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Eur J Cardiothorac Surg 2000;18:194-201
© 2000 Elsevier Science NL
Department of Cardio-thoracic Surgery, Glenfield General Hospital, 1 Groby Road, Leicester, LE3 9QP, UK
Received 8 September 1999; received in revised form 2 May 2000; accepted 10 May 2000.
Corresponding author. Tel.: +44-116-287-1471; fax: +44-116-232-1282
e-mail: m.deja{at}btinternet.com
| Abstract |
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Key Words: Ventricular septal rupture/ventricular septal defect Myocardial infarction-mechanical complications Surgical treatment Retrospective analysis
| 1. Introduction |
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The first surgical repair of post infarction VSD was performed by Cooley in 1957 [3]. Several series have been reported since [410]. As the condition is relatively rare, published series are small. The largest reported series from the Wessex Centre [10] consists of 179 patients. The early mortality reported varies from as low as 19% [6] to as high as 66% [11] and predictors of early and late clinical outcome are still not well established.
The aim of our study was to identify predictors of early and late outcome among patients treated surgically for post infarction VSD over a period of 12 years.
| 2. Materials and methods |
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One hundred and seventeen patients were treated in the reviewed period. Mean age was 65.5±7.8. There were 43 females.
We were able to obtain full perioperative data on 110 patients only, and we therefore present retrospective analysis of these cases. The mean age was 65.6±8.0 (median 66, range 3586). There were 41 females (37%). Seventy-six patients (69%) presented with anterior VSD and 34 (31%) with posterior. The ventricular septal rupture occurred on average 5.6±7.8 days post infarction (median 4 days, range 067). Twenty-eight patients (26%) were thrombolysed.
A history of previous coronary artery disease was found in nine patients (8.2%), six of whom (6.5%) had suffered MI in the past. Preoperative angiography was performed in 90 patients (81%). This showed single vessel disease in 46 patients (51%), double vessel disease in 20 patients (22%), and triple vessel disease in 24 patients (27%). The left main stem was involved in three cases (3.3%).
Other medical problems and risk factors are listed in Table 1.
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On admission 27 patients (25%) were in cardiogenic shock with signs of right ventricular failure and low cardiac output; another 29 (26%) had radiological evidence of pulmonary venous congestion with clinical signs of pulmonary oedema. The haemodynamic status of 18 patients deteriorated and the status of seven patients improved between the time of admission to hospital and operation. Therefore by the time of operation 33 (30%) patients were in cardiogenic shock and another 33 (30%) in pulmonary oedema. In addition nine patients (8.2%) on admission and three (2.7%) at surgery presented with right ventricular failure with no signs of pulmonary congestion or of cardiogenic shock. Fifteen patients (13%) required mechanical ventilation before surgery. Inotropic support was necessary in 54 patients (49%). Intraaortic balloon pump (IABP) counterpulsation was used in 66 patients (60%) before operation. The average time of IABP support prior to surgery was 2.4±2.1 days (median 2, range 013). One patient was supported with extra corporeal membrane oxygenation (ECMO) prior to surgery.
The period from admission to surgery averaged 2.5±4.6 days (median 1, range 027). The operation was performed on the day of admission in 35 cases (31%) and on the next day in 39 (35%). The time that elapsed from MI to surgery and from septal rupture to surgery averaged 14.8±29.7 (median 6) and 9.0±28.1 days (median 2), respectively. There were six patients with chronic post-infarction VSD in our group, who were operated more than 30 days post septum rupture (maximum 215 days). Three of them had been discharged home between septal rupture and operation, but then were readmitted and operated on an urgent basis due to haemodynamic deterioration.
The operations were performed by nine surgeons. The VSD closure with no patch material buttressed mattress sutures, as originally described by Daggett at al. [12], was used in six patients (5.5%): apical amputation in four cases, and posterior VSD repair in two. A patch was used in the remaining patients. This was dacron in the majority of cases (72 patients, 65%), additionally covered with pericardium in one case and with teflon in another. In 16 cases (14%) teflon patch was used. We used also autogenous pericardium, bovine pericardium, polytetrafluroroethylen (Gore-Tex) (PTFE) and PTFE with pericardium in five, two, two and one patient, respectively. The exclusion technique was used increasingly throughout the later half of our series [6].
Excision of left ventricular (LV) aneurysm was performed in ten patients (9.1%), nine of them involving anterior wall. Pseudoaneurysm of LV was found and repaired in further six patients (5.5%).
