Ann Thorac Surg 1995;59:1079-1084
© 1995 The Society of Thoracic Surgeons
Arrhythmogenic Ventricular Aneurysms Unrelated to Coronary Artery Disease
Hiranya A. Rajasinghe, MD,
H. Peter Lorenz, MD,
Michael T. Longaker, MD,
Melvin M. Scheinman, MD,
Scot H. Merrick, MD
Divisions of Cardiothoracic Surgery and Cardiology, University of California, San Francisco, California
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Abstract
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Malignant ventricular tachycardia occurs most frequently in patients with coronary artery disease who have had a previous myocardial infarction and in whom a ventricular aneurysm subsequently develops in the scarred section of myocardium. Ventricular tachycardia in the presence of normal coronary arteries and a left ventricular aneurysm is unusual and can be refractory to medical therapy. We retrospectively reviewed our experience of 10 patients treated at our institution from 1983 to 1993. Age ranged from 22 to 76 years, and all patients presented with sustained ventricular tachycardia. All patients underwent complete electrophysiologic testing. Cardiac catheterization was performed in 9 patients, and each had normal coronary artery anatomy without evidence of significant fixed lesions. A left ventricular aneurysm, diagnosed by either echocardiography, thoracic cine computed tomography or magnetic resonance imaging, or ventricular angiography was present in all patients. Ventricular tachycardia could not be suppressed pharmacologically in 7 of 10 patients using multiple agents including procainamide, quinidine, flecanide, tocainide, propaferone, and amiodarone. Six patients were treated surgically by intraoperative electrophysiologic mapping, endocardial resection of foci, and left ventricular aneurysmectomy. An implantable cardiac defibrillator device was implanted in 2 patients. One patient died on the second postoperative day after simultaneous mapping-guided aneurysmectomy and implantable cardioverter defibrillator placement. There was one late postoperative death. All other surgically treated patients had postoperative electrophysiologic studies demonstrating no inducible ventricular tachycardia, and these patients remain without antiarrhythmic therapy in follow-up extending from 29 to 86 months (mean, 56 months). Surgical pathologic examination showed nonspecific myocardial scarring and fibrosis in the aneurysm walls, which ranged in size from small apical to large broad-based basilar aneurysms with a cavity volume equal to that of the left ventricle. Our experience supports surgical therapy for medically refractory arrhythmogenic left ventricular aneurysms unrelated to coronary artery disease.
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Introduction
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Refractory ventricular tachycardia (VT) occurs most frequently in patients with coronary artery disease who have had a previous myocardial infarction and in whom a ventricular aneurysm subsequently develops in the scarred section of myocardium. Other less common causes of ventricular aneurysm are bacterial endocarditis, sarcoid, anomalous origin of the left coronary artery, trauma, syphilis, mycotic infections, cardiomyopathy, and congenital heart disease, among others [1–7]. A left ventricular aneurysm (LVA) may be well tolerated initially, but the long-term prognosis is poor, and treatment is recommended for patients who manifest signs of congestive heart failure, recurrent systemic thromboembolism, refractory angina, or refractory ventricular tachycardia [7–11]. Ventricular tachycardia usually will respond to conventional antiarrhythmic medications that are administered either empirically or with programmed electrical stimulation as a guide. If medical therapy fails, however, a number of surgical procedures including directed endocardial resection, encircling endocardial resection, and cryoablation of ectopic foci have proved successful in the management of refractory VT.
