator was used in the first 28 patients and a membrane oxygenator in the next 57. Pulsative flow has been used since All operations were performed from 1 to 6 days (mean 3.4) after the septal defect occurrence. The ventricular septal defect repair was performed according to the principles of the technique described by Daggett [9,12]. The main principles were: approach to the interventricular septum through the area of the infarcted myocardium; closure of the VSD without tension with a dacron patch; closure of the ventriculotomy without tension, usually with prosthetic material, mainly for posterior infarction; buttressing of suture line with Teflon (pledgets or strips) and use of glue to reinforce friable tissue. GRF w glue was first used since 1982, followed in 1997 by Bioglue w (Cryolife International w, USA). From 1970 to 1986, the patch was placed over the VSD in the left ventricle and sutured through a unique left ventriculotomy as previously described [8,11]. Since 1986, we introduced the double patch and glue technique using a double ventriculotomy. The left ventriculotomy, similarly to that done in the one patch technique, is made in the infarct area and parallel either to the left anterior descending artery or to the posterior descending artery. So, the exact position of the VSD and of the septum is confirmed, and then allows to make the second incision through the right ventricle, parallel to the first one and nearer as possible of the septum. By this second ventriculotomy, another Dacron patch is positioned widely over to the VSD and sutured to the left Dacron patch with a continuous 4-0 polypropylene suture. Special attention to shape the right patch is required. Indeed, usually two incisions have to be done in the patch to allow a way for the moderator band and for the for tricuspid s papillary muscle tip. Thus, each patch is used as a support for the suture on the other. Moreover, biological glue (GRF w replaced in 1997 by Bioglue w ) is placed between the two patches to reinforce necrotic myocardium septal tissue, which is not resected at all. After that, ventriculotomies are closed as in the usual technique. Associated procedure included aneurysmectomy in 23

3 L. Labrousse et al. / European Journal of Cardio-thoracic Surgery 21 (2002) patients, coronary artery bypass graft in 40 (mean of 1.2 graft per patient), mitral valve replacement in one and permanent pacemaker implantation in four. Recurrences were established by clinical examination and echocardiography analysis when it became available (1978) Data collection and statistical analysis Preoperative and perioperative data (Appendix 1) were collected on retrospective review of patients record. Follow-up information were obtained between February and May 2001 by physician or patient contact and was obtained in all patients except three. Hospital mortality was defined as death within 30 days of operation or during the same hospital admission. SPSS for Windows version 10.0 (SPSS Inc., Chicago, IL) was used to perform statistical calculations. Data are expressed as mean ^ standard deviation. Continuous variables were analyzed using independent t-test or Mann Whitney U-test when data was not normally distributed. Pearson x 2 or Fisher s exact test were used to determine differences when variables were expressed by dichotomous values. The univariate analysis was followed by multivariate logistic regression to determine independent risk factors. Preoperative factors that were significant or with a P value,0.3 were retained in the analysis. Survival was examined by the Kaplan Meier product limit method and p values for difference between survival were obtained by the log-rank test. A value of P, 0:05 was considered statistically significant. 3. Results 3.1. Early The hospital mortality was 42% (36 patients). With the classic repair, mortality concerned 28/56 patients (50%) compared to eight/29 patients (28%) in the double patch technique (P ¼ 0:06) (Table 3). The mode of death is listed in Table 1. The most common mode of hospital death was persistent low cardiac output and recurrence of the VSD. Table 2 Recurrence of the VSD related to the technique of repair (Fisher s exact test: P ¼ 0.09) We observed six recurrences, three in patients with anterior VSD and three with posterior VSD (Table 2). No recurrence was observed with the double patch technique (P ¼ 0:09). Two were reoperated with success, but the four others dead in spite of reoperation in one patient Late Late death occurred in 31 patients between 45 days and 12.5 years after operation. Causes of death were non-cardiac in 