Forty patients (36%) received coronary artery bypass grafts (CABG) (average 1.5 grafts per patient; median 1, range 14). Grafts supplied the infarcted area in seven cases and the remote myocardium in 38 cases.
In 38 cases (34%) no aortic cross-clamp was used, and the heart was either beating (13 patients) or fibrillating (23 patients). Intermittent ischaemia with fibrillation was used in two cases. In the remaining 70 patients (66%) the myocardium was managed with either crystalloid (58 cases) or blood (12 cases) cardioplegia. The mean cross-clamp time was 63.2±23.2 min (median 62, range 10105). Cardiopulmonary bypass time averaged 98.2±38.8 min (median 92.5, range 32240). We used normothermia in 12 cases. The remaining patients were cooled down on average to 28.9±2.7°C (median 28, range 2235).
| 3. Statistical analysis |
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The risk factors for early outcome were analysed using multiple logistic regression. Table 2 contains pre- and perioperative factors included in the analysis. The haemodynamic statuses on admission and at surgery were analysed in two separate models. Similarly we either entered the time between MI and surgery into the model or substituted it with the two time periods, from MI to VSD and from VSD to surgery. Additionally, we separately analysed the influence of some postoperative factors (Table 3) on the outcome of those patients who did not die at surgery. Because some of the independent variables (like time periods) had a skewed distribution, logarithmic transformation was used before entering those variables into the analysis. To estimate logistic regression models the stepwise backward Wald method was used. The variables were entered in the model if the probability of their score statistic was less than 0.05 and removed if the probability was greater than 0.1. The results are presented only for factors that remained in the equation. Their estimated odds ratio (OR) together with 95% confidence interval (CI) is quoted.
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As time periods were log-transformed (using decimal logarithm) before being entered into analysis, the odds ratios quoted for this variables correspond to an increase in the original variable by a factor of 10.
The P<0.05 was considered significant.
| 4. Results |
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In the group of 110 patients, in whom complete analysis was possible, 30-day mortality was 35% (38 patients). The mortality in the anterior VSD group was 34% and in the posterior VSD group 35% (NS).
When weaning off bypass, significant inotropic support (more than 5 µg/kg per min of Dopamine) was used in 102 patients (92.7%), temporary pacing in 40 (36%) and intraaortic balloon counterpulsation in 82 patients (74%).
Seven patients (6.4%) died during surgery. The remaining 103 patients were managed in intensive therapy unit (ITU). The details of ITU stay and postoperative course are presented in Table 4.
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The presence of cardiogenic shock at the time of surgery or on admission increased the risk of postoperative renal failure requiring continuous veno-venous haemofiltration (CVVH) OR 8.5 (CI 2.035.6) (P=0.004) and OR 3.6 (CI 1.211.3) (P=0.03), respectively, but we failed to show any influence of preoperative renal impairment or the length of cardiopulmonary bypass.
No pre- or perioperative factor was found to correlate with the occurrence of a residual VSD postoperatively. However, we observed a residual shunt on postoperative echocardiography somewhat less frequently in the patients who were operated upon in cardiogenic shock (P=0.053) (OR 0.3; CI 0.11.0).
We failed to find any significant predictors of other postoperative complications including postoperative respiratory failure, low cardiac output state or requirement for permanent pacing.
Analysing the postoperative period of the group of patients who did not die in theatre (103 patients), we found low cardiac output syndrome and renal failure requiring haemofiltration, but not the presence of a residual shunt to be an independent predictor of mortality OR 18.5 (CI 1.933.2) (P=0.00001) and 18.6 (CI 3.2105.7) (P=0.001), respectively. However, the presence of a shunt was a strong predictor of reoperation OR 7.7 (CI 1.440.9) (P=0.02).
We observed 63 deaths in the group of all 117 patients. The 10 years survival was 46±5%. The 5 years survival was 41±6% (Fig. 1) .
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In multivariate analysis, preoperative cardiogenic shock was found to affect late survival OR 2.7 (CI 1.54.9) (P=0.001) (Fig. 2) (Table 6a,b). This effect is secondary to the influence on the first months survival since when the analysis was performed on those 72 patients who survived the first postoperative month, perioperative shock was no longer a significant predictor. In this group, age above 70 proved to have a significant effect on life expectancy -OR 2.4 (CI 1.015.6) (P=0.048). Interestingly we found that posterior VSD location improved late survival in those who survived the early period OR 0.2 (CI 0.10.9) (P=0.03). (Table 6c) No other preoperative, perioperative or early postoperative factors, including concomitant CABG, patch material or persistent shunt proved significant. In the group of 72 patients who survived longer than 30 postoperative days, 12 (16.7%) were in NYHA class III or IV and five (6.9%) in CCS class III or IV at the last follow-up. We were unable to identify any perioperative factor to significantly influence functional outcome.
