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a Department of Thoracic and Cardiovascular Surgery, Johann-Wolfgang-Goethe University Hospital, Frankfurt/Main, Germany
b Center of Health Science, Institute for Biostatistics and Mathematical Modelling, Johann-Wolfgang-Goethe University Hospital, Frankfurt/Main, Germany
Accepted for publication February 6, 2009.
* Address correspondence to Dr Papadopoulos, Department of Thoracic and Cardiovascular Surgery, Johann Wolfgang Goethe University, Theodor Stern Kai 7, Frankfurt/Main, 60590, Germany (Email: nestoras.papadopoulos{at}gmail.com).
| Abstract |
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Methods: A total of 32 consecutive patients (mean age, 62.5 ± 10.5 years) underwent postinfarction VSD repair using a standardized technique in our department. A retrospective analysis of clinical and operative data, predictors of early mortality, and long-term survival was performed. The localization of VSD was posterior in 50% and anterior in 50% of the patients.
Results: The hospital mortality was 31.2% (10 patients). The most common cause of hospital death was persistent low cardiac output. The mortality of the posterior VSD group was significantly lower than that of the anterior VSD group (18.7% and 43.7%, respectively, p = 0.01). Intra-aortic balloon pump support and absence of cardiac shock were significantly associated with a lower risk of hospital mortality (p = 0.0001 and p = 0.0009, respectively). The actuarial survival rates of in-hospital survivors at 5 and 10 years were 79% ± 2% and 51% ± 3%, respectively.
Conclusions: The repair of postinfarction VSD by the infarct exclusion is feasible and safe. This technique seems to offer sufficient favorable early and long-term results compared with other techniques. Early indication, preoperative intra-aortic balloon pump support may improve the surgical results. Preoperative cardiogenic shock carries a poor prognosis for this patient group.
| Introduction |
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David and colleagues [2, 3] introduced a new operative procedure in 1987, whereby both the left to right shunts can be eliminated and the ventricular remodeling and aneurysm formation of the infarcted myocardium can be prevented. This report describes our long-term results after surgical repair of postinfarction VSD, as described by David and colleagues [2, 3] for this high-risk group.
| Patients and Methods |
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Preoperatively, echocardiography and coronary angiography were performed in all patients, whereas right-side heart catheterization was performed only in 8 patients. The mean left to right shunt was 51% ± 21.5%, and the mean left ventricular ejection fraction (LVEF) was 47.18% ± 18.57%. Seven patients (21.8%) were operated on within 24 hours after the septal rupture. Ten patients (31.2%) were referred to our unit within 2 to 7 days after the septal rupture, and another 15 patients (47%) were operated on between 8 and 35 days after the septal rupture. The operation was performed urgently 1 ± 1.4 days after admission to our department. The mean interval from infarct to operation was 9.3 ± 7.6 days, whereas the mean interval from onset of VSD and operation was 7.1 ± 6.7 days.
There were 12 women (37.5%) and 20 men (62.5%). The mean age was 62.5 ± 10.5 years (range, 43 to 77). Sixteen patients (50%) presented with posterior VSD and 16 (50%) with anterior VSD. Coronary angiography showed triple-vessel disease in 4 patients (12.5%), double-vessel disease in 13 patients (40.6%), and single-vessel disease in 10 patients (31.2% [right coronary artery stenosis in 7 patients and left anterior descending artery stenosis in 3]).
At the time of admission, 10 patients (31.2%) were in cardiogenic shock with low cardiac output. An IABP was inserted in 13 patients (40.6%) before operation. Table 1 contains patient demographics and preoperative risk profile of 32 patients.
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Myocardial revascularization was performed in all patients at the surgical repair. Excision of left ventricular aneurysm was required in 4 patients (12.5%). Other associated procedures included replacement of the ascending aorta in 1 patient, aortic valve reconstruction in 1 patient, and mitral and tricuspid valve reconstruction in 1 and 2 patients, respectively.