8 cases. In all others cases, the cause was cardiac related (usually either by cardiac failure or due to sudden death). The Kaplan Meier curve of survival after early repair of post infarction ventricular septal defect (hospital mortality excluded) is presented in Fig. 1 with a mean follow-up of 7 years 2 months. Long term survival (excluding hospital mortality) at 2, 5 and 8 years was respectively 85, 63 and 51%. After the 8th year, survival rate dropped down and at 10 years reached only 23%. On the late 18 survivors, 13 (72.2%) are in NYHA classes I or II Risk factors N.pts a Recurrence n % SD % 1 patch patches a N.pts: number of patients. All variables were studied for hospital and late death. The significant risk factors for hospital death are listed in Table 3 in order of decreasing importance. Hospital death was strongly related to preoperative clinical status and its evolution under IABP. Right ventricular function assumed as the percentage of mid-cavity diameter reduction was the second Table 1 Hospital mortality Mode of death n % SD % Low cardiac output VSD recurrence a Cerebral stroke IABP complication b Renal failure Ventricular tachycardia Other Total a b VSD: ventricular septal defect. IABP: intra-aortic balloon pump. Fig. 1. Kaplan Meier survival curve for patients undergoing repair of post infarction ventricular septal defect. Hash marks represent censored data. In brackets: numbers of patients at risk.

4 728 L. Labrousse et al. / European Journal of Cardio-thoracic Surgery 21 (2002) significant difference has been found in the long-term survival rate in both cases. Similarly, none of the others variables studied were significant Multivariate analysis All variables which reached a significant level,0.3 were studied in a logistic regression analysis. In this way, four incremental risk factors of hospital mortality were identified: poor preoperative clinical status, right ventricular dysfunction, lack of clinical evolution under IABP and type of repair (one patch technique). Fig. 2. Survival in patients undergoing repair of post infarction ventricular septal defect comparing those repaired with the one patch technique (solid line) to those repaired with the double patch technique (dashed line). Hash marks represent censored patients. most important risk factor for hospital mortality. Year of the procedure (,1991) and type of repair (one or two patches) were less significant. Concomitant CABG was associated with a lower risk of hospital mortality (33 ^ 14 versus 51 ^ 14%), but did not reach a significant level (P ¼ 0:1). Other factors with a p value at less than 0.3 included proximal coronary lesion, previous myocardium infarction and older age. No significant factors was found in the remaining 35 variables studied (Appendix 1). Especially, it concerns localization of the VSD, sex of the patient, pre and postoperative coronary score and all hemodynamic variables. Concerning long term survival, Kaplan Meier survival curves of patients related to the type of closure, and related to associated CABG are presented in Figs. 2 and 3. No 4. Discussion Post infarction VSD is uncommon, and still associated with a high mortality rate [1 7]. In our previous study [8], the same as in others [3 7,11,13,15], we observed that a shorter interval between the perforation of the septum and the surgical repair was an important risk factor, with no death in patients operated on after the 15th day. Moreover, the delay of surgery was directly correlated to the preoperative status because a lots of the patients die before surgery. As it seems not ethical to delay patients of 15 days and impossible to detect patients who might be able to wait this period, an emergency procedure has to be proposed for all patients with post infarction VSD. Thus, as others [3,14], we believe that these patients should be operated on urgently if they are in hemodynamically stable condition and immediately if they are in cardiogenic shock. Because when the necrotic muscle has been replaced by fibrous tissue technical problems are largely different, we have Table 3 Predictors of increased hospital mortality a Variables Number of patients Hospital death n % P Preoperative group , % reduction in RV diameter, ,0.05 $ Clinical evolution under IABP Impairment ,0.05 Stabilization or improvement Type of repair One patch ,0.06 Two patches Year of operation Before , Associated CABG Yes ,0.1 No Previous myocardial infarction Yes ,0.2 No Proximal coronary lesion Yes ,0.3 No Age (years) ,0.3 # a RV: right ventricle; CABG: coronary artery bypass graft; and IABP: intra-aortic balloon pump.

