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Ann Thorac Surg 2003;76:719-725
© 2003 The Society of Thoracic Surgeons

Original article: cardiovascular

Repair of left ventricular aneurysm: surgical risk and long-term survival

Runar Lundblad, MDa*, Michel Abdelnoor, PhDb, Jan L. Svennevig, MDa

a Department of Cardiothoracic Surgery, Rikshospitalet, Oslo, Norway
b Research Forum, Clinical Epidemiology Unit, Ullevaal University Hospital, Oslo, Norway

Accepted for publication April 3, 2003.

* Address reprint requests to Dr Lundblad, Rikshospitalet, N-0027 Oslo, Norway.
e-mail: runar.lundblad{at}rikshospitalet.no


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 References
 
BACKGROUND: The aim of the study was to identify predictors for survival after repair of postinfarction left ventricular aneurysm.

METHODS: We retrospectively reviewed the records of 149 patients who had an operation for postinfarction left ventricular aneurysm between 1989 and 2001. The following variables were recorded: preoperative clinical, angiographic, and echocardiographic findings and operative procedures. Outcomes were early mortality (<30 days) and long-term survival. Risk factors were pinpointed using t test or Mann-Whitney test, contingency tables, and survival curves. Independent risk factors were identified by logistic regression and Cox regression methods. Mean follow-up was 5.8 years (range, 0 to 13.8 years).

RESULTS: The early mortality (<30 days) rate was 8.7% altogether, and the 5-year cumulative survival rate was 77%. Advanced age, history of ventricular arrhythmia, three-vessel disease, and linear repair technique were independent risk factors for early and total mortality. Poor left ventricular function predicted reduced long-term survival but did not increase surgical risk. Survival was not affected by gender, diabetes, type and severity of symptoms, anterior or posterior aneurysm, revascularization of the left anterior descending artery, or number of distal anastomoses.

CONCLUSIONS: Postinfarction left ventricular aneurysm can be repaired with acceptable surgical risk and long-term survival. Survival is reduced in cases with advanced age, history of ventricular arrhythmia, three-vessel disease, poor left ventricular function, and linear repair of the aneurysm.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 References
 
Left ventricular aneurysm (LVA) is a serious complication of acute myocardial infarction (MI) that can lead to congestive heart failure (CHF), ventricular arrhythmia and, rarely, thromboembolic events. The usual cause is acute occlusion of the left anterior descending artery (LAD), with LVA formation in the distal part of the anterior wall and septum. The operative goal is to correct the size and geometry of the left ventricle (LV) in order to reduce wall tension and paradox movement and to improve systolic function. Intracavitary thrombi are removed, and coronary artery bypass grafting (CABG) is usually performed. Aneurysmectomy and linear repair of LV using cardiopulmonary bypass was introduced by Cooley in 1958 [1]. This remained the standard procedure until the mid 1980s, when the technique of endoventricular patch plasty (EVPP) gradually took over [2–4]. Surgical treatment is indicated in established cases of CHF, angina pectoris, malignant ventricular arrhythmia, or recurrent embolization from LV, whereas operation in asymptomatic patients is controversial. The present study identifies risk factors for premature death in 149 patients operated on for LVA.


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 References
 
Baseline patient characteristics
Between January 1989 and June 2001, 149 consecutive patients were operated on for nonruptured postinfarction LVA. The cases were reviewed retrospectively in March 2003. The diagnosis and criteria for aneurysmectomy were based on a dyskinetic aneurysm with systolic paradoxical movement. Linear repair (n = 74) of the LV was performed mostly in the early part of the period and EVPP (n = 75) in the later part. Baseline clinical data are summarized in Table 1. There were 116 men and 33 women, with a mean age of 61.6 ± 9.5 years. Ninety percent of the patients had sustained one or two MIs preoperatively, and 10% had multiple MIs. All patients had symptoms from their LVA, and 77% were in New York Heart Association functional class III or IV. Indications for operation were as follows: angina pectoris (23%), CHF (20%), angina pectoris and CHF (25%), ventricular arrhythmia (5%), and ventricular arrhythmia combined with angina pectoris or CHF (26%). No patient had implantable cardioverter defibrillator preoperatively.