Ventricular tachycardia in a patient with normal (disease-free) coronary artery anatomy and an LVA is rare and can be refractory to medical therapy. In 2 previously published case reports, Fontaine and associates [12] (3 patients) and Aizawa and colleagues [13] (5 patients) reported their experience in the medical and surgical management of arrhythmogenic left ventricular aneurysm unrelated to coronary artery occlusive disease. In both studies, all patients with inducible VT refractory to pharmocologic therapy and foci identified by complete electrophysiologic testing (EPS) (combined total of 6 patients) underwent operative resection. No early deaths were reported, and postoperative EPS in Aizawa and colleagues' series showed no inducible VT in 3 of 5 surgical cases [13]. However, data regarding the mean follow-up is limited to 14 months, and the cause of the LVA was assumed to be idiopathic [12]. In the present study, we retrospectively reviewed 377 patients who presented to the Electrophysiology Laboratory at the University of California, San Francisco, with sustained VT between 1983 and 1993. Ten patients were found to have normal coronary arteries and an LVA. The purpose of this study is to present our experience in the management of VT and LVA unrelated to coronary artery disease.
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Material and Methods
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Selection of Patients
A retrospective analysis was performed on 377 patients referred to the Electrophysiology Laboratory at the University of California, San Francisco, Moffitt/Long Hospital for sustained ventricular tachycardia between 1983 and 1993. Fifty patients were treated directly surgically including ventricular mapping and ablation. A total of 10 patients were identified from the electrophysiology laboratory records at the University of California, San Francisco, with sustained ventricular tachycardia, left ventricular aneurysms, and normal (disease-free) coronary artery anatomy and absence of ischemic heart disease. Patients with a documented prior myocardial infarction within 6 months of presentation were excluded. There was no prior history of cocaine or drug abuse suggesting small vessel coronary artery disease in these patients.
Clinical Features
Patient parameters analyzed included age, sex, symptoms, rhythm, number of ventricular tachycardia episodes, medications administered, imaging studies, complete EPS, medical and surgical treatment, surgical pathology, and follow-up by review of medical records and telephone interviews with the patient or his or her physician. The patient profile of our group and main clinical data are summarized in Table 1
. There were 5 men and 5 women; their mean age was 49 years (range, 22 to 76 years). All patients presented with symptomatic recurrent ventricular tachycardia in the preoperative period, and 8 patients previously had failure of standard antiarrhythmic therapy.
Diagnostic Studies
All 10 patients who presented with sustained or recurrent ventricular tachycardia underwent initial diagnostic evaluation with an electrocardiogram and complete EPS. The electrocardiogram was analyzed during sinus rhythm and during VT for the electrical axis and probable origin of the arrhythmia. The goal of EPS was to induce and locate a source of VT similar to the presenting clinical syndrome. Programmed pacing was applied to different zones of the right and left ventricle to determine if VT could be induced and terminated by either single, multiple, or burst extrastimulus technique [14].
Patients with inducible VT on EPS underwent coronary angiography and ventriculography to document the presence or absence of atheromatous coronary artery disease as a cause of the arrhythmia. Left ventricular aneurysm was diagnosed angiographically using the Coronary Artery Surgery Study protocol [15]. An LVA was determined to be present if two of the following criteria were present: (1) systolic bulging of the involved segment, (2) absence of trabeculation in the involved segment, and (3) well-defined demarcation of the aneurysmal segment from normally contracting myocardium [15]. Two-dimensional echocardiography, thoracic cine computed tomography, or thoracic magnetic resonance imaging of the heart also was performed in the majority of patients to aid or confirm the diagnosis of LVA.
Operative Procedure
We used the technique of Josephson and associates [16] of aneurysmectomy and ventricular mapping with directed endocardial resection to treat malignant ventricular arrythmias with LVA. In all cases of map-guided aneurysmectomy, the heart was exposed with standard median sternotomy. The patient was placed on cardiopulmonary bypass after ascending aortic root and bicaval right atrial cannulation at normothermia. Right ventricular pacemakers were used for reference electrogram and stimulation, and epicardial mapping was performed using a hand-held probe to identify the focus of early activation. After successful completion of epicardial mapping, a small ventriculotomy was performed through the thinnest portion of the aneurysmal segment and endocardial mapping was performed. If an area of early activation was identified, the entire aneurysm was opened and endocardial resection was performed to include the focus of early activation. Either the large ventriculotomy incision was closed primarily or a Dacron patch was used to reconstruct the left ventricle. The standard deairing maneuvers were carried out, the heart was defibrillated, and the patient was decannulated after weaning from cardiopulmonary bypass.
