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Ann Thorac Surg 2000;70:553-557
© 2000 The Society of Thoracic Surgeons

Original articles: cardiovascular

Surgical treatment of acquired left ventricular pseudoaneurysms

René Prêtre, MDa, André Linka, MDb, Rolf Jenni, MDb, Marko I. Turina, MDa

a Department of Cardiovascular Surgery, University Hospital Zürich, Zürich, Switzerland
b Department of Cardiology, University Hospital Zürich, Zürich, Switzerland

Address reprint requests to Dr Prêtre, Cardiovascular Surgery, University Hospital, 100 Rämistrasse, CH-8091 Zürich, Switzerland
e-mail: rene.pretre{at}chi.usz.ch


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Comment
 References
 
Background. We present a review of our experience with acquired pseudoaneurysms of the left ventricle in order to establish the risk of surgical repair.

Methods. Ten patients operated upon for a left ventricular pseudoaneurysm in our clinic between 1984 and 1999 were reviewed. The pseudoaneurysm, a complication of myocardial infarction (four acute and three chronic) or previous cardiac surgery (three chronic), was resected in all patients and the ventricular wall defect closed with direct sutures (five cases) or a patch (five cases). Coronary artery bypass graft was performed in 6 patients.

Results. Three patients died (postoperative mortality 30%) after repair of an acute postinfarction (2 patients) or a chronic postsurgical (1 patient) pseudoaneurysm. Three patients died during follow-up (median 4 years) of a carcinological (2 patients) or cardiac (1 patient) cause. Two years after repair, 5 patients were in New York Heart Association class I or II, and 1 patient was in class III.

Conclusions. Repair of left ventricular pseudoaneurysms can be performed with acceptable results, although mortality is significant in acute myocardial infarction and redo operations. Propensity for fatal rupture, however, is higher than the surgical risk in acute pseudoaneurysms or in large or expanding chronic ones and warrants surgical repair. The best approach to small asymptomatic chronic pseudoaneurysm is unsettled.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 References
 
Acquired pseudoaneurysm of the left ventricle is a rare disorder that usually occurs after transmural myocardial infarction or after cardiac surgery [1–4]. The wide use of echocardiography nowadays allows detection of asymptomatic pseudoaneurysms occurring a few days after acute myocardial infarction or surgery. These acute pseudoaneurysms, a variant of myocardial rupture, are extremely unstable and bound to fatal rupture. Chronic pseudoaneurysms are usually detected because of symptoms, less often incidentally [1, 4]. Their natural history is imperfectly known. The danger of secondary rupture is real for large pseudoaneurysms, but uncertain for small ones [1, 4]. The risk of surgical repair, on the other hand, is also barely known, due to the extremely small number of series published. Our experience with this disorder has been reviewed in order to evaluate this risk and propose guidelines for management.


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 References
 
The chart history of all the patients operated upon in our clinic for a pseudoaneurysm of the left ventricle between 1984 and 1999 was reviewed. Two types of pseudoaneurysms were encountered: postinfarction ones (Fig 1), which occurred after transmural myocardial infarction, and postsurgical ones (Fig 2), which occurred after cardiac surgery. The pseudoaneurysms were divided into acute when discovered within 2 weeks and chronic ones when discovered more than 3 months after myocardial infarction or surgery. Acute postinfarction pseudoaneurysm is a variant of myocardial free-wall rupture characterized by the absence of pericardial tamponade and hemodynamic collapse. During this time period, we treated 9 patients with a postinfarction myocardial free-wall rupture: 5 had a hemopericardium with impaired hemodynamics [5], and 4 (the patients included in this study) had an acute pseudoaneurysm. Acute pseudoaneurysms were discovered incidentally by echocardiography, and chronic ones during investigations of cardiac failure. Coronary arteries were evaluated in all patients. Six patients had a three-, 4 had a two-, and 1 had a single-vessel disease, and 1 patient had no vessel disease. Two patients with a postsurgical pseudoaneurysm had open coronary artery bypass grafts.