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  		Table 1. Preoperative Patient Characteristics

 
For LVA diagnosis, we relied on echocardiography and cardiac catheterization with left ventriculography and selective coronary angiography. From left ventriculography, LV ejection fraction (LVEF) was calculated in 126 patients, and LV end-diastolic pressure was measured in 136 patients. Preoperative cardiac performance is shown in Table 2. Left ventricular function was significantly reduced, with LVEF of 34 ± 12% and LV end-diastolic pressure 21 ± 8 mm Hg. All patients had significant coronary lesions identified by angiogram. Three-vessel disease was present in 37%, left main stenosis in 10%, and significant LAD lesion in 95%. Anterior location of the aneurysm was seen in 140 patients (94%) and nonanterior location in nine cases (inferoposterior wall n = 5, posterolateral wall n = 4). Coronary pathology was complex in the nine cases with nonanterior aneurysm. Five had right main coronary pathology with normal circumflex artery (three occlusions, one 90% stenosis, one 90% stenosis with right coronary dominance). Three of these five cases also had significant LAD lesion. Another four patients had significant lesions of both right main coronary and circumflex vessels (one had occlusion of both vessels, one had stenosis of both vessels, two had stenosis of right main coronary artery and occluded circumflex artery). Two of these patients also had LAD stenosis, and another had left main stenosis. Isolated pathology of the circumflex artery was not seen.


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  		Table 2. Preoperative Cardiac Performance

 
Operative technique
The procedure was performed using cardiopulmonary bypass and moderate systemic hypothermia. The aneurysm was incised parallel to the interventricular septum; intracavitary clots were removed; and the ventricular vent was inserted. Distal coronary anastomoses were performed, and, finally, the LV wall was repaired. In six patients who did not have CABG, LVA repair was performed on the beating heart. In 143 cases, the aorta was cross-clamped, and cold antegrade crystalloid cardioplegic solution was infused. In 58 of these 143 cases, the whole procedure was done with the aorta cross-clamped. In 85 of 143 cases, the LVA repair was performed on a beating heart, as the cross-clamp was removed after the aneurysm was opened, and eventually distal anastomoses were performed. For linear repair, the edges were readapted with two strips of felt or pericardium for reinforcement, using a combination of continuous sutures and interrupted mattress stitches. For EVPP, a patch of Dacron (n = 66) or polytetrafluoroethylene (n = 9) was attached to the border zone between normal and scarred tissue, after a circular purse string suture was eventually used to restore a new apical neck (n = 5). The patch was secured with continuous (n = 35) or interrupted (n = 6) mattress sutures or a combination of both (n = 34). The aneurysm sac was closed over the patch with two strips of felt or pericardium for reinforcement, using a combination of continuous sutures and interrupted mattress stitches. When performed, cryoablation was based on mapping or just visually directed.

Statistical analysis
Continuous numeric data are presented as mean ± standard deviation (range), whereas discrete numeric data and categoric data are presented as frequencies. Endpoints were early mortality (<30 days) and total mortality.

Univariate analysis of early mortality was performed using 2 x 2 tables with {chi}2 or Fischer exact test for discrete numeric data or categoric data, and the two-tailed t test or the Mann-Whitney test was used for continuous numeric data. Analysis of total mortality was done according to the Kaplan-Meier method, and differences between survival curves were estimated by the Breslow test and the log rank test [5].

Multivariate analysis was performed for variables that were statistically significant (p < 0.05) or marginally significant (p < 0.2) in the univariate analysis, or that were considered clinically or pathophysiologically important (age, gender, diabetes, and LVEF). Logistic regression was used to identify independent risk factors for early mortality. The Cox proportional hazards regression method was used to identify independent risk factors for total mortality [6]. Manual, backward elimination of variables was performed, based on the following criteria: clinical or pathophysiologic importance, correlation matrix between the variables, and statistical significance of the Wald test.


