Ann Thorac Surg 2009;87:e37-e39. doi:10.1016/j.athoracsur.2009.01.046
© 2009 The Society of Thoracic Surgeons
Case Reports
Use of Initial Biventricular Mechanical Support in a Case of Postinfarction Ventricular Septal Rupture as a Bridge to Surgery
Lenard Conradi, MDa,
Hendrik Treede, MDa,
Jens Brickwedel, MDa,
Hermann Reichenspurner, MD, PhDa,b,*
a Department of Cardiovascular Surgery, University Heart Center Hamburg, Hamburg, Germany
b University Medical Center Hamburg-Eppendorf, Hamburg, Germany
Accepted for publication January 20, 2009.
* Address correspondence to Dr Reichenspurner, Department of Cardiovascular Surgery, University Heart Center Hamburg, Martinistr 52, Hamburg, D-20246, Germany (Email: lconradi{at}uke.de).
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Abstract
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The incidence of postinfarction ventricular septal rupture is declining as coronary revascularization techniques have become available for a large number of patients [1]. However, morbidity and mortality rates associated with this complication remain high. We report the case of a patient suffering from acute myocardial infarction who developed a postinfarction ventricular septal defect. Instead of attempting surgical closure, he was placed on biventricular mechanical support. After 2 weeks, surgical closure of the defect and concomitant explantation of the assist device were successfully performed. This approach may represent a new treatment option restoring hemodynamic stability and avoiding surgery on freshly infarcted myocardium.
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Introduction
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The incidence of ventricular septal rupture after acute myocardial infarction is declining as interventional and thrombolytic coronary revascularization techniques have become readily available for a large number of patients [1]. However, morbidity and mortality rates associated with this severe complication remain high, particularly when patients arrive in cardiogenic shock despite established surgical and transcatheter-based rescue efforts [2]. In ventricular septal defect (VSD) surgery the alternatives of early surgical repair to avert hemodynamic instability, and surgical delay to allow for the tissue surrounding the infarcted myocardium to solidify, must be carefully weighed against one another. Percutaneous treatment strategies using modern Amplatzer VSD occluder devices can represent a reasonable alternative to surgery. However, mortality rates after interventional treatment are reported to be within the range of emergency surgery and residual or recurring shunt formation is a frequent phenomenon [3]. A novel strategy in the surgical management of postinfarction ventricular septal rupture may be a staged approach of initial biventricular mechanical support followed by secondary surgical repair to avoid surgery on freshly infarcted myocardium.
We report the case of a 48-year-old man who developed posterior ventricular septal rupture after suffering from acute inferior myocardial infarction. He had experienced symptoms of unstable angina pectoris since the previous night and presented to his attending physician where electrocardiography revealed signs of myocardial ischemia in the inferior leads. After referral to a local hospital without prior thrombolytic therapy, elevated enzymes confirmed the presumptive diagnosis of acute myocardial infarction. Transthoracic echocardiography revealed severe inferior wall hypokinesia and a large ventricular septal defect, not isolating pressures in the two ventricular chambers with subsequent right ventricular volume overload. The localization near the ventricular apex and the complex character made an interventional attempt at VSD closure impossible. Emergency coronary angiography diagnosed single-vessel coronary artery disease with complete occlusion of the right coronary artery. Subsequent percutaneous coronary intervention was performed with successful recanalization of the occluded vessel. In the face of rapid further deterioration of the patient's hemodynamics an intra-aortic balloon pump was inserted and high-dose inotropes had to be administered. The patient was urgently transferred to our center in cardiogenic shock. On arrival, the patient presented with impending multiple organ failure. Despite intra-aortic balloon counterpulsation and high-dosed inotropic and vasopressor support, a mean arterial pressure of 50 mm Hg could barely be sustained. He was in a state of metabolic acidosis with a pH value as low as 7.2 and blood lactate levels up to 14 mmol/L. The central venous pressure was at 13 to 16 mm Hg, his pulmonary artery pressure was at 22 to 27 mm Hg, and pulmonary-to-systemic flow ratio was calculated to be 3.8, indicating a massive left-to-right shunt. The decision was made to immediately take the patient to the operating room and place him on cardiopulmonary bypass to stabilize hemodynamics and thereby resuscitate the patient.
