Ann Thorac Surg 2004;78:2178-2180
© 2004 The Society of Thoracic Surgeons
Case report
Long-Term Survival With Acquired Ventricular Septal Defect After Myocardial Infarction
Peter Alter, MDa,*,
Bernhard Maisch, MDa,
Rainer Moosdorf, MDb
a Department of Internal Medicine–Cardiology, Marburg, Germany
b Department of Cardiovascular Surgery, Philipps University of Marburg, Marburg, Germany
Accepted for publication July 25, 2003.
* Address reprint requests to Dr Alter, Philipps University of Marburg/Lahn, Department of Internal Medicine–Cardiology, Baldingerstrasse, 35033 Marburg, Germany
alter{at}mailer.uni-marburg.de
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Abstract
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Acquired ventricular septal defects (VSD) are rare and devastating complications after myocardial infarction. The long-term prognosis with medical therapy is extremely poor. We report on a patient who developed progressive heart failure within 3 months after myocardial infarction due to an unknown VSD. The left ventricular function was severely impaired. After diagnosing VSD by echocardiography, surgical occlusion was performed. In addition, a biventricular pacemaker was applied using epicardial leads. The patient recovered almost completely 6 weeks postoperative. Beside hemodynamic changes, biventricular pacing is potentially sufficient to improve the postoperative outcome of patients with severe heart failure in these conditions.
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Introduction
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Development of ventricular septal defect (VSD) is a rare devastating complication after myocardial infarction with an incidence of 0.2% to 2% [1]. The prognosis remains extremely poor with a mortality of 20% to 50% in patients undergoing surgical therapy and 95% in those treated medically, being highest within the first month after myocardial infarction (overall mortality 74% at 30 days, 78% at 1 year) [2]. Accordingly, patients with long-term survival for several months after medical treatment of myocardial infarction are absolutely rare. Potentially, biventricular pacing is sufficient to improve the postoperative outcome of patients with initially severely reduced left ventricular function.
We report a 69-year-old patient who had suffered from angina pectoris. Because of delayed consultation of his physician at the following day, the underlying inferior myocardial infarction has been treated medically without thrombolysis or acute revascularization. Three days later, coronary angiography revealed triple-vessel disease with medial occlusion of the right coronary artery (RCA) as well as high grade stenoses of the left anterior descending (LAD) and circumflex artery (RCX). Angiography revealed severe impairment of left ventricular function with an ejection fraction of 21% and an extended inferior wall dyskinesia. Therefore, surgical bypass grafting had been recommended, but the patient initially preferred medical therapy, because of his increased surgical risk resulting from enormous obesity (BMI 35.6 kg/m2). The next 2 weeks of hospital stay were unobtrusive and the patient was discharged. Three months later, the patient gradually developed dyspnea (New York Heart Association [NYHA] III–IV), edemas, and ascites ongoing with an increase of body weight of 12 kg within a few days leading to recurrent hospital admission. Recurrent nonsustained ventricular tachycardia was supposed to be causative for the deterioration. Subsequently, heart failure and antiarrhythmic therapy were modified and thepatient was transferred to our hospital after giving his informed consent to surgical therapy.
Physical examination revealed systolic-diastolic murmur. The 12-lead standard electrocardiogram revealed an atrioventricular conduction delay (block I°) and left bundle branch block (intrinsic QRS duration 150 ms). Transthoracic echocardiography confirmed the previous diagnosis of an inferior wall aneurysm ongoing with a markedly reduced left ventricular function (ejection fraction 30%) and dilated diameter (end-diastolic 68 mm). The right ventricle diameter was distinctly pronounced (Fig 1). Angulation of the echocardiographic four-chamber view to the inferior heart basis revealed for the first time an extended VSD of the inferobasal septum (Fig 2). Color Doppler illustrated blood shunting from left to the right ventricle. Transesophageal echocardiography was performed during surgery. After central injection of echo-contrast medium into the superior caval vein, there was evidence for bubbles passing the septum (minor shunt) and occurring in the left ventricle (Fig 3). An expected "washout" phenomenon due to an dilution of right ventricular contrast medium resulting from left to right shunting was not observed markedly. Consistent with the diagnosis of (major) left-to-right shunt, blood gas analysis demonstrated an increase of oxygen from the caval vein (pO2 36 mm Hg) to the pulmonary artery (pO2 55 mm Hg). In addition, thermal dilution measurement using Swan-Ganz catheter (Baxter Healthcare, Deefield, IL) concealed an up to 9.5 L/min increased cardiac time volume in discrepancy to the severely reduced left ventricular function.
