JTCS Email Content Delivery
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Hooshang Bolooki
Kushagra Katariya
Richard J. Thurer
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bolooki, H.
Right arrow Articles by Duncan, R. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bolooki, H.
Right arrow Articles by Duncan, R. C.
Related Collections
Right arrow Congestive Heart Failure
Right arrow Myocardial infarction

J Thorac Cardiovasc Surg 2003;126:374-385
© 2003 The American Association for Thoracic Surgery


Surgery for acquired cardiovascular disease

Factors affecting late survival after surgical remodeling of left ventricular aneurysms

Hooshang Bolooki, MDa,*, Eduardo DeMarchena, MDb, Stephen M. Mallon, MDb, Kushagra Katariya, MDa, Michael Barron, MDc, H. Michael Bolooki, BSa, Richard J. Thurer, MDa, Stana Novaka, Robert C. Duncan, PhDd

a Divisions of Thoracic and Cardiovascular Surgery, University of Miami School of Medicine/Jackson Memorial Hospital, Miami, Fla, USA
b Cardiology, University of Miami School of Medicine/Jackson Memorial Hospital, Miami, Fla, USA
c Departments of Anesthesiology, University of Miami School of Medicine/Jackson Memorial Hospital, Miami, Fla, USA
d Epidemiology, and Public Health, University of Miami School of Medicine/Jackson Memorial Hospital, Miami, Fla, USA

Read at the Twenty-eighth Annual Meeting of The Western Thoracic Surgical Association, Big Sky, Mont, June 19-22, 2002.

Received for publication July 15, 2002; revisions received September 3, 2002; revisions received October 11, 2002; accepted for publication October 28, 2002.

* Address for reprints: Hooshang Bolooki, MD, FRCS (C), University of Miami/Jackson Memorial Hospital, PO Box 016960 (R-114), Miami, FL 33101, USA
hbolooki{at}med.miami.edu


    Abstract
 Top
 Abstract
 Patients and methods
 Results
 Discussion
 Discussion
 References
 
OBJECTIVES: Surgical remodeling of the left ventricle has involved various techniques of volume reduction. This study evaluates factors that influence long-term survival results with 3 operative methods.

METHODS: From 1979 to 2000, 157 patients (134 men, mean age 61 years) underwent operations for class III or IV congestive heart failure, angina, ventricular tachyarrhythmia, and sudden death after anteroseptal myocardial infarction. The preoperative ejection fraction was 28% ± 0.9% (mean ± standard error), and the pulmonary artery occlusive pressure was 15 ± 0.07 mm Hg. Cardiogenic shock was present in 26 patients (16%), and an intra-aortic balloon pump was used in 48 patients (30%). The type of procedure depended on the extent of endocardial disease and was aimed at maintaining the ellipsoid shape of the left ventricle cavity. In group I patients (n = 65), radical aneurysm resection and linear closure were performed. In group II patients (n = 70), septal dyskinesis was reinforced with a patch (septoplasty). In group III patients (n = 22), ventriculotomy closure was performed with an intracavitary oval patch.

RESULTS: Hospital mortality was 16% (25/157) and was similar among the groups. Actuarial survival up to 18 years was better with a preoperative ejection fraction of 26% or greater (P = .004) and a pulmonary artery occlusive pressure of 17 mm Hg or less (P = .05). Survival was worse in patients who had intra-aortic balloon pump support (P = .03). Five-year survival for all patients in group III was higher than for patients in group II (67% vs 47%, P = .04).

CONCLUSIONS: Factors that improved long-term survival after left ventricular surgical remodeling were intraventricular patch repair, preoperative ejection fraction of 26% or greater, and pulmonary artery occlusive pressure of 17 mm Hg or less without the need for balloon pump assist.


Key Words: 22 • 30


Dr Bolooki


Surgical methods to restore the volume and shape of the left ventricle (LV), after an extensive myocardial infarction (MI) that has resulted in cavity remodeling (LV aneurysm), have evolved over the years. Present techniques attempt to reconstruct the natural ellipsoid shape of the LV cavity, which offers the most favorable geometry for LV performance and patient survival.1-3 The long-term surgical results have been reported as an observational experience by various centers, most recently by the RESTORE group.4,5 This study evaluates the factors affecting the long-term survival of patients who underwent 3 methods of LV cavity restoration.


