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Ann Thorac Surg 1996;61:1752-1757
© 1996 The Society of Thoracic Surgeons
Departments of Cardiothoracic Surgery and Cardiology, St. Antonius Hospital, Nieuwegein, the Netherlands
Accepted for publication January 31, 1996.
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Abstract |
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 TopFootnotes Abstract IntroductionMaterial and MethodsResultsCommentReferences |
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Methods. Between 1980 and 1992 109 patients were treated surgically for ventricular septal rupture using a standardized technique. A division in time periods was made. The rupture was categorized according to its anterior or posterior site and proximal or distal location.
Results. The 30-day mortality rate was 27.5%. Multivariate logistic regression analysis identified preoperative shock (p = 0.0007) and right atrial oxygen saturation less than 60% (p = 0.021) as predictors for early death; the risk for early death declined over the time periods from 50% to 12.8% (p = 0.0007). Proximal ventricular septal rupture location (p = 0.0092) and interval between infarction and ventricular septal rupture less then 1 day (p = 0.034) were risk factors for the occurrence of preoperative shock.
Conclusions. Proximal ventricular septal rupture location was the main determinant of preoperative cardiogenic shock, which in turn was the strongest predictor of early mortality. Over the time periods a decrease in early mortality was reached.
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Introduction |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
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Postinfarction ventricular septal rupture (VSR) is an infrequent but serious complication of myocardial infarction [1]. It is associated with a high mortality if treated conservatively, as only 13% of the patients survive longer than 2 months [1, 2]. The first successful repair was reported by Cooley and associates in 1957 [3]. After improvements in perioperative management [4] and surgical technique [5], surgical repair has become the treatment of choice. The current approach is to consider postinfarction VSR as a surgical emergency [6–10]. The overall early surgical mortality is high (21% to 51%) [5–13] and is influenced by the presence of cardiogenic shock [8, 13–15], posterior site of the infarction [4, 9, 13, 14], and a short interval between infarction and the occurrence of the VSR [13]. It has been suggested that impaired right ventricular function due to right ventricular infarction may lead to increased early mortality [9, 14, 6–10]. The present retrospective analysis was undertaken to identify factors that may influence the early outcome of surgical treatment for postinfarction VSR. Regional location of the VSR was included as a variable.
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Material and Methods |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
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Diagnostic Procedures
Right heart catheterization was performed in 105 patients, echocardiography in 79 patients, and coronary angiography in 104 patients.
Surgical Technique
In all patients cardiopulmonary bypass, systemic hypothermia, and antegrade cold crystalloid oxygenated cardioplegia were used. The septum was approached through the infarct-related left ventricular myocardium. Prosthetic material was used to repair the septum after resection of the infarcted tissue. In the anterior approach suture closure of the left ventricle was used, whereas in the posterior approach the ventricle was closed using the onlay patch technique as described by Daggett [5].
Ventricular Septal Rupture Location and Site of Infarction
The defects were categorized into four VSR types according to anterior or posterior site of the infarction and proximal or distal location of the VSR, as demonstrated in Figure 1
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2 or Fisher's exact test. Stepwise multivariate logistic regression analysis was used to relate clinically meaningful variables to dichotomous or ordinal outcome variables. |
Results |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
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The infarction that led to the VSR was anterior in 54 patients (49.5%) and posterior in 55 patients (50.5%). Twenty-one patients (19.2%) were hospitalized owing to the signs of the VSR, after an ambulant or silent infarction. The mean interval between the onset of the infarction and the occurrence of the VSR was 4.5 days (SD, 4.5 days), with a median of 3 days and a range from less than 12 hours to 21 days.