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  		Fig 1. Transoesophageal echocardiography (left) and ventriculography (end diastolic frame, right anterior oblique view) (right) showing an acute postinfarction pseudoaneurysm of the left ventricle. Note the absence of hemopericardium on echocardiography. (LV = left ventricle; arrow points the neck of the pseudoaneurysm.)

 


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  		Fig 2. Transthoracic echocardiography (left) and ventriculography (end diastolic frame, right anterior oblique view) (right) showing a chronic postsurgical pseudoaneurysm. The pseudoaneurysm was detected 5 years after redo mitral valve replacement. (LV = left ventricle; MV = mitral valve prosthesis; arrow points the neck of the pseudoaneurysm.)

 
The repair was performed with the aid of cardiopulmonary bypass in 9 patients and without it in 1 patient. This patient, a 76-year-old man with a recent partially reversible stoke, had an acute postinfarction pseudoaneurysm on the inferior surface of the left ventricle (Fig 1). He received bypasses to the left anterior descending and right coronary artery on a beating heart. The heart was then gently mobilized from pericardium and loose adhesions were taken down. The bleeding site was identified and controlled by finger compression. A patch of Teflon was applied on the bleeding site and fixed with Histoacryl glue and a second layer of xenopericardium was sutured on the epicardium. Cardioplegic arrest of the heart was considered during cardiopulmonary bypass when thrombi in the pseudoaneurysm had been detected by echocardiography and during performance of bypass grafts. When a danger of systemic embolisation existed, dissection was initially limited to the anterior surface of the heart and completed after cross-clamping of the aorta. Without this danger, complete dissection of the heart and repair of the pseudoaneurysm were performed on a perfused heart. Ventricular fibrillation was electrically induced during repair of the pseudoaneurysm. Various techniques were used to obliterate the neck of the pseudoaneurysm. In 4 patients with chronic pseudoaneurysms, the defect was closed with direct sutures reinforced with Teflon felt. In 3 patients with a defect located close to the basal part of the left ventricle, the ventricular defect was closed with a patch of Gore-Tex to avoid potential distortion of the heart structures or excessive traction on the edges of the defect. In 2 patients with an acute pseudoaneurysm, no attempt was made to approximate the edges of the defect on a friable myocardium. The defect was covered with a patch of xenopericardium in 1 patient, and with a double patch of Teflon and xenopericardium in the other, as explained above. In 1 patient with a postsurgical mycotic pseudoaneurysm, infected tissues were debrided, the edges of myocardial defect approximated with polypropylene sutures, and the underlying pericardium was used to buttress the infected area. This avoided insertion of foreign material in the infected area. Coronary artery bypasses were performed for significant stenosis in 6 patients (mean number of distal anastomosis = 2.0). In 2 patients with postsurgical pseudoaneurysm, previous bypasses were open. In 1 patient with one-vessel coronary artery disease, the marginal branches of the occluded circumflex artery became entrapped in the repair and were not bypassed. In the last patient with previous mitral valve replacement, the coronary arteries were normal.

Follow-up was established in summer of 1999 in all patients by telephone contact with the patient or his physician. It ranged from 2 to 77 months (median 45 months).


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 References
 
During this 16-year period, 10 patients were treated for a left ventricular pseudoaneurysm in our unit. Demographic and clinical data are summarized in Table 1. Seven pseudoaneurysms complicated a transmural myocardial infarction, and three previous cardiac surgeries. The latter pseudoaneurysms occurred after a ventriculotomy in 2 patients and after a redo mitral valve replacement in 1 patient. Ventriculotomy had been performed to repair a ventricular aneurysm in 1 patient and a ventricular septal rupture in the other [6]. In this patient, an infection developed on the Teflon strips that had been used to reinforce the ventriculotomy closure.