    Patients and methods
 Top
 Abstract
 Patients and methods
 Results
 Discussion
 Discussion
 References
 
Patient selection
A retrospective review was performed of 157 consecutive patients who underwent LV volume reduction surgery by 1 of 3 surgical techniques from 1979 to 2000. All procedures were performed by the senior author (H.B.). Table 1 summarizes the characteristics of all patients. The age range of the patients was from 30 to 85 years (mean 61 ± 0.08 years SEM). There were 134 male patients (85%). All patients had had an anteroseptal MI in the past, and 66 patients (42%) had had an MI within the month before admission. All patients had a large anterior wall LV dyskinetic aneurysm. The indications for operation were congestive heart failure, cardiogenic shock (systolic blood pressure < 80 mm Hg and cardiac index < 1.8 L · min-1 · m-2), angina pectoris, ventricular tachyarrhythmia (VT), and sudden death. The preoperative data on LV systolic function and pulmonary artery occlusive (PAO) pressure are shown in Table 2. Patients with isolated lateral or posterior wall aneurysm or with LV dysfunction and predominant mitral valve insufficiency were not included in this survey.


View this table:
[in this window]
[in a new window]
 
TABLE 1. Preoperative patient characteristics

 

View this table:
[in this window]
[in a new window]
 
TABLE 2. Preoperative hemodynamic findings

 
Complete myocardial revascularization was performed in 126 patients (80%) by using saphenous vein segments and the left internal thoracic artery (Table 3). The left anterior descending artery was bypassed whenever possible. If the left anterior descending artery or any other major coronary artery had an extensively narrowed lumen, endarterectomy was performed to establish proximal blood flow, especially to the septal perforators. In 3 patients, the right internal thoracic artery was used as a free graft to bypass the left coronary artery branches. Sequential coronary grafts were performed whenever possible.6


View this table:
[in this window]
[in a new window]
 
TABLE 3. Operative procedures: Early and late mortality and follow-up

 
The operations were performed on an emergency or urgent basis (within 12 to 24 hours of admission) in 74 (47%) of the patients. Additional procedures included mitral valve repair or replacement in 3 patients, aortic valve replacement in 1 patient, and atrial septal defect closure in 1 patient. An automatic implantable cardioverter-defibrillator was implanted in 16 patients. In our early experience, intrapericardial automatic implantable cardioverter-defibrillator patches were placed in 44 patients during surgery.

Surgical techniques
The details of techniques used in our center have been published.7,8 In brief, normothermic cardiopulmonary bypass was established, and the heart was maintained beating, empty, and in sinus rhythm. The blood pressure was kept at 70 to 80 mm Hg. Left ventriculotomy was made parallel and lateral to the course of the left anterior descending artery. Endocardial mapping was performed in all patients with VT, and cryoablation or subendocardial scar resection was performed according to our VT protocol.9 Thereafter, under mild hypothermia (33°C-35°C), the aorta was crossclamped and antegrade cold-blood (4°C) cardioplegic arrest was induced.

Aneurysm resection and LV volume restoration were performed using 3 methods. The type of operation was selected depending on the extent of endocardial disease. The goal was to restore an elliptical LV cavity and a cone-shaped apex.

In patients with minimal septal dyskinesis (group I, n = 65), radical aneurysmectomy was performed.7 This involved resection of the entire scarred aneurysm wall, leaving a narrow rim near the contracting endocardium laterally and medially, avoiding the left anterior descending artery injury and entry into the right ventricular cavity. A linear anterior ventriculotomy closure was performed usint interrupted sutures with Teflon (DuPont, Wilmington, Del) pledget reinforcement with minimal plication of the lateral wall. Attempts were made to reconstruct the LV apex without creating mid-ventricular narrowing.

In patients with a large dyskinetic septal scar (group II, n = 70), septal plication was performed by using interrupted sutures reinforced with Teflon pledgets. A Teflon patch (1 mm thick) was cut to an oval shape (with an average size of 3 x 5 cm) to support the septum (septoplasty).8 The ventriculotomy was closed by including the supported septum that was sewn to the junction of the visible scar tissue and the myocardium (septal inclusion).

In group III (n = 22), there was minimal involvement of the septal wall. The borders of the scarred and viable (contracting) myocardium were identified, and the ventriculotomy opening was used to size a teardrop-shaped (or oval) patch of Dacron (Hemashield; Boston Scientific Corporation, Natick, Mass) to reconstruct the anterior wall of the LV. Moderate plication of the LV opening was achieved by an encircling purse-string suture or spacing of the sutures to secure the patch (Figure 1). Attempts were made to avoid oversizing the patch (the size averaged 2 x 4 cm). It was sewn in place with 1 row of continuous sutures ensuring an ellipsoid LV cavity and a cone-shaped apex. Intraoperative transesophageal echocardiography was used extensively to assess the LV cavity size before and after the operation (Figure 2). The medial (septal) and the lateral remnants of the scarred aneurysm tissues were then trimmed, and the ventriculotomy was closed over the patch (septal exclusion).



View larger version (158K):
[in this window]
[in a new window]
 
Figure 1. Surgeon’s view of the anterior wall of the heart after LV volume restoration operation with an oval endoventricular Dacron patch. The black arrowheads point to the sutures that secure the patch and the purse-string suture.