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
References
 
Operative and postoperative characteristics
Operative and postoperative data are shown in Table 3. Coronary artery bypass grafting was performed in 118 patients, and the number of distal anastomoses was 2.2 ± 1.0 (range, 1 to 6). The LAD was significantly diseased in 141 patients, and it was revascularized with the internal mammary artery in 62 cases and with vein graft in 13 cases. Cryoablation, eventually combined with endocardial scar resection, was done in 23 of 47 patients with ventricular arrhythmia. One patient had a previous inferior wall infarction and a large mitral regurgitation and received a mitral valve and EVPP. Intraaortic balloon pump was used in 8.7% of patients, and 24.2% needed inotropic agents for more than 24 hours. Noncardiac organ failure developed in 6%, and all these patients had sustained low output syndrome postoperatively. No patients had sternal dehiscence.


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  		Table 3. Operative and Postoperative Characteristics

 
Mortality rates
The early mortality (<30 days) rate was 8.7% (13 patients). Independent risk factors for early mortality were advanced age, three-vessel disease, history of ventricular arrhythmia, and linear repair of the aneurysm (Table 4). Follow-up was 5.8 ± 3.8 years (range, 0 to 13.8 years), and total observation time was 861 years. Overall the 5-year cumulative survival was rate 77% (Figure 1). Independent risk factors for total mortality were advanced age, three-vessel disease, low LVEF, more than one previous MI, history of malignant ventricular arrhythmia, and linear repair technique (Table 5 and Fig 2–7). The following factors had no influence on early and total mortality rates: gender, diabetes, angina pectoris, CHF, New York Heart Association class, left main stenosis, LV end-diastolic pressure, mitral regurgitation, location of aneurysm, time between last MI and operation, number of distal coronary anastomoses, and date of operation.


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  		Table 4. Risk Factors for Early Mortality by Multivariate Analysis in 149 Patients

 


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  		Fig 1. Cumulative survival after left ventricular aneurysm repair in 149 patients. Numbers on curve indicate patients at risk.

 

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  		Table 5. Risk Factors for Total Mortality by Multivariate Analysis

 


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  		Fig 2. Effect of age on cumulative survival after left ventricular aneurysm repair. Numbers on curves indicate patients at risk. Circles = age less than 70; squares = age greater than 70.

 


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  		Fig 3. Effect of left ventricular function on cumulative survival after left ventricular aneurysm repair. Numbers on curves indicate patients at risk. Squares = left ventricular ejection fraction (LVEF) less than 0.35; circles = LVEF greater than 0.35.

 


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  		Fig 4. Cumulative survival after left ventricular aneurysm repair. Effect of number of preoperative myocardial infarctions (MI). Numbers on curves indicate patients at risk. Circles = number of MI equaling 1; squares = number of MI greater than 1.

 


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  		Fig 5. Effect of history of ventricular arrhythmia (VA) on cumulative survival after left ventricular aneurysm repair. Numbers on curves indicate patients at risk. Circles = VA negative; squares = VA positive.

 
Operations during follow-up
Three patients in the linear repair group underwent subsequent heart transplantation. One patient received a transplant after 7 weeks and died 6 years later. Another patient received a transplant 6 months after the aneurysm repair and is still alive 6 years after the transplantation. The last patient received a transplant 5 years after the primary operation and is still alive 7 years after the transplantation. No patient in the EVPP group has received a transplant, but the follow-up time has been shorter. Eleven patients received implantable cardioverter defibrillator during follow-up, and one patient in the linear repair group has removed cardiac Teflon felt because of chronic, fistulating sternal infection.



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  		Fig 6. Effect of coronary disease on cumulative survival after left ventricular aneurysm repair. Numbers on curves indicate patients at risk. Circles = one- or two-vessel disease; squares = three-vessel disease.

 


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  		Fig 7. Effect of aneurysm repair technique on cumulative survival. Numbers on curves indicate patients at risk. Squares = linear repair; circles = endoventricular patch plasty.

 
Comment
Left ventricular aneurysm behaves according to the law of La Place. Left ventricular wall tension increases with increasing LV diameter, intracavitary pressure, and wall thinning. A large and thin-walled aneurysm has high wall tension, poor coronary perfusion, and further dilation. The ultimate stage of LVA is enlargement, not only of the aneurysm, but of the global LV. As the impaired LV can not generate high blood pressure, this will limit the increase in wall tension and protect against further dilation of the aneurysm and eventually free rupture, which seems extremely rare.