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  		Table 1. Clinical Characteristics of Patients With LV Pseudoaneurysm

 
Resection of the pseudoaneurysm and closure of the ventricular wall defect was achieved in all patients without embolic, bleeding, or mechanical complications. The ventricular function was unchanged after repair, as assessed by perioperative transoesophageal echocardiography. Three patients died postoperatively, 2 after repair of an acute postinfarction pseudoaneurysm and 1 after repair of a chronic postsurgical pseudoaneurysm. In the postinfarction group, 1 patient died after a protracted course of progressive multiple organ failure and the other suddenly after transfer on the regular ward 10 days after repair. Autopsy was inconclusive regarding the cause of death. In the postsurgical group, 1 patient died of multiple organ failure due to persistent sepsis. This patient, with a mycotic pseudoaneurysm, was moribund on admission. He had been operated on in the hope that eradication of the septic focus would result in improvement. Overall, postoperative mortality was 30%; in the postinfarction group, it was 28%. Three further patients died after hospital discharge. One patient, with myocardial ischemic disease and preoperative New York Heart Association (NYHA) cardiac failure class III, died suddenly 2 months after repair without a clear cause at autopsy. The other 2 patents (who were free of cardiac symptoms) died of unrelated cause 3 and 5 years later. Among 6 patients alive 2 years after surgical repair, 5 were in NYHA class I or II, and 1 was in class III because of preexisting reduced ventricular function.


   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
References
 
Major findings and limitation of the study
The major finding of this study is that the repair of acquired pseudoaneurysms of the left ventricle, combined with appropriate myocardial revascularization, can be performed with acceptable mortality and good long-term results. Mortality is, however, significant during the acute phase of myocardial infarction and in redo operations.

The major limitation of this study resides in the small number of patients included. The occurrence of a single negative event tremendously slants the results against surgical repair. In this regard, the occurrence of two sudden deaths (without anatomic substrate at autopsy) and our decision to operate on a patient in desperate condition were particularly penalizing for surgery. Our results, therefore, need be interpreted with allowance to these unfavorable circumstances, and need be compared with the postulated natural evolution of acquired pseudoaneurysms. This evolution has constantly been grim for acute and for large chronic pseudoaneurysms. Natural evolution has not been established for small chronic pseudoaneurysms [1, 4].

Etiology of ventricular pseudoaneurysms
Acquired left ventricular pseudoaneurysms develop after transmural myocardial infarction (55% in reviews), surgery (33%), trauma (7%), or infection (5%) [1, 4]. Rupture of the left ventricle after myocardial infarction usually leads to acute pericardial tamponade and immediate death [7–9]. Pathologists have established that ventricular rupture occurs in stages and progresses from endocardium to pericardium [10, 11]. A few patients are able to survive this disorder if an adherent thrombus or pericardial adhesions seal the rupture and contain the bleeding. Adhesions may already exist at the time of infarction or more frequently develop de novo during the process of rupture. Postsurgical pseudoaneurysms occur after replacement of the mitral valve or arise on a previous ventriculotomy [2, 3, 12–14]. The complication occurs in 0.02% to 2.0% of mitral valve replacements [3, 7]. Predisposing factors include resection of the posterior leaflet, overzealous decalcification of the annulus, insertion of an oversized prosthesis, and redo mitral valve replacement (as was the case in this series), especially if the stent of a bioprosthesis has eroded the posterior ventricular wall [3, 7, 12]. A technical failure and tearing of a suture in a friable myocardium are recognized causes for pseudoaneurysms arising on the closure line of a ventriculotomy. Infection of foreign material like Teflon felts and myocarditis are other possible causes. A combination of infectious and mechanical factors was certainly responsible for the delayed development of a septic pseudoaneurysm on a previous ventriculotomy in 1 of our patients.

Diagnosis and indication for surgery
The salient feature that distinguishes a pseudoaneurysm from a true aneurysm is the discontinuity of the myocardium around the cavity [1, 15, 16]. The discontinuity is best captured by magnetic resonance or by echocardiography (Fig 1) [16]. The presence of a neck smaller than the aneurysmal cavity is strongly suggestive of a pseudoaneurysm, especially if color Doppler records a turbulent flow at the neck. Contrast ventriculography can also suggest a pseudoaneurysm when a narrow neck is detected (Figs 1 and 2), but cannot always rule it out when an aneurysmal cavity is found.