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Results
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All ten patients presented with recurrent ventricular tachycardia, and 7 required cardioversion upon initial presentation. The most common presenting symptoms were palpitations and syncope, and 8 patients had been using antiarrhythmic medications.
All patients underwent complete EPS with programmed stimulation as part of the initial diagnostic evaluation. Electrophysiologic testing showed sustained inducible ventricular tachycardia in 9 of 10 patients. All foci of VT were monomorphic in pattern. Ventricular tachycardia could not be pharmacologically suppressed in 7 of 10 patients. Multiple agents were used including procainamide, quinidine, flecanide, tocainide, propaferone, and amiodarone. One patient's VT was suppressed with verapamil, and this patient remains asymptomatic with more than 6 years of follow-up. Another patient's VT was suppressed with amiodarone; this patient remains asymptomatic with more than 5 years of follow-up. Nine of 10 patients underwent cardiac catheterization and were found to have normal coronary anatomy without evidence of angiographically fixed obstructive lesions.
Left ventricular aneurysm was present in each patient, diagnosed by ventricular angiography, echocardiography, or thoracic cine computed tomography or magnetic resonance imaging, alone or in combination (Table 2; Fig 1). Gross aneurysmal morphology by imaging studies included large anteroseptal aneurysms, thin-walled inferior aneurysms, and small apical aneurysms. Estimates of ejection fraction by echocardiography or ventricular angiography ranged from 0.50 to 0.86, and only 2 patients had evidence of mural thrombus.
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Fig 1. . Representative coronary angiogram from a selected patient. (A) Right anterior oblique projection of normal left anterior descending and left circumflex coronary arteries. (B) Left anterior oblique view of normal right coronary artery and branches. (C) Right anterior oblique view of discrete large-mouth left ventricular aneurysm at the base of the heart.
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Seven patients with inducible VT by programmed stimulation that could not be pharmacologically suppressed upon initial evaluation were referred for surgical management. Surgical and medical therapy for patients with refractory ventricular tachycardia, LVA, and normal coronary arteries are summarized in Table 3. Electrophysiologic testing identified a focus of VT in 7 patients, 6 of whom were treated subsequently by intraoperative mapping, endocardial resection of foci, and left ventricular aneurysmectomy or aneurysm plication. In 1 patient (patient 2) EPS failed to identify a focus of VT, and an implantable cardioverter defibrillator (ICD) device was implanted. Another patient (patient 10), a 32-year-old pregnant woman in her second trimester with inducible VT who initially responded to amiodarone, subsequently required ICD placement for recurrent VT while receiving antiarrhythmic drugs. There was one early postoperative death (patient 1) that resulted in a 69-year-old woman with refractory VT who suffered a cardiac arrest on the second postoperative day after simultaneous mapping, aneurysmectomy, and ICD placement. Her clinical course was notable because, despite repeated episodes of VT and antiarrhythymic drug resistance, preoperative EPS could not induce VT and intraoperative mapping failed to identify a focus adjacent to the LVA. The postoperative course was complicated by multiple episodes of VT after extubation. During the fourth episode of VT on the second postoperative day this patient converted into ventricular fibrillation rhythm and could not be resuscitated. Postoperative EPS could not be performed before she died, and autopsy study revealed diffuse interstitial myocardial fibrosis, a hypertrophied left ventricle, and normal epicardial coronary arteries without evidence of intramyocadial microvascular disease. A single late death occurred in a 19-year-old man in whom a cardiomyopathy developed requiring cardiac transplantation 34 months after successful mapping-guided aneurysmectomy and symptom-free midterm follow-up. He died of multiple organ system failure 6 weeks after cardiac transplantation.