After emergency median sternotomy, the heart exhibited massive posterior wall infarction with extensive hematoma and severely compromised biventricular contractility. As tissue surrounding the infarcted myocardium appeared edematous and fragile, and primary repair seemed likely to fail, the decision was made to implant an Abiomed AB 5000 biventricular assist device (Abiomed Inc, Danvers, MA) without attempting repair of the large VSD. Standard cannulation was performed, and cardiopulmonary bypass was established with mild hypothermia. The assist device was implanted, introducing inflow cannulas through the left ventricular apex and the right atrium, outflow cannulas were anastomosed to the ascending aorta and the pulmonary artery. The patient was then weaned from cardiopulmonary bypass, establishing excellent hemodynamic support by the assist device (5 L/min) transferred to the intensive care unit. He awoke showing no signs of neurological damage, and improved rapidly. Hepatic and renal functions normalized during the first postoperative week after impending multiple organ failure due to the initial low cardiac output.
On day 12 after initial admission, the patient was taken back to the operating room for surgical closure of the VSD. At this time, the hemodynamic condition had stabilized, multiple organ failure due to end-organ malperfusion had been successfully averted, and infarcted myocardial tissue could be expected to have sufficiently consolidated by now. Access to the VSD was gained by incision of the inferior wall of the left ventricle through the area of infarction. Intraoperative findings confirmed the previous echocardiographic diagnosis. The apical interventricular septum proved to be detached from the inferior wall in a large portion resulting in an extensive and complex VSD with a maximal diameter of 3.2 cm. Septal myocardial tissue surrounding the VSD proved to be sufficiently stable to support pledgeted transseptal interrupted sutures, firmly anchoring a Dacron patch in an infarct exclusion technique. Closure of the ventriculotomy required the use of a second Dacron patch, since the edges of the defect in the left ventricular free wall created by infarctectomy could otherwise not be approximated without tension. Teflon felt-armed mattress sutures were placed to secure the patch to the margins of the defect.
Concomitant explantation of the assist device was successfully performed. Finally, the patient was successfully weaned from cardiopulmonary bypass under constant echocardiographic control of ventricular function, and once again transferred to the intensive care unit under mild inotropic and vasopressor medication, with a reinserted intra-aortic balloon pump.
The further postoperative course was uneventful, and the patient was discharged 9 days after ventricular assist device explantation to a rehabilitation facility. At the latest follow-up in our outpatient heart failure clinic 4 months after surgery, the patient remains alive and in excellent condition. Echocardiographic control shows no signs of recurrent interventricular shunt formation and a stable left ventricular function with an ejection fraction of 50%.
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Comment
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Postinfarction ventricular septal rupture has been recognized to complicate approximately 1% to 2% of acute myocardial infarctions. Even though strategies for surgical management of this severe complication have been described as early as 1957 by Cooley and colleagues [4], and have been continuously refined since then, the outcome after surgical repair has improved little, and perioperative mortality remains as high as 30% to 50% [5]. The most common cause of death is represented by low cardiac output followed by recurrent or residual VSD formation. Interventional approaches using modern occluder devices may represent a therapeutical alternative, although there is little experience with such devices under the emergency conditions of postinfarction VSD. The largest published series presents data of 18 patients from a United States registry. Even though only a minority of 5 patients received interventional treatment in the acute phase of myocardial infarction, with the remaining patients undergoing VSD closure between 14 to 95 days after the infarction, overall mortality is stated to be a high 41% [3]. Nonetheless, percutaneous attempts at VSD closure may be justified in cases of well-defined, smaller lesions, which are more common in an anterior location. Results after medical treatment alone are even worse, with up to 80% of patients dead after 4 weeks. Only a small minority of patients are hemodynamically sufficiently stable to be managed medically with surgical or interventional repair at a later time. The overwhelming majority of patients are in a state of impending or manifest cardiogenic shock and require immediate surgical treatment before multiple organ failure becomes irreversible. As a consequence, the diagnosis itself may be considered as an indication for surgery. Other attempts to gain hemodynamic stability, such as inotropic support, diuretics, and intra-aortic balloon counterpulsation to reduce left ventricular afterload and increase cardiac output can only be regarded as additional measures while preparing patients for the operation. While early surgery has been widely recognized as the only feasible strategy to restore hemodynamic stability and to avert adverse outcome due to end-organ ischemia, the theoretical option of deferring surgery to wait for consolidation of the infarcted myocardium remains intriguing.
