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Ann Thorac Surg 1997;63:138-142
© 1997 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

Early Repair of Postinfarction Ventricular Septal Rupture

MidAmerica Heart Institute, Saint Luke's Hospital, and Department of Surgery, University of Missouri-Kansas City School of Medicine, Kansas City, Missouri

Accepted for publication July 22, 1996.

	Abstract

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

 
Background. Postinfarction rupture of the interventricular septum is usually fatal without surgical intervention. The optimal timing and the most appropriate technique of surgical repair remain unsettled.

Methods. The results of surgical closure of postinfarction ventricular septal defect in a consecutive series of patients seen over a 24-year period were reviewed and analyzed. Late follow-up was obtained in all patients who survived the operation.

Results. Sixty of 76 patients treated surgically exhibited cardiogenic shock, low cardiac output syndrome, or both at the time of operation. A plan of early operative intervention was followed in these unstable patients, with 60% of them undergoing repair within 24 hours of septal rupture. For the entire series of patients, the hospital mortality rate was 40.8%; survival was 41.5% at 5 years and 25.6% at 10 years postoperatively.

Conclusions. Significant trends observed during the period of study were a more aggressive stance regarding surgical intervention in all patients who presented with hemodynamic instability and improved survival in those patients who presented with septal rupture complicating an inferior myocardial infarction.

	Introduction

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

 
Rupture of the ventricular septum is an ominous complication of acute myocardial infarction, usually resulting in death unless surgical repair is performed [1–3]. Other therapeutic measures, such as pharmacologic or mechanical circulatory support, as well as application of innovative percutaneous techniques of defect closure, have not been consistently effective as modalities of palliative or definitive treatment [4, 5]. The longer the interval between septal rupture and surgical repair, the less the operative mortality; however, the argument for operative delay is mitigated by the large early attrition from the condition, resulting in a lower overall salvage rate [3]. Therefore, we and others have adopted a policy of prompt surgical intervention in these seriously ill patients [1, 3, 6]. This report documents our experience with a consecutive series of patients with postinfarction ventricular septal rupture treated surgically at our institution.

	Patients and Methods

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

 
During a 24-year period ending in December 1994, 76 patients underwent primary repair of a postinfarction ventricular septal defect at the MidAmerica Heart Institute. The first 27 of these cases have been reported previously [3]. Of the total series, 42 patients (55.3%) were male, and the ages ranged from 48 to 90 years (mean, 69.1 years; 39 were 70 years and 6 were 80 years). The 34 women were slightly older (mean, 70.8 years) than the men (mean, 67.8 years). Four patients had previously (9 months, 7 years, 7 years, and 8 years) undergone a coronary artery bypass procedure. The ventricular septal rupture occurred as a consequence of an anterior myocardial infarction in 42 patients (55.3%) and secondary to an inferior myocardial infarction in the remaining 34 patients (44.7%). Preoperative coronary angiography, performed in 75 patients (98.7%), revealed the incidence of single, double, and triple coronary artery disease (luminal diameter narrowing >50%) to be 42.7%, 38.6%, and 18.7%, respectively. No patient exhibited substantial left main coronary artery stenosis. Single-vessel disease was observed more frequently in those patients with an anterior myocardial infarction (48.8%) than in those with an inferior myocardial infarction (35.3%). The 4 patients who had undergone previous myocardial revascularization each had multivessel disease.

Sixty patients (78.9%) presented for surgical therapy with frank cardiogenic shock or low cardiac output syndrome (hypotension, oliguria, decreased mentation, metabolic acidosis, or requirement of continuous inotropic infusions). Two of these patients had undergone successful resuscitation from ventricular fibrillation, 3 exhibited third-degree heart block, and 1 had intractable cardiac arrest at initiation of the operative intervention. The intraaortic balloon pump, first used preoperatively in1980, had been placed preoperatively in 28 of 36 patients encountered since then, and in each of the last 14 patients. Operation in these hemodynamically unstable patients, undertaken as early as 2 hours after rupture, was begun within 6 hours in 11 patients (18.3%), within 12 hours in 18 patients (30%), within 24 hours in 36 patients (60%), and within 72 hours in 54 patients (90%). The remaining 6 patients underwent operation 3 to 17 days after occurrence of the septal rupture. In these latter patients, operation was delayed because of late diagnosis or transfer of the patient from another hospital, or because an initially stable clinical presentation deteriorated into a low cardiac output state. In addition to the 1 patient transferred to the operating room while undergoing mechanical ventilation and external cardiac massage, it was necessary to initiate cardiac massage in 4 other patients between arrival in the operating room and institution of cardiopulmonary bypass. In 2 of these patients, poststernotomy open cardiac massage was complicated by ventricular free-wall rupture before bypass cannulation.