The mean cross-clamp time was 87 ± 24.4 minutes (range, 48 to 122) and cardiopulmonary bypass time was 166 ± 54.3 minutes (range, 70 to 270).
Statistical Analysis and Data Collection
All statistical analyses were performed with the Statview program (SAS Institute, Cary, NC). Categorical variables are expressed as percentage and were evaluated with the
2 or Fisher exact tests. Continuous variables are expressed as mean ± SD, as well as median and range, and were evaluated using the Student t test. Logistic regression analysis was used to determine the predictors of survival and in-hospital mortality. Long-term survival was calculated by the Kaplan-Meier method. Follow-up information was collected between December 2007 and January 2008 by patient or physician contact. Operative mortality was defined as death within 30 days of operation. A p value less than 0.05 was considered as significant. The follow-up period ranged between 8 months and 12 years (mean follow-up time, 4.5 ± 4.4 years).
| Results |
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Reexploration for postoperative bleeding or tamponade had to be performed in 3 patients (9%); renal failure occurred in 10 patients (31%) with need for continuous venovenous hemofiltration. Fourteen patients (44%) needed prolonged inotropic support (need for inotropic agents longer than 3 days) because of low cardiac output, and 7 (22%) required prolonged assisted ventilation. One patient (3%) had a neurologic event 1 week after the operation, and 1 patient (3%) had a complete atrioventricular block and required permanent pacemaker implantation. Five patients (12.5%) required extracorporeal membrane oxygen support owing to severe biventricular failure; 2 of them died within 30 days of operation.
The mean intensive care unit stay for survivors was 18.5 ± 35 days The mean hospital stay for patients who needed inotropic support because of low cardiac output was 39 ± 56 days, and for hemodynamically stable patients, it was 21 ± 21 days.
The following variables were tested for in-hospital mortality: age older than 60 years, VSD location, single- or multiple-vessel disease, cardiogenic shock, IABP support, one or more cardiovascular disease risk factors in the medical history, previous MI, renal insufficiency in the medical history, and left ventricular function. The influence of these variables on early mortality is illustrated in Table 2.
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| Comment |
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In 1977, Daggett and coworkers [6] reported lower perioperative mortality rates achieved by the use of prosthetic material to replace necrotic muscle and by a transinfarct incision regardless of infarct location. Since that time, other classic operative techniques, including infarctectomy and reconstruction of the ventricular septum and free wall of the heart with Dacron (C.R. Bard, Haverhill, PA) patches, have been performed [7–9]. David and colleagues [2–4] introduced, in 1987, a new operative procedure, whereby both the left to right shunts can be eliminated, and the ventricular remodeling and aneurysm formation of the infarcted myocardium can be prevented. The prevention of additional damage of the already dysfunctional right ventricle and the restoration of the left ventricle geometry, by the above-described method, may be the reason it leads to a lower operative mortality rate [4].
Because of the very impressive results of using this technique, this operative procedure has been applied in all of the 32 consecutive patients who underwent repair of postinfarction ventricular septal rupture in our department between June 1995 and September 2007. In our series, the hospital mortality was 31.2%, a rate that is similar to the mortality reported in previous studies, especially the results of the last 10 years [10–14]. Indeed, the hospital mortality in our series was higher than the 19% mortality reported by David and Armstrong [15], who were using the same technique. Delay in surgical indication to repair VSD may result in multiple organ failure and early death [16].
In our series, we found also a significantly low mortality rate for the posterior VSD group (19%), which is similar to the mortality rate of the posterior VSD group reported by David and coworkers [4]. Conversely, the delay in surgical intervention for half our patients because of late admission through the cardiologists to our cardiac unit may explain our patients' outcomes.