Sixty-two patients (58.7%) were in cardiogenic shock, defined as a systolic blood pressure less than 80 mm Hg, signs of increased peripheral resistance, and oliguria (diuresis <20 mL/h). In 11 of these (10.1%) the clinical condition deteriorated to such extent (systolic blood pressure less than 40 mm Hg) that external cardiac massage was carried out before emergency operation. The mean preoperative serum creatinine level was 178 µmol/L (SD, 99 µmol/L; range, 67 to 720 µmol/L). An atrioventricular conduction block was present in 15 patients (13.8%) and a complete conduction block in 8 patients. At coronary angiography single-vessel disease was found in 57 patients (54.8%), double-vessel disease in 29 patients (27.9%), and triple-vessel disease in 18 patients (17.3%). At right heart catheterization the mean right atrial pressure was 11.0 mm Hg (SD, 5.2 mm Hg) and the mean pulmonary artery pressure was 29.3 mm Hg (SD, 6.7 mm Hg). The mean left-to-right shunt was 3.1:1 (SD, 1.1). The mean right atrial oxygen saturation was 52.6% (SD, 11.8%). Pulmonary artery wedge pressure and cardiac output were measured in too limited a number to allow statistical analysis. Their mean values were 19.5 mm Hg (SD, 8.1; n = 79) and 3.7 L/min (SD, 1.3; n = 74), respectively.
Initial treatment of the VSR consisted of fluid resuscitation, inotropic support, and afterload reduction. Preoperatively, intraaortic balloon pumping (IABP) was initiated in 51 patients (46.8%): in 37 cases for cardiogenic shock and in 14 as a precaution. Of the patients in cardiogenic shock, 19 were immediately transferred to the operating theater without an IABP.
Operative Data
The mean delay between the onset of the VSR and operation was 5.6 days (SD, 7.7 days) with a median delay of 1 day and a range from less than 12 hours to 36 days. The mean aortic cross-clamp time was 86 minutes (SD, 32 minutes). Coronary artery bypass grafting was performed in 45 patients (41.3%). In 1 patient an aortic valve replacement was performed for stenosis.
Postoperative Morbidity
Postoperative morbidity occurred in 36 patients, not including the patients who could not be weaned from bypass. Postoperative cardiac failure occurred in 20 patients, which required prolonged inotropic support and the insertion (10 patients) or continuation of IABP support. Respiratory insufficiency was seen in 5 patients (4.6%). Twenty patients (18.3%) experienced a period of renal failure with anuria and severely elevated plasma creatinine levels; 17 (15.6%) required temporary dialysis. Five patients suffered from multiple organ failure (4.6%). Of the 5 patients (4.6%) who suffered a perioperative cerebrovascular accident, 3 recovered without any sequelae, whereas the other 2 died of cardiac complications. One case of gastrointestinal hemorrhage was treated conservatively. Three patients suffered from transient IABP-related leg ischemia for which thromboembolectomy was necessary after the removal of the IABP. Recurrence was seen in 25 patients (22.9%), needing reoperation in 15 patients. In 1 patient severe iatrogenic tricuspid valve incompetence had to be repaired due to the involvement of the chordae in a suture fixing the patch to the proximal septum. In 6 patients (5.5%) a permanent pacemaker was inserted for persistent complete atrioventricular conduction block.
Early Mortality
Thirty patients (27.5%) died within 30 days after the operation (early mortality). In 3 cases the operation was abandoned due to absence of adequate substrate to repair the septum or the free wall. Nine patients (8.3%) could not be weaned from cardiopulmonary bypass after repair.
Risk factors for early death are listed in Table 1. Significant clinical factors were the presence of preoperative cardiogenic shock and right atrial oxygen saturation less than 60%.
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). Multivariate logistic regression analysis of the periods identified only increasing age (odds ratio, 1.13; p = 0.0003) and an increase in pulmonary artery pressure (odds ratio, 1.08; p = 0.0066) as independent factors.
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). Proximal location of the VSR and an interval between infarction and onset of the VSR less then 1 day were predictors for cardiogenic shock. The relative risk for cardiogenic shock was 3.3 times higher for proximal VSR location and was more favorable with an interval between myocardial infarction and VSR longer than 1 day. Figures 2 and 3 demonstrate the relationship between preoperative shock and early mortality, respectively, and the four VSR types. A significant difference was found between preoperative shock and early mortality, respectively, and combined proximal and combined distal VSR location (Table 4).