 


View larger version (111K):
[in this window]
[in a new window]
 
Figure 2. Intraoperative transesophageal echocardiogram. The views are in systole (A, C) and diastole (B, D) before (A, B) and after (C, D) volume reduction surgery in a patient in group III. Left atrium (LA), left ventricle (LV), mitral valve (MV), aneurysm (A), and right ventricle (RV) are identified. The arrowheads show the extent of the anterior endoventricular patch in systole (C) and diastole (D). Note the extent of LV volume reduction and apical restoration.

 
Follow-up
Patients were followed up by direct contact, telephone interviews, and outpatient clinic visits. Follow-up intervals ranged from 15 months to 22 years (group I, 260 months; group II, 186 months; group III, 104 months). Follow-up management was performed by the primary care physicians. Patients were maintained on an optimized regimen for treatment of congestive heart failure that included use of ß blockers and angiotensin-converting enzyme inhibitors. Follow-up cardiac catheterization was performed if the patients became symptomatic. Twenty patients (14%) were lost to follow-up because of tertiary referrals, patient migration, and unknown reasons.

Statistical analysis
Data were analyzed using the SAS System (SAS Institute Inc, Cary, NC). Continuous variables were expressed as mean ± SEM and categorical variables as frequency and percent. Univariable analysis of categorical determinants of mortality was performed by the {chi}2 test and the Fisher exact test. Continuous variables were analyzed using the analysis of variance and Student t tests. Actuarial survival curves (Kaplan-Meier) were used to assess differential mortality among the 3 groups. Multivariable regression analysis (Cox model) was used to assess the effect of independent variables on survival. Wilcoxon and log-rank statistical analyses were applied to evaluate the survival curves.


    Results
 Top
 Abstract
 Patients and methods
 Results
 Discussion
 Discussion
 References
 
The operative procedures were performed from 1979 to 2000. Initially (1979-1992), most patients underwent radical aneurysmectomy with linear closure (group I, n = 47) or septal inclusion (group II, n = 57). Septal exclusion with endocardial patch was the technique used from 1992 to 2000 (group III, n = 22), whereas other operative techniques (group I, n = 18; group II, n = 13) were used according to the pathologic findings as previously described. One patient underwent septoplasty in 1977 for acute MI, LV false aneurysm, and cardiogenic shock. He lived 80 months.

Hospital mortality included all deaths within the same hospitalization or within 30 days. There were 25 early postoperative deaths (16%). The major causes of deaths were persistent congestive failure, recurrent ventricular arrhythmia, and multiorgan failure. There was no significant difference in early deaths among the 3 groups of patients (Table 3). For the entire group, the risk factors associated with early mortality included class III and IV (New York Heart Association) congestive failure (P = .04), cardiogenic shock (P < .0001), use of an intra-aortic balloon pump (IABP) (P = .0001), and emergency or urgent operations (P = .0003).

For the entire group (including early mortality), the actuarial survival at 5, 10, and 15 years was 53%, 30%, and 18%, respectively (Figure 3, A). Excluding the early death, the actuarial survival for the same intervals was 63%, 37%, and 22%, respectively (Figure 3, B). A comparison of the actuarial survival for the hospital survivors among the 3 groups is shown in Figure 4. At 5 years, 74% of group III patients (with endoventricular patch) were alive in comparison with 63% of group I and 58% of group II (P = .229). Comparison of actuarial survival for all patients at risk in group I (radical resection) and patients in group III showed no significant difference (Figure 5, A), whereas there was a significant difference in survival comparing all patients at risk in group III with those in group II (septoplasty). Survival at 5 and 7 years was 47% and 37% for group II, respectively, compared with 67% and 67% for group III, respectively (P = .04) (Figure 5, B).



View larger version (13K):
[in this window]
[in a new window]
 
Figure 3. Actuarial survival for all patients at risk including (A) and excluding (B) early (operative) mortality.

 


View larger version (24K):
[in this window]
[in a new window]
 
Figure 4. Comparison of actuarial survival in the 3 patient groups after LV volume reduction surgery: group I, radical resection; group II, septoplasty; group III, endoventricular patch. P = .2290.

 


View larger version (15K):
[in this window]
[in a new window]
 
Figure 5. Actuarial survival including the early mortality comparing the results for the 3 operative techniques. A, All patients at risk in groups I and III are compared. P = .1591. B, All patients at risk in groups II and III are compared.

 
There were significant differences in the preoperative incidence of cardiogenic shock and of urgent or emergency operations and use of IABP among the groups. Group III patients had the lowest number of urgent or emergency operations 9% (2/22) compared with 40% (26/65) and 65% (46/70) in groups I and II, respectively (P = .003) (Table 3). There was a significant difference in survival among all patients undergoing operations electively (n = 83) compared with those undergoing emergency or urgent operations (n = 74). Survival was 64% versus 41% at 5 years and 53% versus 34% at 7 years for elective versus urgent or emergency operations, respectively (P = .0006, Wilcoxon; P < .02 log-rank). However, the difference in long-term survival among hospital survivors was not significant (P = .31) (Figure 6, F).