5 L. Labrousse et al. / European Journal of Cardio-thoracic Surgery 21 (2002) Fig. 3. Survival in patients undergoing repair of post infarction ventricular septal defect comparing those with concomitant CABG (dashed line) to those without concomitant CABG (solid line). Hash marks represent censored patients. excluded from this study late repair (.15 days) of post infarction VSD. Hospital mortality in our series is similar to that reported by others groups since 1990, especially results of the last 10 years [2 4,15]. However, comparison of mortality between different institutions remains unreliable. Indeed, patients are usually first referral to cardiologist centers, and a part of the patients (depending of cardiologist habit) might be considered not suitable and then not referred to surgery. So, a part of the discrepancy in operative results between institutions might be attributed to variable recruitment. As in our series, the improvement of hospital mortality in the last years is usually found in other studies [3,4]. Risk factors for early death have been determined in our previous series [8], and confirmed in others [3 7,13,16,17]. Concerning clinical status, all authors found a higher mortality rate in patients with preoperative cardiogenic shock. However, we have to consider not only the cardiogenic shock itself, but also its intensity and its evolution under medical therapy. Worst results were observed in patients with lack of improvement hemodynamic status in spite the use of an IABP. This last point is likely the reflect of a large amount of infarcted left myocardium, which will Table 4 Hospital mortality in patients treated with the double patch technique related to the localization of the VSD (Fisher exact test: P ¼ 0.4) Localization N.pts Hospital mortality n % SD Anterior ^ 19 Posterior ^ 24 have to switch patients to circulatory assist devices as a bridge to heart transplantation if patient s conditions allow it. Right ventricular function, important risk factor in our study, was not detected again in a recent publication [16]. Right ventricular dysfunction is related to several factors: left ventricular dysfunction, right ventricular infarction or ischaemia and right ventricle volume overload. Only the last is reversible. Analysis of the part of these three components is not easy, and as sample size of VSD series is small, analysis and conclusions are likely not very reliable, and would need much larger samples to determine exact predictors of outcome. About surgical technique, few technical aspects need to be pointed. The double patch technique with glue used since 1986 is done without infartectomy at all. So, it avoids additional detrimental damages on the septum. Moreover, as the right ventriculotomy is achieved through an infarcted area, any detrimental effect of its function remains hypothetical, and identical long term follow-up preclude for that on long term. As each patch is used as a support for the suture on the other, they make the suture easier and less prone to tear than pledgets. Another role of the second patch is to contain the glue. By that way, the glue homogenize, reinforce and maintain the friable septal tissue which become dense and solid. In literature, VSD recurrences are not infrequent [2 4]. In a recent series [2] a residual shunt was found in 40% of patients with reoperation in a third of them and subsequent mortality. The absence of recurrence in patients treated with the double patch and glue technique could be an explanation for a part of the decrease of mortality since this technique was used. Moreover, a recent publication [5] mentions perioperative failure of the repair and the need of a re-repair with long time of cardiopulmonary bypass. Such pejorative

6 730 L. Labrousse et al. / European Journal of Cardio-thoracic Surgery 21 (2002) complication does not occur in our experience with the double patch technique. So the double patch appears more reliable than the one patch technique. Posterior VSD has been traditionally associated with increased operative mortality. Difficulties in operative exposition and repair are usually advanced to explain that result [5,12]. In our series, there is no significant difference in operative mortality according to the localization of the VSD when the repair is performed with the double patch technique (Table 4). However, our sample is not big enough to totally ensure that. As for classic repair, and even if surgical exposure is improved by the double ventriculotomy, the repair is usually more demanding than in anterior localization. And the absence of recurrence of the VSD even in this localization confirms that the double patch technique allows a perfect and