Indications for operation
Two thirds of the patients had one MI, and one third had more than one MI. The interval between last MI and aneurysm repair ranged from 1 month to 27 years. Early intervention (<2 months) did not increase the operative mortality rate. All patients had symptoms from their LVA. Angina with or without CHF led to surgical intervention in two thirds of the cases, whereas ventricular arrhythmia, alone or in combination with other symptoms, was the indication in the rest of the cases. Like other studies, we found that a history of ventricular arrhythmia resulted in reduced long-term survival [7, 8]. Ventricular arrhythmia arises in the border zone between viable and dead myocardium, particularly on the interventricular septum. Simple aneurysmectomy, with or without concomitant CABG, often fails to control ventricular arrhythmia, and it is hypothesized that EVPP can have an inherent antiarrhythmic effect [9]. Endoventricular patch plasty can reduce wall tension on the interventricular septum, and, by sewing the patch there, may act on the arrhythmia substrate like an endocardial excision or cryoablation, converting it to a homogeneous and nonarrhythmogenic scar. Moreover, because much of the aneurysm sac is retained, EVPP facilitates the use of an internal mammary artery graft to LAD, which may be particularly important to improve septal perfusion. Intraventricular thrombus formation is common, but the incidence of arterial embolism is low. No patient in our series had embolic episodes.

Although the surgical risk is increased, patients with low LVEF and multivessel disease have a particular survival benefit after CABG [10]. The biologic basis for this is recruitment of hibernating myocardium. It is not known whether an operation improves survival in the subset of patients with extensive MI and LVA formation, and no controlled studies have been done to evaluate surgical and modern medical treatment. Afterload reduction with angiotensin-converting enzyme inhibitors may control symptoms and hemodynamic deterioration for a period of time, but the effect on life expectancy is unknown. In accordance with other reports on LVA repair [11–15], we show that low LVEF is a predictor for reduced long-term survival, as a 10% reduction in LVEF reduces mean survival time by 30% (Table 5). Unless it is extremely low, a reduced LVEF per se should not contradict operation, because historical data show a short life span without operation in symptomatic patients [16]. Global LVEF represents both the contractile and the noncontractile, aneurysmic parts of the left ventricle. Because noncontractile tissue is removed during LVA repair, the contractile LVEF or segmental wall-motion analysis is the preferred method to predict the benefit of an operation.

Low LVEF indicated poor long-term survival, but the clinical correlate, heart failure, was not correlated with adverse outcome in the present study. Neither the presence nor the severity of CHF was associated with premature death. Conflicting data exist on the association between CHF and late outcome after LVA repair. Some studies identify severe CHF as an independent determinant for premature death [7, 12–14, 17], whereas others show no association [8, 11, 18]. This controversy may have several explanations. Dyspnea varies over time because of natural variations of the disease and response to medical treatment. In addition, New York Heart Association classification per se is not accurate and bears a great deal of uncertainty because the patients adapt to their poor physical state. In agreement with this, our study showed no association between LVEF and severity of CHF. Clinical heart failure is an established indication for LVA repair, but the degree of symptoms should not influence the decision for surgical treatment.

It is controversial whether aneurysmectomy should be performed prophylactically to prevent irreversible damage of LV. Although LVA repair may improve long-term survival, operation is traditionally not recommended in asymptomatic cases because of the surgical risk involved. An early mortality rate of 8.7% in the present study is in accordance with those of other reports [8, 9, 11, 14, 15, 17–21]. However, the early mortality rate was 4% in the 75 patients who had EVPP repair in the later part of the series. Because these patients all had symptoms from their LVA, aneurysmectomy can probably be performed with comparable or even lower surgical risk in asymptomatic patients.

Location of aneurysm
In clinical reports, LVA is usually located in the anterior wall, whereas inferoposterior or posterolateral aneurysms are less common [13]. Postinfarction LVA follows pathology of the LAD-diagonal system (anterior aneurysm), circumflex branches (posterolateral aneurysm), or right coronary artery (inferoposterior aneurysm). In our series, a significant LAD lesion was present in 95% of patients, and the aneurysm was located anteriorly in 94%. The prevalence of inferoposterior aneurysms is significantly higher in autopsy series than in clinical reports [22]. This may be due to the extensive infarction necessary for LVA formation. When this occurs in the inferoposterior wall, the result is often acute, severe mitral regurgitation, and the patients die in the acute phase rather than develop LVA.