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| 5. Discussion |
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The 30-day mortality in our series was 35%. This is much lower than the 66% reported by Hill and Stiles in a pooled series from four cardiac centres from Northern California [11], corresponds with the mortality reported by Cooley or Chaux et al. [4,5], is higher than 27% (31% in acute VSD) reported from Wessex Centre [10], and much in excess of 19% reported by David and Armstrong who were using the exclusion technique [6].
The interesting finding in our series is the similar mortality in anterior and posterior VSD groups (34 vs. 35%). Most reports identify posterior VSD location as a risk factor for higher mortality [911,1418]. This, however, is not a universal finding [6,19]. Higher mortality reported in posterior VSD can either be related to greater technical difficulties associated with surgical repair or to a higher incidence of right ventricular failure [1518]. The infarct exclusion technique advocated by David may be the answer to technical difficulties, as his survival/mortality in this series has been similar in both VSD locations [6,20]. Our surgical technique was not consistent throughout the series. Interestingly, we treated only few patients with right ventricular failure without signs of shock or pulmonary congestion. This may account for the similar mortality in both anterior and posterior VSD cases.
Thirty percent of our patients developed LV failure and 15 of them (14%) required mechanical ventilation before surgery. We have not found such high numbers in other studies. The need for mechanical ventilation was not a result of delaying operation but to aid in management of pulmonary oedema and/or cardiogenic shock. Thirteen of these patients underwent surgery on the day of admission. Interestingly the need for preoperative IPPV did not influence early survival.
As a routine, our patients were managed with dopamine infusion and diuretics. Only in half of them (54 patients) the dose of dopamine was greater than 5 µg/kg per min. IABP support was used in 66 patients. The routine use of intraaortic counterpulsation increased in the second half of our series. Preoperative IABP will increase cardiac output and decrease the left to right shunt, and will also improve coronary perfusion. Nevertheless, there are no data to show an improvement in early mortality with preoperative IABP use [8,10,14]. Furthermore, there are reports of increased mortality associated with IABP [19,21]. The reasons for this are unclear. It seems however, that the IABP was used in the most gravely ill patients only. We failed to show any benefit of preoperative IABP use in multivariate analysis of our data. Still, it was our impression that intraaortic balloon pumping allowed for some clinical stabilisation in the patients in whom it was used. There is some data showing that the peak improvement occurs in 24 h and no further benefit can be expected with prolonged balloon pumping [22]. It may well be that, at least in some patients, we missed the best opportunity window and the patients underwent surgery once their haemodynamic status started to decline again. After all, we implemented IABP in 60% of our patients preoperatively for average of 2.4 days and, although it seemed to improve patients status, we eventually operated on only seven patients in better haemodynamic condition than they were on admission. The haemodynamic deterioration between admission and operation as well as shock prior to surgery is strong predictors of early mortality, much stronger than the shock on admission. The finding of cardiogenic shock significantly increasing mortality has been well established [5,6,811,17,19,20].
Another independent predictor of early mortality in our series was the time period from infarction to surgery. The odds ratio of 0.1 in multiple logistic regression may suggest, that the early survival be significantly improved by delaying the surgical procedure. One of the appealing concepts may be, that the more chronic VSD is easier to repair since the septum is well scarred and the patch can be securely sutured [2]. Another simple explanation given by authors who described this relationship is, that sicker patients select themselves and are treated surgically much earlier in face of intractable shock [2,5,11]. However in our series the time from infarct to surgery was a predictor independent from patient haemodynamic status (by multivariate analysis). Thus, it wasn't just clinical shock that influenced higher mortality in patients operated soon after infarction.
When we analysed the time intervals from infarct to rupture and from rupture to surgery it was the first one that appeared to be a highly significant predictor of survival (OR 0.1). It suggests that early rupture represents a separate patient characteristic predictive of early mortality. We propose, that patients with a larger MI developed septal rupture earlier and because of extensive myocardial damage did worse, even if they didn't develop overt shock preoperatively. At the same time in the model in which shock on admission and haemodynamic deterioration are included instead of shock at the time of surgery the time period between septal rupture and surgery reaches significance, with a longer time interval favouring survival. This is in agreement with the mentioned concept of easier operation in more chronic VSDs [2], however one shall remember that deterioration of patient haemodynamic status during the hospital stay is an ominous sign.