Other studies also identify posterior VSD location as a risk factor for high mortality [11, 17–21] due to difficulties of the surgical exposition and repair or due to a higher incidence of right ventricular failure. Moore and colleagues [22] reported that the increased mortality in their series was due to a greater impairment of right ventricular function and greater elevation of right ventricular pressure. The repair of postinfarction VSD by infarct exclusion described by David and associates [4] seems to improve the results of surgery for patients with posterior VSD, as shown in our series. This technique may solve the difficulties of the posterior VSD repair, as this is physiologically sound and may leave the right ventricle undisturbed [4].
Other predictors of early mortality have been determined in our series. The influence of these variables on early mortality is illustrated in Table 2. As described by other groups, there is a high mortality rate for patients with preoperative cardiogenic shock, especially for those whose hemodynamic status is not improved by IAPB support [11, 12, 14–17, 23, 24].
Intra-aortic balloon counterpulsation, implantable turbine-pump, and percutaneous cardiopulmonary bypass support are counted among the different cardiac-assist devices available to cardiologists and cardiac surgeons to stabilize the patient after acute MI before operation. The basic goals of the less invasive IABP counterpulsation are to stabilize circulatory collapse, to increase coronary perfusion and myocardial oxygen supply, and to decrease left ventricular workload and myocardial oxygen demand. Counterpulsation has also been shown to be useful in achieving pulsatile cardiopulmonary bypass and in assisting high-risk patients through the operation [25]. In our series, preoperative IABP support and absence of cardiogenic shock were associated with a significantly lower risk of hospital mortality (p = 0.0001 and p = 0.0009, respectively). Based on this finding, we believe that patients with preoperative cardiogenic shock should be promptly treated with IABP, inotropic agents, and vasodilators before any diagnostic examination. Preoperative intra-aortic counterpulsation may increase cardiac output and improve coronary perfusion, and may lead to a decrease of the left to right shunt.
In all of our patients, we performed coronary artery angiography and myocardial revascularization before the repair of VSD, when a 70% stenosis existed. Because the hemodynamic status of the postinfarct VSD patient can suddenly deteriorate, some reports [17] strongly advise against coronary artery angiography. In our experience, none of our patients with septal rupture died during the angiography. We believe, as do others [4, 14, 23], that coronary artery angiography should be performed in every patient who can be stabilized hemodynamically. Patients in cardiogenic shock who cannot be stabilized with IAPB support or medical treatment should immediately undergo operation.
The incidence of residual VSD reported varies from as low as 4.7% [12] to as high as 43% [10]. Cox and colleagues [23] described a residual VSD in 22.9% of the patients in their series; 60% of them have undergone reoperation because of clinically significant shunt. In our series, only 1 patient (3.1%) received a redo procedure after 24 months of the first correction because of clinically significant residual shunt. The low incidence of residual VSD in our series as well as in the series by David and associates [4] may be explained by the application of the infarct exclusion technique with the suturing of the pericardial patch to the healthy endocardial tissue surrounding the infarcted muscle of the ventricular septum and the ventricular wall.
Several limitations of this study must be considered. In 2 follow-up cases, it was impossible to report precisely the cause of death, mainly because autopsy was not performed in these cases. Also, the study investigates a small number of patients. Overall, a larger number of patients are necessary to corroborate our findings.
Percutaneous closure of the smaller VSDs with catheter-based devices may now offer a different treatment option for critically ill patients who have a small postinfarction ventricular septal rupture [26]. However, the same authors raise concerns over the possibility of further increasing the size of the rupture and destroying the atrioventricular valves or the ventricles through the devices [27].
In conclusion, the repair of postinfarction ventricular septal rupture by the infarct exclusion technique described by David and associates [2–4] can be done safely. This technique seems to improve the results of surgery for patients who have posterior VSD and avoids the recurrence of the VSD after the first correction. From our data, it appears that preoperative cardiogenic shock carries a dismal prognosis. We support the strategy of preoperative IABP implantation as an important tool for the preoperative support of hemodynamically unstable patients with postinfarction ventricular septal rupture.
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