Sixteen patients exhibited evidence of congestive heart failure (tachycardia, pulmonary congestion, fluid retention, tachypnea, and dyspnea) preoperatively without shock or low cardiac output syndrome. Eight of these patients underwent early (range, 20 hours to 20 days; mean, 5.4 days) closure of their septal defects. In 2 patients with progressive congestive heart failure, the intraaortic balloon pump was placed before operation. Seven of the 16 patients underwent elective late (range, 31 days to 7 months after rupture) closure of their septal defects, and the remaining patient underwent closure of a defect only after some 7 years.

The operative technique for all patients included standard bicaval and ascending aortic cannulation, cardiopulmonary bypass with mild (28° to 30°C) systemic hypothermia, and induced cardiac arrest. Since 1979, cold hyperkalemic cardioplegia has been used, and in 4 recent cases, the cardioplegic solution was administered through the coronary sinus. Routine operative technique modifications in the later part of the series included use of the membrane oxygenator and intraoperative transesophageal echocardiography.

Ventricular septal defects associated with an anterior myocardial infarction (42 patients) were approached by an anterior or anteroapical left ventriculotomy through the infarcted tissue. Necrotic left ventricular free-wall muscle was excised (during repair of the septal defect) in at least 32 patients, and septal debridement of necrotic myocardium was usually performed. Patch reconstruction of the septum was performed in 31 patients, and direct closure of the defect with pledgeted sutures was performed in the remaining 11 patients. Ventriculotomy closure usually was accomplished using large through-and-through horizontal mattress sutures (with external strips of pledget material), incorporating the left ventriculotomy wall, the septum or septal patch, and the right ventricular wall.

Defects secondary to inferior myocardial infarctions (34 patients) were approached through a left ventriculotomy in 20 patients, a right ventriculotomy in 9 patients, and through both right and left ventriculotomies (with excision of intervening ventricular wall) in 5 patients. Repair of the defect was accomplished by patch reconstruction of the septum in 22 patients and by direct closure using pledgeted sutures in 12 patients. When incised and resected, the left ventricle was repaired by direct closure using externally pledgeted mattress sutures in 16 patients and by patch replacement of the posterior left ventricular free-wall defect in 9. Two patients, whose defects were approached through a right ventriculotomy only, required suturing of an external onlay reinforcing patch over a portion of the posterior left ventricle.

In the entire series of 76 patients, concomitant operative procedures included coronary artery bypass(es) in 29 patients (2 of whom had previously undergone a coronary artery bypass procedure), intraaortic balloon pump insertion in 14, implantation of a permanent pacemaker in 2, mitral valve replacement in 1, and placement of a left ventricular assist device in 1. Thirty-nine of the last 49 patients undergoing early (20 days) repair have had insertion of an intraaortic balloon pump either preoperatively or intraoperatively.

There was an intraoperative recurrence of the septal defect, as evidenced by recurrence of the palpable thrill or an oxygen step-up in the right ventricle, in 3 patients after removal from cardiopulmonary bypass. In each instance, the repair was taken down and redone. Two patients exhibited disruption of the left ventricular free-wall suture line after discontinuation of cardiopulmonary bypass; each underwent attempts at repair.

	Results

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

 
Four patients (5.3%), each presenting in shock (3 undergoing operation within 8 hours of their ventricular septal rupture), died in the operating room. In one instance, there was repeated left ventricular suture-line disruption, which could not be repaired successfully. The other 3 patients (2 having cardiac arrest during sternotomy) exhibited persistently inadequate cardiac function and could not be separated successfully from cardiopulmonary bypass.