reliable repair. David recently described a technique of repair by exclusion of the VSD with a large bovine pericardial patch [14]. His results are very impressive; but in his last series [16], David noted that in anterior localization patch exclusion would have the same results than traditional repair; and that the improvement of early results are in particular observed in case of posterior VSD. As our results in patients with posterior VSD seem to be similar to those with anterior VSD, up to now we have had no opportunity to evaluate David s technique. About preoperative coronarography, as other authors [4,14,18,19], we systematically performed it as soon as the patient is admitted. It allows in the same time the systematic insertion of an IABP, and concomitant CABG are achieved if necessary. No detrimental effect has been found with that policy. Especially, no mortality or morbidity has been found to be related to coronarography. Moreover, associated CABG did not appeared as a risk factor for early and late death. Recently report from Zûrich [18] has highlighted the interest of concomitant CABG. Our results confirm its conclusions. As long term follow-up of patients with associated coronary lesions is similar to those without coronary lesion, and as no complications can be related to concomitant CABG, preoperative coronarography had to be recommended and CABG performed if necessary to eliminated a potential ischemic added risk due to other coronary arteries lesions. Some limitations of this study need to be noted. We have to point to the known disadvantages of a retrospective study, which covers 30 years. Especially, the quality of operative (cardioplegia, etc.) and intensive care management has dramatically changed and improved over this period. That makes any analysis of early mortality partially inaccurate. So, our results of the impact of the double patch and glue technique on early mortality have mainly to be analyzed in the lack of early recurrence of the VSD and subsequent mortality. However, this study reflects the intake of patients from a particular institution, and thus reflects similar patterns of patients recruitment and surgical indications. 5. Conclusion However better patients management during the years may have play a role in the improvement of surgical results in the treatment of post infarction VSD; the use of the double patch technique by avoiding recurrence of the VSD played a role in that reduction of the hospital mortality. In front of this and the absence of long term detrimental effects, this technique has to be recommended in the early repair of post infarction VSD. Moreover, our study confirms that CABG can be done safely to control the added risk of an associated coronary artery lesion. References [1] Crenshaw BS, Granger CB, Birnbaum Y, Pieper KS, Morris DC, Kleiman NS, Vahanian A, Califf RM, Topo EJ. 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(1): [2] Deja MA, Szostek J, Widenka K, Szafron B, Spyt TJ, Hickey MS, Sosnowski AW. Post infarction ventricular septal defect can we do better? Eur J Cardiothorac Surg 2000;18(2): [3] Prêtre R, Ye Q, Grünenfelder J, Lachat M, Vogt PR, Turina MI. Operative results of repair of ventricular septal rupture after acute myocardial infarction. Am J Cardiol 1999;84: [4] Cox FF, Morshuis WJ, Thijs Plokker HW, Kelder JC, van Swieten HA, Brutel de la Rivière AB, Knaepen PJ, Vermeulen FE. Early mortality after surgical repair of post infarction ventricular septal rupture: importance of rupture location. Ann Thorac Surg 1996;61: [5] Dalrymple-Hay MJR, Monro JL, Livesey SA, Lamb RK. Post infarction ventricular septal rupture: the Wessex experience. Semin Thorac Cardiovasc Surg 1998;10(2): [6] Chaux A, Blanche C, Matloff JM, de Robertis MA, Miyamoto A. Post infarction ventricular septal defect. Semin Thorac Cardiovasc Surg 1998;10(2): [7] Skillington PD, Davies RH, Luff AJ, Williams JD, Dawkins KD, Conway N, Lamb RK, Shore DF, Monro JL, Ross JK. Surgical treatment for infarct-related ventricular septal defects. Improved early results combined with analysis of late functional status. J Thorac Cardiovasc Surg 1990;99(5): [8] 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: [9] Daggett WM, Buckley MJ. The surgical treatment of post infarction ventricular septal defect: indications, techniques and results. In: Moran J, Michaelis L, editors. Surgery Fort the Complications of Myocardial Infarction, New York: Grune and Stratton, pp [10] Fannapazir L, Bray CL, Dark JF, Moussalli H, Deiraniya AK, Lawson RAM. Right ventricular dysfunction and surgical outcome in post infarction ventricular septal defect. Eur Heart J 1983;4: [11] Jones MT, Schofield PL, Bray CL. Surgical repair of acquired ventricular septal defect: determinants of early and late outcome. J Thorac Cardiovasc Surg 1987;93: [12] Madsen JC, Daggett Jr WM. Repair of post infarction ventricular septal defects. Semin Thorac Cardiovasc Surg 1998;10(2): [13] Kirklin JW, Barratt-Boyes BG. Post infarction ventricular septal defect. In: Wiley J, editor. Cardiac Surgery, New York: Wiley, pp