Aneurysm repair technique
Endoventricular patch plasty was introduced as a more physiologic repair than the linear closure technique, especially when the aneurysm extends into the septum. In small aneurysms not involving the septum, the theoretical advantages of EVPP are less convincing. Endoventricular patch plasty can improve LV function [12, 19, 23] more effectively than the linear repair method [9, 24]. There is still controversy whether EVPP is superior to simple aneurysmectomy with regard to early and late clinical outcome. Both methods clearly improve functional status [7, 9, 11, 15, 18, 19, 21, 24, 25]. Some studies report superior functional improvement after EVPP than after linear repair [9, 15, 18, 21], whereas others fail to demonstrate any difference between the methods [11, 13, 24]. Alternatively, LVA can be repaired by a modified linear technique, eventually combined with septoplasty, which offers a more physiologic shape of the LV than traditional linear closure. This technique can provide good symptomatic relief and long-term survival and is associated with improvement in LV function [7, 26]. No randomized trials have evaluated long-term survival after EVPP and linear repair. In the present study, EVPP was associated with better long-term survival than linear repair, but other retrospective reports failed to demonstrate any difference in survival between the two methods [8, 11, 13, 15, 18, 21, 24]. However, these studies include relatively small numbers of patients and cover a long period of time, making interpretation of data and statistical evaluation difficult.

There are no controlled studies that determined the benefit of CABG during LVA repair. Because CABG is usually performed whenever indicated and technically possible, the present study and other retrospective reports give no data to evaluate the effect of concomitant revascularization on early and late outcomes. Nevertheless, CABG is highly recommended for two reasons. First, it reduces or prevents angina pectoris. Second, although the LAD is occluded and the periphery on the free wall seems poor, an internal mammary artery graft to LAD may be particularly important in order to revascularize viable interventricular septum and to control ventricular arrhythmia originating in the transitional zone. In the present study, a graft to LAD was significantly more frequent in the EVPP group (67%) than in the linear repair group (39%). The importance of an internal mammary artery graft to LAD during complex operations was probably underestimated in the first period of the series, when linear repair dominated. Moreover, with that technique, the aneurysmal sac is partially removed, and the remnant is used for closure of the left ventricle, which may render revascularization of LAD impossible.

Limitations of the study
Left ventricular aneurysm can be defined as an area of asynergy (akinetic or dyskinetic) that is large enough to reduce LV function. This is a very loose definition, and the lack of uniformity regarding aneurysm criteria complicates almost all discussions of LVA repair. In the present report, the diagnosis and criteria for aneurysmectomy were based on a dyskinetic aneurysm with systolic paradoxical movement. However, there is a continuum between akinesia and dyskinesia, and there are obvious border zones between these entities. Aneurysmectomy was introduced originally for dyskinetic aneurysms, and there is controversy about whether cases with akinetic aneurysms would benefit from surgery. Recent reports suggested that both LV dysfunction and the outcome of surgery depended on the extent of asynergy rather than the type of asynergy (akinetic or dyskinetic) [7, 12, 20, 27]. Wall thinning of the aneurysm was not systematically quantified in our study, neither preoperatively nor perioperatively. Dyskinetic aneurysms can have a surprisingly thick LV wall, consisting of a mixture of scar and viable myocardium. If a certain amount of viable, but hibernating, myocardium exists, there are probably cases that will benefit most from revascularization alone and not aneurysmectomy.

Our study was retrospective, covering a period of 12 years, with several surgeons involved. Linear repair was performed during the first half of the period and EVPP in the last. Although risk profiles were not different between these two groups, the operative experience, surgical strategies, and postoperative care may have changed over time, and differences in outcome should be interpreted with care.

In summary, postinfarction LVA can be repaired with acceptable surgical risk and good long-term survival. Survival is reduced in cases with advanced age, history of ventricular arrhythmia, three-vessel disease, poor left ventricular function, and linear repair of the aneurysm.


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 References
 

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Eur J Cardiothorac Surg, July 1, 2004; 26(1): 125 - 128.
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