Postoperatively, low cardiac output was an almost universal occurrence in patients exhibiting preoperative shock or the low cardiac output syndrome. One patient underwent emergency sternotomy shortly after arrival in the intensive care unit because of hemorrhage. Three patients were returned to the operating room within the first postoperative day because of bleeding/tamponade (1 patient), for insertion of a right ventricular assist device (1 patient), or for secondary closure of a recurrent ventricular septal defect (1 patient). Another patient underwent closure of a recurrent ventricular septal defect on the third postoperative day. One patient required reclosure of a disrupted sternotomy wound during the postoperative period. One patient underwent delayed (38 days) repair of a recurrent ventricular septal defect before discharge from the hospital. Other major postoperative complications included respiratory insufficiency (6 patients), severe central nervous system injury (5 patients), renal failure (7 patients, 3 requiring dialysis), major gastrointestinal bleeding (2 patients), bloodstream sepsis (2 patients), third-degree heart block requiring pacemaker implantation (1 patient), and leg ischemia leading to toe amputation (1 patient).

Of the entire series, 31 patients (40.8%) died within the first 30 postoperative days or while still in the hospital. Only 1 of the 4 patients who had undergone a previous coronary artery bypass procedure survived. Twenty-nine of the 31 deaths occurred in the 60 patients who were subjected to operation while exhibiting shock or the low cardiac output state (48.3% mortality rate). There were two postoperative deaths (12.5%) among the 16 patients with preoperative symptoms of only congestive heart failure. Both of these patients were operated on urgently (26 hours and 30 hours after septal rupture) because of worsening cardiac decompensation. One of these patients, hemodynamically stable 1 hour after arrival in the intensive care unit, suddenly exsanguinated from rupture of the left ventricular suture line, and the other died on the first postoperative day of progressive cardiogenic shock.

The precise cause of death was difficult to establish in some instances; however, an apparent cause was determined for each of the 31 postoperative deaths. Two patients died of exsanguination, 2 died of respiratory insufficiency, 2 of uncontrolled sepsis, 2 after attempted early closure of a recurrent ventricular septal defect, and one of a massive stroke. Twenty patients died as a result of low cardiac output and its immediate consequences. Finally, 2 patients died after multiple complications, 41 days and 43 days postoperatively, of progressive multisystem organ failure.

Among the 68 patients undergoing early (20 days) repair, univariate analysis (² method) was done for the risk factors of age (<70 years versus 70 years), sex (male versus female), clinical presentation (shock/low cardiac output syndrome versus congestive heart failure), location of acute myocardial infarction (anterior versus inferior), vessels diseased (single versus multiple), time of repair after septal rupture (<24 hours versus 1 to 20 days), and position in the series (first 34 patients versus last 34 patients). The results revealed nonsignificant differences (p > 0.05) in in-hospital mortality for each risk factor tested (Table 1). In the entire series (76 patients), however, there was a progressive decrease in operative mortality associated with delayed repair. The operative mortality rate was 51.4% in patients who underwent repair within 24 hours, 47.1% when performed at 1 to 5 days, and 28.6% when the operation was done 6 to 20 days after septal rupture. Eight patients underwent late (>1 month) repair, with no deaths.

Forty-five patients (59.2%) were discharged from the hospital alive. The discharged patients have been followed up for a total of 276.5 patient-years, during which time 29 late deaths have occurred. The survival and causes of death in these 29 patients are summarized in Table 2. Sixteen patients currently are surviving up through 20 postoperative years (mean, 5.3 years). The actuarial survival for the entire series was 49.7%, 41.5%, and 25.6% at 1, 5, and 10 postoperative years, respectively.

	Comment

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

The natural history of patients suffering a postinfarction ventricular septal rupture is dismal, with approximately 15% surviving 2 months and only about 7% alive at 1 year [1, 8, 10, 11]. The mortality rate is greatest early after rupture and is approximately 40% within the first 48 hours. Attempts to manage patients with postinfarction septal rupture by nonoperative regimens have, in general, proven ineffective [2–48, 13]. Use of the intraaortic balloon pump has been championed by some as a helpful treatment, but it has neither decreased nor substantially delayed the necessity for operative repair [9, 10, 14].