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Comment |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
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Patient Selection
Of the 109 patients, 94 were referred to our center from 31 different hospitals. It is inevitable that a substantial patient selection was made beyond our scope at the level of the patient, the family physician, and cardiologist based on actual clinical condition, general health status, and age. Due to its rare occurrence and the different attitudes of physicians toward VSR, it may not be possible to approximate an overall view on the results of its treatment. However, it is important to note that the preoperative variables are not essentially different from those of other studies [8, 9, 13, 15, 18].
Use of Intraaortic Balloon Pump
Less then half of our patients received an IABP preoperatively. If the hemodynamic situation was stable and operation could be performed without delay, a balloon was not inserted preoperatively. In case of cardiogenic shock developing before or during diagnostic procedures or in case operation could not be performed immediately after diagnosis, IABP was initiated.
Time Periods
Over the three time periods a significant decline in early mortality was noted. Other authors also noticed a considerable decline in early mortality in their late time period [8, 13]. As no significant differences were found in patient-related variables between the three time periods, apart from increased age, it seems justified to conclude that the improved results of operation are due to improved preoperative, perioperative, and postoperative management and improved surgical confidence and experience.
Surgical Technique
In this series a surgical technique was used based on a transinfarction approach, infarct resection, and synthetic patch repair of the septal and free wall defect, with changes when demanded by the local situation. Favorable experience with a new technique was recently described by David and coworkers [18]. Their technique of excluding the infarction and rupture site from the left ventricular cavity might be particularly useful in cases in which sufficient myocardial substrate to repair the septum or free wall is not present. A patch of bovine material may divide the pressure generated by the left ventricle in a more natural way compared with synthetic material, preventing recurrence and aneurysm formation.
Early Mortality, Preoperative Shock, and Ventricular Septal Rupture Location
The presence of preoperative cardiogenic shock was found to be the most significant independent clinical determinant of early mortality, which confirms the experience of others [9, 13, 14, 18]. Low right atrial oxygen saturation was another independent predictor of early mortality.
Some unexpected factors emerged when the determinants of preoperative cardiogenic shock were analyzed. Previous reports mentioned the posterior infarction site as a predominant risk factor for cardiogenic shock and early death [9, 13, 14]. In our series we found that the proximal VSR location was the main determinant of preoperative shock. Skillington and associates [13] have speculated that surgical results in the inferobasal located VSR, close to the mitral valve, might be unfavorable. We were not able to confirm that the posterior site of the infarction had any influence on early mortality or preoperative shock. The posterior infarction group included the proximal-posterior VSR type with the highest risk for early death, whereas the anterior infarction group included the distal-anterior type of VSR with a lower risk for early death. This may explain the differences in early survival between posterior and anterior site infarctions found in this study using univariate analysis. Moreover, the infarction site was not shown to be an independent risk factor by multivariate analysis.
The influence of the proximal VSR location on preoperative shock is not likely to be related to an intrinsic effect of the VSR itself. The size of the infarction is probably the most important factor [4]. A proximally located VSR may be related to a more proximal occlusion of the coronary artery and a larger infarcted area, with an increased tendency to early and extensive necrosis and hence an increased tendency to cardiogenic shock and early death. The interval less then 1 day between infarction and the onset of the VSR as a determinant for cardiogenic shock also supports this hypothesis. We could speculate that a larger infarcted area either by the very proximal location of the occlusion or absence of collateral circulation with a considerable amount of necrosis probably results in a short interval to the development of a VSR.
Right ventricular failure is generally thought to be an important factor in the poorer prognosis of VSR in association with posterior infarction [9, 13, 14]. In this study, however, the infarction site was not related to the surgical outcome. Temporary volume and pressure overload of the right ventricle by the left-to-right shunt in combination with impaired septal and left ventricular function due to an extensive transmural infarction may play an important role [7, 16–18]. The interventricular septum, which is of greater importance to right ventricular function compared with the right ventricular free wall, may be functionally equally impaired in an anteroseptal infarction as in a posteroseptal infarction [19, 20].
Conclusion
We conclude that proximal VSR location rather than the posterior infarction site was the main determinant of preoperative cardiogenic shock, which in turn was the strongest determinant of early mortality. Over the time periods a significant decrease in early mortality was reached, probably caused by improved perioperative management and confidence.
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Footnotes |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
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References |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
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