7 L. Labrousse et al. / European Journal of Cardio-thoracic Surgery 21 (2002) [14] David TE, Dale L, Sun Z. Post infarction ventricular septal rupture: repair by endocardial patch with infarct exclusion. J Thorac Cardiovasc Surg 1995;110: [15] Lemery R, Smith HC, Giulani 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: [16] David TE, Armstrong S. Surgical repair of post infarction ventricular septal defect by infarct exclusion. Semin Thorac Cardiovasc 1998;10(2): [17] Moore CA, Nygaard TW, Kaiser DL, Cooper AA, Gibson RS. Post infarction ventricular septal rupture: the importance of location of infarction and right ventricular function in determining survival. Circulation 1986;74: [18] Prêtre R, Ye Q, Grünenfelder J, Zund G, Turina MI. Role of myocardial revascularization in post infarction ventricular septal rupture. Ann Thorac Surg 2000;69: [19] Muehrcke D, Daggett W, Buckley M, Akins C, Hilgenberg A, Austen W. Post infarct ventricular septal defect repair: effect of coronary artery bypass grafting. Ann Thorac Surg 1992;54: Appendix A. The variables entered into the univariate analysis included: Demographic variables: sex, age at time of operation. Medical history variables: hypertension, diabetes mellitus, nicotinism, angina, previous myocardial infarction, dyslipidemia. Clinical variables: preoperative status (group), supraventricular or ventricular arrhythmia, atrio-ventricular conduction failure, preoperative intra-aortic balloon pump, evolution (impairment, stabilization, improvement) under intra-aortic balloon pump. Ventricular septal defect variables: myocardial infarction, site of myocardial infarction, delay infarction-ventricular septal defect. Angiographic variables: site of ventricular septal defect, left ventricular ejection fraction, right ventricular function, left ventricular aneurysm, mitral insufficiency, delay infarction-angiography. Coronarography variables: preoperative coronary score, post-operative estimated coronary score, site of the coronary lesion related to myocardial infarction. Catheterization data variables: pulmonary artery pressure (systolic, mean, diastolic), right ventricular pressure (systolic, diastolic), pulmonary capillary pressure, left ventricular pressure (systolic, diastolic), cardiac index, corrected cardiac index, enrichment in O 2 in volumes, pulmonary to systemic flow ratio, left ventricular work index. Operative variables: operative myocardial ischemic time, extra corporeal circulation time, type of repair, year of operation, associated coronary bypass graft, associated left ventricular aneurysmectomy. Appendix B. Conference discussion Dr D. Wheatley (Glasgow, Scotland): Thank you very much for this very well presented and interesting series. One of the questions I had you partly answered but I wonder if you could just clarify for us the policy regarding coronary angiography. Many cardiologists are understandably reluctant to do a coronary angiogram in a very ill patient a day or two after an infarct, and I wondered what your policy is about that. It appears that you have this done routinely now, but having seen that, do you then bypass all significant stenoses, including the infarct-related artery, or do you do a more limited intervention? Dr Deville: Now our policy is systematic coronarography in our patients. We have not noted detrimental effect of this procedure. The time required for the coronarography is short. All the patients with a significant coronary lesion (more than 70%) underwent a coronary bypass. It is generally not on the infarcted coronary artery but on a collateral of this artery. The discussion could concern patients with very poor hemodynamic condition with persistent cardiogenic shock. In such cases could be discussed the possibility of a perioperative coronarography, but in some patients there is no associated lesion. I think Prof. Turina brings a good clarification of this problem in a recent publication. Mr A. Ritchie (Cambridge, UK): Thank you very much for your interesting and very long study, and your results are much more experienced than my personal limited clinical experience, but can I ask you a question that is very important to me. Is the improvement in both the short-term and long-term outcome more related to your management of patients when they present to you? And what I am really trying to