The operative mortality rate is high with early operative repair, the preoperative presence of cardiogenic shock, and an inferior location of the acute infarction. Late repair (>1 to 2 months) is associated with significantly fewer operative deaths; however, only approximately 15% of patients will survive to undergo operation if such an approach is taken routinely. Therefore, despite the increased mortality associated with early operative intervention, many investigators advocate early repair in these desperately ill patients with the goal of improving overall salvage [1, 2, 10, 11]. Although preoperative use of the intraaortic balloon pump has been disappointing with regard to long-term support of these patients, it has been used more frequently in recent years to stabilize the patient during diagnostic studies or in preparation for operation. Nevertheless, as the results of this experience demonstrate, early repair is associated with substantial morbidity and mortality despite every effort to lessen the risks.

The technical difficulties associated with early repair of the defect in necrotic, friable myocardium may be related more to the interval after the acute infarction than to the interval after the actual septal rupture. The interval between infarction and repair in those patients undergoing early (20 days) repair in the present series is shown in Figure 1. Approximately 50% of patients underwent operation within 4 days, and 75% within 10 days of their acute myocardial infarction. The use of thrombolytic agents in the treatment of acute myocardial infarction may shorten the interval between infarction and septal rupture [7]. Some believe that the higher operative mortality rate associated with early repair of a septal rupture may be related more to the limited myocardial reserve and multiple organ system injury associated with poor systemic perfusion than to the actual technical performance of the operation [2].

View larger version (14K): [in this window] [in a new window]   Fig 1. . Cumulative percentage of patients undergoing early operation relative to the interval after rupture of the ventricular septum (solid line) and the interval after the acute myocardial infarction (dashed lineme zero, labeled "septal rupture," relates to the solid line; time zero is the time of occurrence of myocardial infarction for the dashed line. Note the time scale change at 5 days.

The operative technique for repair continues to evolve. Most surgeons advocate repairing the defect through a left ventriculotomy, through the infarcted free wall when possible. Our experience suggests that repair of an infarct secondary to an inferior acute myocardial infarction may be performed successfully through a right ventriculotomy, with the theoretic advantage of less left ventricular compromise. Others also have used this approach to repair a posterior septal rupture [7]. How aggressive the debridement of necrotic tissue should be in the ventricular septum and left ventricular free wall is uncertain. The technique of replacing the resected, infarcted inferior left ventricular free wall with a patch was introduced by Dagget [11]. More recently, David and co-workers [15] described a technique of left ventricular remodeling with a large pericardial patch. Unfortunately, the incidence of residual or recurrent ventricular septal defect remains in the range of 15% to 20% [9, 12].

It is disappointing that the overall salvage rate did not seem to improve with time. However, increasingly during the 24-year period, fewer patients were deemed inoperable and higher-risk patients were accepted for early operation. Thirty-one of the first 38 patients in this series were referred early (20 days) for operation, and during this earlier time frame, 7 other patients with clinically recognized septal rupture after myocardial infarction died without attempted repair. All but 1 of the last 38 patients in the series were referred early (20 days) for operation; and, during this latter half of our experience, no patient at our institution with clinically recognized postinfarction ventricular septal rupture died before operation. In addition, an improving salvage rate of patients undergoing repair of septal ruptures complicating an inferior myocardial infarction has been documented. Therefore, it appears that in fact, the overall salvage of patients presenting with postinfarction septal rupture has probably improved. Although there is a high operative mortality rate associated with early repair, overall a good long-term survival is attainable.

	Footnotes

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

 
Address reprint requests to Dr Killen, Medical Plaza II-50, 4320 Wornall, Kansas City, MO 64111.

This article has been selected for the open discussion forum on the STS Web site:

http://www.sts.org/annals

	References

Top Footnotes Abstract Introduction Patients and Methods Results Comment References

 

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4. Daggett W. Surgical management of ventricular septal defects complicating myocardial infarction. World J Surg 1978;2:753–66.[Medline]
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This Article Abstract 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 Author home page(s): Duncan A. Killen Jeffrey M. Piehler A. Michael Borkon Michael E. Gorton William A. Reed Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Killen, D. A. Articles by Reed, W. A. Search for Related Content PubMed PubMed Citation Articles by Killen, D. A. Articles by Reed, W. A.