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Fig 2. Angulation of the view to the inferior basis reveals the extended ventricular septal defect at the inferobasal septum.
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Fig 3. Transesophageal echocardiography illustrates a few contrast medium bubbles (injected into the superior caval vein) passing the septal wall (inferior to the image plane) and occurring in the angle between septum and mitral leaflet. An expected "washout" phenomenon due to a dilution of right ventricular contrast medium resulting from left to right shunting was not observed markedly.
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After median sternotomy and cannulation of aorta and right atrium with a standard two-stage cannula, open exploration of the ventricle confirmed the diagnosis of an extended VSD of the inferobasal septum adjacent to the inferior wall aneurysm. Subsequently, the aneurysm was resected and VSD plication was performed using buttressed sutures. Laser ablation of arrhythmogenic foci guided by intracardial mapping was done before closure of the ventricle in a linear wedge fashion. The internal mammary artery was grafted to the LAD, each one vein was connected to RCA and RCX. Because of the preoperatively severely reduced left ventricular function, an intraaortic counterpulsation was initiated prophylactically with release of the cross clamp. In order to improve the heart function, a biventricular pacemaker was implanted using an epicardial approach for all three leads. Each of the bipolar leads were sutured to the epicardial surface of the right atrial and ventricular wall. Because of epicardial fat and the posterior ventricular reconstruction, a unipolar screw-in lead was fixed at the lateral left ventricular wall. Within the ongoing surgical procedure, the pacemaker's atrioventricular delay was shortened resulting in active biventricular stimulation for resynchronization therapy. After 3 days of intraaortal balloon pumping at our intensive care unit, the patient recovered. Follow-up echocardiography 6 weeks later revealed markedly improved left ventricular function (ejection fraction 50%) and nearly normalized diameter (end-diastolic 60 mm).
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Comment
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Development of VSD postmyocardial infarction remains a serious event with poor and relative static outcome within the last decade. After surveillance of the acute period and surgical repair, the prognosis appears to be relatively good [2, 3]. Assumably, our patient developed VSD within the first month after myocardial infarction resulting in gradual worsening of heart failure. Usually thrombolysis or acute revascularization is recommended in acute myocardial infarction. Therefore, most of the recent studies lack patients undergoing conservative treatment. The latter is estimated to worsen the prognosis of VSD [4]. Analysis of the GUSTO-I trial data revealed an anterior infarct location and female sex as predictors of VSD [2]. An inferior VSD is accompanied by a worse outcome. Despite these negative predictors and late surgical intervention (performed 5 months after myocardial infarction), the patient survived.
This report is a reminder that every new onset or progression of right or left heart failure following myocardial infarction should lead to further diagnostic procedures including regular physical examinations in respect to new murmur and immediate echocardiography [5]. We focus on the diagnostic importance of transthoracic echocardiography to reveal an inferior VSD. The apical four-chamber view or the subxiphoidal access seem to be favorable in the detection of inferobasal VSDs. Beside right ventricular dilatation, an increased pulmonary artery mean pressure (assessed as Doppler gradient at the tricuspid valve), an abnormal mitral leaflet motion, and echo-contrast medium passing the septal wall as indirect signs, the morphologic appearance of VSD should be visualized directly. Color Doppler technique is suited to improve the diagnosis [6]. It cannot be generalized that the transesophageal approach is superior for this pattern because the inferior septum cannot be visualized obligatory. Thus, early diagnosis of acquired VSD after myocardial infarction is required quoad vitam, and echocardiography seems to be most helpful.
Biventricular pacing is probably beneficial for patients with severely reduced left ventricular function and intraventricular conduction delay. Several reports describe improvement of left ventricular function and exercise capacity of heart failure patients (NYHA III–IV) of different causes in addition to standard medical therapy [7, 8]. This report demonstrates that patients with VSD and severe heart failure undergoing cardiac surgery potentially benefit from early biventricular pacing. We have seen similar developments after other types of ventricular reconstruction in patients with severe heart failure and concomitant left bundle-branch block, so that we have adopted this type of early resynchronization therapy as a routine for this special cohort of patients. In contrast to other groups, we prefer permanent leads, as our experience demonstrates longer periods of biventricular pacing are mandatory for stabilization of the hemodynamics. Despite an initially severely reduced heart function, our patient recovered almost completely within 6 weeks. However, the contributory extent of VSD closure and biventricular stimulation to the improvement of heart function cannot be separated exactly.
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References
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Abstract
Introduction