All other surgically treated patients had postoperative EPS demonstrating no inducible VT and were discharged from the hospital without antiarrhythmic therapy. These patients remain asymptomatic with a mean follow-up of 56 months. Patient 5 required placement of an ICD for recurrent ventricular tachycardia that was inducible on late postoperative EPS several months after endocardial resection of foci and aneurysmectomy.
Surgical pathology specimens of resected aneurysm segments were sent on all patients undergoing mapping-guided aneurysmectomy. Microscopic pathologic examination demonstrated a pattern of extensive interstitial fibrosis and replacement of cardiac muscle with scar in 5 of 6 specimens. Blood vessels were examined carefully for evidence of calcification and thrombus formation and none were found. There was no evidence of myocarditis, sarcoidosis, fatty infiltration, or myofibrillar disarray such as that seen in idiopathic hypertrophic cardiomyopathy. No specific cause could be established for the aneurysms. In a single patient a predominantly lymphocytic infiltrate containing giant cells and eosinophils was found scattered within necrotic myocardial tissue. Special stains for acid-fast bacilli and fungal organisms were negative. Trypanosoma cruzi (Chagas' disease) was not identified. The histopathologic changes in this patient were thought to be most consistent with a focal myocarditis.
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Comment
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Ventricular aneurysms were first recognized in the 18th century, with the vast majority due to myocardial infarction [17]. Left ventricular aneurysms can be expected to develop after approximately 12% to 15% of known myocardial infarctions. Congestive heart failure, thromboembolism, angina, and ventricular arrhythmias generally are accepted as indications for LVA resection or plication [18]. Despite improvement in therapy for myocardial infarction, cardiothoracic surgeons are faced with increasing numbers of patients who have life-threatening arrhythmias associated with LVAs. Even with the advent of pharmocologic therapy, a 47% mortality was reported among patients with VT developing more than 8 weeks after acute myocardial infarction [19]. Frequently, these malignant arrhythmias do not respond to aggressive medical management [20].
The work-up of a patient with a malignant ventricular tachycardia includes thorough EPS with attempts to induce and localize a focus of VT similar to the clinical syndrome. Most VTs in the presence of LVA are thought to result from ischemia in the border zone surrounding the LVA. In the majority of cases, VT can be controlled by antiarrhythmic medications or overdrive suppressive pacing. The goal, therefore, of the evaluation is to locate a treatable source for the arrhythmia, either in a scar or aneurysm.
In patients with LVA and VT refractory to medical therapy, surgical therapy has been shown to be efficacious [16]. Surgical attempts to correct LVA have been relatively recent. Cooley and associates [21] reported the first excision of LVA on total cardiopulmonary bypass in 1958. Approaches to control refractory VT surgically in patients with LVA followed the disappearance of VT in resected LVAs first observed by Couch [22]. ``Blind'' aneurysmectomy, however, has been associated with a high rate of recurrent VT and early mortality [20]. Furthermore, the use of concomitant coronary artery bypass grafting has not been shown to improve results [23]. The most favorable results in the surgical treatment of arrhythmogenic ventricular aneurysms have been achieved with mapping-guided subendocardial resection in combination with aneurysmectomy [24, 25].
The standard mortality rate reported for surgical correction of recurrent VT associated with postinfarction aneurysm has been reported to be 10% in one series of 40 patients [24] and has ranged between 16% and 17% in other series of 30 patients or greater [26, 27]. Our overall 17% hospital mortality rate in patients undergoing surgical therapy compares favorably with previously reported mortality rates. Although a previous history of cardiac operation, advanced New York Heart Association functional class, low left ventricular ejection fraction, and operation within 30 days of myocardial infarction have been cited as variables influencing early survival, none of our patients had evidence of ischemic heart disease or cardiomyopathy, and all were found to have good left ventricular systolic function preoperatively [26].