The distinction is important to establish, especially when the anomaly is detected shortly after myocardial infarction. Unlike true aneurysms, which have a resistant fibrotic wall, pseudoaneurysms initially consist of loose tissues and have an excessively high propensity for secondary rupture. Prompt surgical correction is mandatory (Fig 3). The risk of rupture seems less dramatic for chronic pseudoaneurysms. Although rupture has been documented [17, 18], a more reassuring evolution has also been reported. Frances and coworkers in a literature review gathered 31 patients treated conservatively [1]. Fifteen died within a median time of less than 1 week after myocardial infarction, confirming the hazard of acute postinfarction pseudoaneurysms. Sixteen survived and were alive at a median time of 156 weeks, suggesting a relative stability of chronic pseudoaneurysms. Likewise, Sakai and associates reported 8 patients with a pseudoaneurysm after mitral valve repair [3]. Seven were observed an did not develop complications at a mean follow-up of 57 months. One patient underwent an operation and died postoperatively.



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  		Fig 3. Management of acquired pseudoaneurysms of the left ventricle.

 
The dilemma regarding the need to operate a chronic pseudoaneurysm is often solved by itself. Most pseudoaneurysms are detected during investigations of angina pectoris or congestive heart failure, which are in part due to associated coronary artery disease or mitral valve insufficiency [1–4]. Surgical cure of the pseudoaneurysm along with myocardial revascularisation or mitral valve repair or replacement improves symptoms in the great majority of patients. In 10% to 20% of the cases, chronic pseudoaneurysms are discovered incidentally [1]. Because of the uncertainties surrounding their natural history, and the relative safety of surgical repair in this subgroup, the decision to operate should prevail over conservative management in case of large or expanding pseudoaneurysms. The unfavorable Laplace’s law components expose the pseudoaneurysms to further dilatation and rupture, or creation of mechanical embarrassment of the heart. Embolization of thrombotic material, induced by stagnant patterns of blood flow, has also been reported with large pseudoaneurysms [1, 4]. Asymptomatic small pseudoaneurysms have a more stable course [1, 3]. Regular echocardiographic or magnetic resonance assessments could be a reasonable approach in the patient who does not require surgical myocardial revascularization or mitral valve surgery. Any increase in size should lead to surgical treatment (Fig 3).

Surgical treatment
The surgical treatment of left ventricular postinfarction pseudoaneurysms raises few problems. If thrombotic material within the pseudoaneurysm has been detected by echocardiography, dissection of the heart should initially be limited to the anterior surface to allow placement of cannulas and institution of cardiopulmonary bypass. The left ventricle should be dissected free from the pericardium after the aorta has been cross-clamped. In the other cases, the pseudoaneurysm can be repaired on a perfused heart, during period of induced ventricular fibrillation. The neck of the pseudoaneurysm can be closed directly in chronic cases because of its fibrotic edges. When the defect is large or located near the base of the heart, a patch may be preferable to avoid excessive traction on the myocardium or distortion of the circumflex artery or sinus coronarius. In acute cases, epicardial patching of the freshly necrotic myocardium is an effective and reliable method [5, 19]. Appropriate myocardial revascularization and correction of associated mitral valve insufficiency should complete ventricular repair [2]. The mortality rate for the cure of postinfarction pseudoaneurysms is difficult to estimate from collected case reports and from the few existing series. In Frances’ review, it was 23%, in Komeda’s series (the largest one with 12 patients), it was 25%, and in ours, it was 28% [1, 2]. In Komeda’s experience, mortality was not associated with technical difficulties in repair of the pseudoaneurysm (a fact confirmed in our experience), but with poor left ventricular function or the need for mitral valve replacement [2].