get at here is has your policy of treating these patients before you actually take them to the operating theater changed? In my institution, for example, I would put a balloon pump into the patient for 3, 4, maybe even 5 days and then take them to the operating theater, and that I have found has decreased the mortality for the procedure but also reduced the number of post repair leaks that subsequently come, and I think that more than any other factor, along with warm blood cardioplegia, which I routinely use, has changed the scenario for these patients. Is that clear in the way you treat your patients or do you take these patients immediately to the operating theater? Dr Deville: Yes, our policy is to take these patients very quickly. If the patient is in stable condition, I think it is important to operate him urgently, but if he is in persistent shock, it is immediately, as soon as an operating room is available. Of course, the in-hospital mortality would be poor, but if you delayed patients, some of them would be dead before the surgery, and even if you have better short-term results, it is not ethical. Dr P. Skillington (Melbourne, Australia): Thank you for your presentation. Most studies have shown an increased mortality with inferior VSD. Did you look at that risk factor? Dr Deville: Yes. In our experience, the early results are not different according to the location of the VSD, and personally I think that the technical management is very important. Most of the problems were related to VSD recurrence. In literature, VSD recurrence appeared between 10 and 40%, and some publications mentioned peri-operative failure of the repair, especially in the posterior localization. We do not observe such complication with the double patch technique and the use of glue, and in our experience the difference was not significant between the early deaths in the two groups of patients. But of course, the technical aspect is more difficult in posterior localization; the exposure is more difficult and the lesion is, most often, more sophisticated. Dr M. Irarrazaval (Santiago, Chile): Two short technical questions. Do you recommend this double patch for all of the VSDs or you are more selective in anterior or posterior? And the second question is, in this 30-year period of time, there have been changes in the decision of where do you put the patch. We have gone more and more suturing the patch very far away from the necrosis, as far as possible. Would that be possibly another reason for the improvement of the results? Dr Deville: To the first question, since 1992, I have systematically used the double patch technique with a double ventriculotomy. The role of the second patch is to constitute a support for the running suture but also to contain the biological glue between the two patches. To your second question, of course we attempt to suture the patch very large away from the border of the lesions and sometimes very close to the mitral annulus. I think it is very important to exclude the most part of the infarcted septum. Dr M. Turina (Zurich, Switzerland): Claude, congratulations on a very interesting paper. I was very surprised to find the right ventricular dysfunction as the independent predictor. In my experience, every patient who comes on the operating table has a major right ventricular dysfunction because of the shunt. So the next question is a logical one. Do you have a level of left to right shunt when you intervene? Some of these patients will have a very minor left to right shunt, something like 20, 25%, and in some of them it will progress quickly. In others, they can be managed with a balloon pump for a longer period of time, as suggested. But every patient who is operated upon has a right ventricular dysfunction. Dr Deville: Yes. In the first part of our study we determined right ventri-

8 732 L. Labrousse et al. / European Journal of Cardio-thoracic Surgery 21 (2002) cular dysfunction as a very important risk factor. It is always significant in the second part, and we believe have identified two groups of patients: patients who have a right ventricular dysfunction compared to 10% who have no survival, and between 10 and 20% who have a high risk of mortality but some survival. I think the problem is related to the fact that right dysfunction is related to three components: the left ventricular dysfunction, the right ventricular infarct, and the overload due to shunt. Only the last component is reversible. So sometimes patients with very poor right ventricular function because of an important shunt have a good outcome. I am not sure that this right ventricular function is a very good factor. I think it is an intricacy of the three components.