The single early death in our series after aneurysmectomy and ICD placement may best be explained as a result of incomplete mapping. Several previous studies have demonstrated the superiority of directed aneurysmectomy over nondirected ``blind'' aneurysmectomy in the days before EPS was available for ablation of medically refractory VT [23]. Nondirected ventricular aneurysmectomy has been associated with recurrence of VT as high as 40% in substantial series [23], yet the results of ``visually directed'' endocardial resection are equal to those of map-directed endocardial resection [28]. Because a reentry mechanism has been postulated to be the most common cause of sustained recurrent ventricular tachycardia, mapping-guided surgical procedures are based on interrupting the reentrant circuit or resecting the point of earliest activation [29]. Several preoperative EPSs were unable to induce VT in patient 1 (see Table 3
), and intraoperative mapping failed to localize a focus. It is possible that this patient's ventricular arrhythmia resulted from a nonreentrant mechanism and was therefore not amenable to mapping. Moreover, surgical therapy may be indicated only for reentrant sustained VT.
Although the vast majority of ventricular aneurysms develop in hearts with previous myocardial infarction and coronary atherosclerosis, a number of less common causes unrelated to ischemic heart disease have been identified including endocarditis, sarcoid, anomalous origin of the left coronary artery, trauma, syphilis, mycotic infections, and cardiomyopathy [1–7]. In our study, microscopic analysis of 6 aneurysm specimens received from the operating room was unable to establish a cause for aneurysm formation. Five of 6 specimens showed extensive areas of interstitial fibrosis and scar formation without evidence of atheromatous changes in surrounding blood vessels. Our remaining specimen was notable for the presence of a predominantly lymphocytic infiltrate consistent with a focal myocarditis; however, special stains for acid-fast bacilli and fungal organisms were negative, and parasitic organisms were not identified. Our histopathologic findings confirm the observations made by other authors in failing to establish a cause in cases of LVA with normal coronary arteries [13].
Although a clear cause could not be established for aneurysm formation, in some cases the gross morphology and distribution of the LVAs may suggest an explanation. In 3 cases, the LVA originated at the midportion of the ventricle forming a saccular apex. These LVAs may represent a severe form of asymmetric hypertrophic cardiomyopathy whereby the pattern of hypertrophy occurs at the level of the papillary muscles (midventricular hypertrophy). Previous reports have described histopathologic abnormalities in hypertrophic cardiomyopathy of extensive interstitial fibrosis and dense scar formation in the absence of major epicardial coronary artery disease [30, 31]. It also has been suggested that VT-related aneurysm is a sequela of chronic myocarditis diagnosed from surgical specimens of so-called idiopathic left ventricular tachycardia [32]. This appears similar to observations made in this study in several of our microscopic pathology specimens. The fibrosis and scar formation may result from myocardial ischemia due to impairment of blood flow through small coronary arteries. Although a causal relationship between small vessel disease and interstitial fibrosis is suggested by these observations, caution must be exercised in making this conclusion.
In conclusion, our study supports the use of mapping-guided endocardial resection in the treatment of medically refractory ventricular tachycardia in patients with LVAs unrelated to coronary artery disease. Despite the limitations of the electrophysiologic evaluation in providing complete mapping, surgical therapy may be undertaken with resultant low perioperative mortality and recurrence-free long-term success. We also conclude that patients who present with recurrent VT, even without evidence of coronary artery disease, should be evaluated carefully for the presence of a ventricular aneurysm. Ventricular aneurysm usually can be detected by noninvasive imaging modalities and confirmed by angiography. Other patients who do not undergo surgical therapy may respond to antiarrhythmic drug or device treatment.
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Footnotes
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Presented at the Poster Session at the Thirtieth Annual Meeting of The Society of Thoracic Surgeons, New Orleans, LA, Jan 31–Feb 2, 1994.
Address reprint requests to Dr Merrick, Division of Cardiothoracic Surgery, M593, University of California, 505 Parnassus Ave, San Francisco, CA 94143.
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Abstract
Introduction