The repair of postsurgical pseudoaneurysms is technically demanding because of tight adhesions, presence of bypass grafts, and, at times, difficult location of the pseudoaneurysm at the base of the heart. We treated 3 such patients. In 1 patient, the pseudoaneurysm was grossly infected. After resection and debridement of infected tissues, the neck of the pseudoaneurysm was approximated with direct sutures and the infected area buttressed with the underlying pericardium. This avoided insertion of foreign material. In another patient, a large pseudoaneurysm developed at the base of the heart after mitral valve replacement. The pseudoaneurysm was approached and repaired from the outside of the heart. Many authors have reported an approach from the inside of the heart with exclusion (not resection) of the pseudoaneurysm in this situation. In this approach, the left atrium is opened, the mitral valve temporarily removed, and the neck of the pseudoaneurysm directly closed or covered with a patch [12–14]. Local characteristics that include the size and location of the pseudoaneurysm, need to replace or refix the mitral valve prosthesis, and course of open bypass grafts should determine the most appropriate approach. The external approach bears, however, a few advantages: the repair can be performed on a perfused heart, access to the pseudoaneurysm is not restricted by a small mitral annulus, and the pseudoaneurysm is removed.


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 

  1. Frances C., Romero A., Grady D. Left ventricular pseudoaneurysm. J Am Coll Cardiol 1998;32:557-561.[Abstract/Free Full Text]
  2. Komeda M., David T.E. Surgical treatment of postinfarction false aneurysm of the left ventricle. J Thorac Cardiovasc Surg 1993;106:1189-1191.[Abstract]
  3. Sakai K., Nakamura K., Ishizuka N., Nakagawa M., Hosoda S. Echocardiographic findings and clinical features of left ventricular pseudoaneurysm after mitral valve replacement. Am Heart J 1992;124:975-982.[Medline]
  4. Yeo T.C., Malouf J.F., Oh J.K., Seward J.B. Clinical profile and outcome in 52 patients with cardiac pseudoaneurysm. Ann Intern Med 1998;128:299-305.[Abstract/Free Full Text]
  5. Prêtre R., Benedikt P., Turina M.I. Experience with postinfarction left ventricular free wall rupture. Ann Thorac Surg 2000;69:1342-1345.[Abstract/Free Full Text]
  6. Prêtre R., Ye Q., Grünenfelder J., Lachat M., Vogt P., Turina M. Operative results in repair of ventricular septal rupture after acute myocardial infarction. Am J Cardiol 1999;84:785-788.[Medline]
  7. Becker R.C., Gore J.M., Lambrew C., et al. A composite view of cardiac rupture in the United States National Registry of Myocardial Infarction. J Am Coll Cardiol 1996;27:1321-1326.[Abstract]
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  10. Perdigao C., Andrade A., Ribeiro C. Cardiac rupture in acute myocardial infarction. Various clinico-anatomical types in 42 recent cases observed over a period of 30 months. Arch Mal Coeur 1987;80:336-344.
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  12. Carlson E.B., Wolfe W.G., Kisslo J. Subvalvular left ventricular pseudoaneurysm after mitral valve replacement. J Am Coll Cardiol 1985;6:1164-1166.[Abstract]
  13. Chatson G., Gallagher R., Quahliero D., Ruffett D., Allmendinger P. Ventricular pseudoaneurysm associated with cardiopulmonary resuscitation 6 weeks after mitral valve replacement. Ann Thorac Surg 1989;48:719-720.[Abstract]
  14. Sutter F.P., Goldman S.M., Werthman P.E., Moghadam A.N. Circumflex artery ventricular fistula and pseudoaneurysm after mitral reoperation. Ann Thorac Surg 1990;50:826-827.[Abstract]
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  16. Brown S.L., Gropler R.J., Harris K.M. Distinguishing left ventricular aneurysm from pseudoaneurysm. A review of the literature. Chest 1997;111:1403-1409.[Abstract/Free Full Text]
  17. Vlodaver Z., Coe J.I., Edwards J.E. True and false left ventricular aneurysms. Propensity for the latter to rupture. Circulation 1975;51:567-572.[Abstract/Free Full Text]
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  19. Padro J.M., Mesa J.M., Silvestre J., et al. Subacute cardiac rupture. Ann Thorac Surg 1993;55:20-23.[Abstract]
Accepted for publication February 8, 2000.




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