The described strategy enabled hemodynamic stabilization of the patient and restoration of peripheral organ perfusion, and allowed for recovery and maturation of the infarcted myocardium before surgical correction of the VSD. Although there have been anecdotal reports of ventricular assist device therapy in VSD patients [6–8], this approach may represent a novel concept in VSD surgery. While Pitsis and colleagues [6] report successful bridging of a patient to surgery on left ventricular support, high right-to-left shunting has been described to result in hypoxic brain damage in another patient placed on left ventricular assist device after suffering from postinfarction ventricular septal rupture [7], suggesting biventricular support to be implemented when considering mechanical assistance. Previously, biventricular mechanical support without VSD closure has been described in a bridge-to-transplantation concept. In a report by Samuels and colleagues [8], a cannulation strategy at the atrial level has been proposed. However, our strategy of transapical left ventricular drainage combined with sufficient right ventricular support proved to be successful with uneventful mechanical support until definite surgical treatment. Thus, a staged approach with initial mechanical support to reach the paramount goal of rapidly stabilizing the hemodynamic situation of the patient and thereby averting end organ failure, followed by secondary surgery after maturation of the freshly infarcted myocardium seems to be a feasible approach. To the best of our knowledge, the presented case is the first existing report in which biventricular mechanical circulatory support has been used in a bridge to surgery setting for delayed correction of postinfarction ventricular septal rupture.
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References
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- Poulsen SH, Praestholm M, Munk K, Wierup P, Egeblad H, Nielsen-Kudsk JE. Ventricular septal rupture complicating acute myocardial infarction: clinical characteristics and contemporary outcome Ann Thorac Surg 2008;85:1591-1596.[Abstract/Free Full Text]
- Crenshaw BS, Granger CB, Birnbaum Y, et al. Risk factors, angiographic patterns and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. GUSTO-I (Global Utilisation of Streptokinase and TPA for Occluded Coronary Arteries) Trial Investigators. Circulation 2000;101:27-32.[Abstract/Free Full Text]
- Holzer R, Balzer D, Amin Z, et al. Transcatheter closure of postinfarction ventricular septal defects using the new Amplatzer muscular VSD occluder: results of a U.S. registry Catheter Cardiovasc Interv 2004;61:196-201.[Medline]
- Cooley DA, Belmonte BA, Zeis LB, Schnur S. Surgical repair of ruptured interventricular septum following acute myocardial infarction Surgery 1957;41:930-937.[Medline]
- In: Cohn Lh, editor. Cardiac Surgery in the Adult. New York, NY: McGraw-Hill; 2008.
- Pitsis AA, Kelpis TG, Visouli AN, Bobotis G, Filippatos GS, Kremastinos DT. Left ventricular assist device as a bridge to surgery in postinfarction septal defect J Thorac Cardiovasc Surg 2008;135:951-952.[Free Full Text]
- Kshettry V, Salerno C, Bank A. Risk of left ventricular assist device as a bridge to heart transplant following postinfarction ventricular septal rupture J Card Surg 1997;12:93.[Medline]
- Samuels L, Entwistle J, Holmes E, Paris T, Wechsler AS. Mechanical support of the unrepaired postinfarction ventricular septal defect with the Abiomed BVS 5000 ventricular assist device J Thorac Cardiovasc Surg 2003;126:2100.[Free Full Text]
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Abstract
Introduction