We observed a high incidence of residual postoperative shunt. Our incidence of 43% is well in excess of what is reported in the literature [9]. This may be a result of very careful echo follow-up. Only 13 patients (12%) required reoperation on clinical grounds. Contrary to reported data the presence of a persistent shunt was not associated with increased early mortality in our series [9]. We failed to show any influence of an echocardiographically evident shunt on late functional status in survivors and on late mortality. It appears therefore, that most of this apparently high shunt incidence was clinically not significant.
The presence of cardiogenic shock at the time of surgery had a major influence on long-term survival, largely due to its adverse impact on early mortality. When Cox proportional hazard analysis was used to find the predictors of outcome in those who survived 30 postoperative days, preoperative shock was no longer a significant factor. Indeed none of the preoperative characteristics apart from the age of above 70 and posterior VSD location prove significant. So we believe that operation can yield a good long-term result in even the sickest patients. It is even more compelling, as the vast majority of survivors remain in NYHA class I or II throughout the follow-up. This relates to elderly patients as well. These conclusions are shared by Dalrymple-Hay et al. [10], David [6], Madsen and Daggett [2] and others.
Another controversial question remains the need for concomitant coronary revascularization. Several studies have failed to show a relationship between CABG and perioperative mortality [10,11,14,19]. This was the case in our experience as well. There are some data to suggest that concomitant myocardial revascularization in patients with post infarct VSD improves late survival [7,23]. This effect may be more evident in posterior VSD [14]. Conversely, the Southampton experience [10], Loisance et al. [24] and Piwnica et al. [25] failed to show any benefit of concomitant grafting on late results. We couldn't prove any influence of concomitant CABG on late survival of our patients using Cox regression model (Fig. 3) . This remains the case when anterior and posterior VSD patients were studied separately as well as, when considering multiple vessel disease only.
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In conclusion it appears from our data that cardiogenic shock and a short interval between MI and septal rupture carry a grave prognosis. We would recommend implementing resuscitative measures initially, especially in patients admitted in cardiogenic shock. We feel strongly that prolonging efforts to improve patients cardiovascular state beyond first 24 h is hazardous and the benefit obtained with initial stabilisation may be lost.
A residual shunt, even if requires reoperation, does not preclude successful late outcome.
| Acknowledgments |
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| Footnotes |
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| Appendix A. Conference discussion |
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You had a very high incidence of residual VSDs, in the region of 40%, many of which, of course, may just have been small ones detected by echo. But have you considered changing your technique as a result of this high incidence of residual VSDs?
Dr M.A. Deja: Actually we didn't want to include this slide in the presentation because it would make it too long. We looked at the early postoperative findings to find whether they can predict survival. And we found, that the low cardiac output and need of CVVH use increased very significantly the early mortality. However, we didn't find any significant influence of residual VSD. And although we needed to reoperate on some of those patients, they remain in a good functional class and most of them are still alive. So indeed, quite a significant proportion of these residual shunts was clinically non-significant and just picked up on echo.
Mr K. Dhital (London, UK): Can you comment on whether the availability and use of thrombolytic therapy has had any influence on the number of VSDs that you have seen and whether this has any effect on the outcome?
And secondly, do you, or members of the audience, have any experience with using percutaneous devices for closing the residual shunt to try and avoid redo surgery?
Dr M.A. Deja: Starting with the second question, we don't have any experience with percutaneous devices.
Regarding the first question, the thrombolysis, we found a trend of increased mortality, early mortality, in the patients who had been thrombolysed, but the P value was around 0.15, more or less, so it wasn't really significant.
Dr. J.R.L. Hamilton (Newcastle-upon Tyne, UK): One of your first slides showed a marked reduction in the number of patients referred over the last few years. Is that a change in the natural history do you think?
Dr M.A. Deja: The last bar that you've seen was up to August of the last reported year, and was much lower. But indeed, we had the highest number of about, I think 16 patients in 1995, and in most years we've seen something like eight cases.
Dr. F. Schoendube (Aachen, Germany): My question concerns your postoperative protocol. I remember you had some intra-aortic balloon pumps. Do you implant them prophylactically or what is your rationale in putting them in?
Dr M.A. Deja: We used a balloon pump in 60% of our patients preoperatively. But at the very moment, our tactic is to put the balloon into every patient who presents with VSD, just to try to stabilize them as much as possible and operate in the best possible hemodynamic status.
Dr A. Merounko (Tomsk, Russia): What is in your mind about transcutaneous close of postinfarction VSD with a special device?
Dr. M. Deja: We haven't tried this, so I can't answer this question.
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