View larger version (28K):
[in this window]
[in a new window]
 
Figure 6. Actuarial late survival excluding early death according to preoperative variables: ejection fraction (EF), pulmonary artery occlusive (PAO) pressure, intra-aortic balloon pump (IABP), and ventricular tachyarrhythmia (VT). D, P = .3356; E, P = .2427; F, P = 3184.

 
The early mortality for patients with cardiogenic shock in groups I, II, and III was 50% (4/8), 47% (8/17), and 0% (0/1), respectively. There was significantly lower survival (36% at 3 years) in all patients with cardiogenic shock than in patients without cardiogenic shock (68% at 3 years, P = .0003 by the log-rank test). However, among hospital survivors, patients with preoperative cardiogenic shock demonstrated 42% survival at 5 years versus 66% in patients without cardiogenic shock (P = .137).

The incidence of myocardial revascularization and the number of coronary bypass grafts per patient were similar in the 3 groups (P = .398) (Table 3). For the entire group, among 98 hospital survivors, the survival at 5 and 10 years was higher in patients with arterial grafts (74% and 35%) than in patients with venous grafts only (60% and 32%), respectively (P = .360).

Multivariate analysis was performed to identify the risk factor(s) that affected the late mortality. A total of 24 factors were considered including the following: operative technique, age, ejection fraction (EF), PAO pressure, cardiac index, VT, cryoablation, congestive heart failure, cardiogenic shock, recent MI, use of arterial grafts, urgency of operation, and need for IABP. Preoperative factors that significantly affected the survival of all patients at risk and hospital survivors included EF (>=26%), PAO pressure (<=17 mm Hg), and no IABP (Table 4 and Figure 6, A-C). Factors that influenced early death but had no significant effect on long-term survival included preoperative congestive failure, VT, cardiogenic shock, recent MI, and emergency versus elective operations (Figure 6, D-F).


View this table:
[in this window]
[in a new window]
 
TABLE 4. Cox regression analysis of multivariable predictors of late mortality in all hospital survivors after left ventricular volume reduction surgery

 
There were 76 deaths during the follow-up period (Table 5). Congestive heart failure was the most frequent cause. Cause of death was unknown in 11 instances. The hearts from 8 patients (in groups I and II) who died 6 months to 3 years postoperatively were examined by pathologists. The position and the extent of healing of the septal patch were impressive (Figure 7).


View this table:
[in this window]
[in a new window]
 
TABLE 5. Causes of late death

 


View larger version (133K):
[in this window]
[in a new window]
 
Figure 7. Heart specimen showing mid-ventricular section 6 months after volume reduction surgery with septoplasty technique (group II). The septal patch (white arrowheads), right ventricle (RV), left ventricle (LV), septum (S), and patent anterior descending artery (A) are shown. This patient died suddenly of cardiac dysrhythmia probably caused by a posterior septal infarction (black arrowheads). White arrows indicate 2 implanted defibrillator patches. Note the suture line (black arrow), the thick wall LV cavity, and the septal wall with the Teflon patch.

 
One patient in group III underwent cardiac transplantation and is doing well. On their last visit, the 36 surviving patients were in New York Heart Association symptom class I or II. Fourteen of these patients were older than 72 years and lived independently. Late cardiac catheterization data (5-16 years postoperatively) from 7 patients were reviewed. The LV angiogram in 5 patients showed decreased LV end-systolic and end-diastolic volumes and a slightly improved EF (Figure 8).



View larger version (154K):
[in this window]
[in a new window]
 
Figure 8. Preoperative (A, B) and postoperative (C, D) left ventriculograms in systole (A, C) and diastole (B, D) in a patient in group III. Preoperatively, the apex contained islands of clots. Note restoration of LV apex and improvement in systolic function.

 

    Discussion
 Top
 Abstract
 Patients and methods
 Results
 Discussion
 Discussion
 References
 
LV remodeling is a natural consequence of transmural MI.10,11 It is enhanced by the extent of infarction and is a sequela of infarct expansion and wall stretch. These anatomic changes initially ameliorate cardiac dynamics in the form of an increase in blood pressure and cardiac output and a decrease in end-diastolic pressure, although at the expense of increase in LV volume, wall stress, and wall tension (La Place law).

Surgical methods of eliminating the noncontractile areas of the LV have been used since 1958.12 The procedure is universally accepted. It improves cardiac systolic performance and in conjunction with myocardial revascularization improves long-term survival results.13-15 In recent years, a combination of medical management using percutaneous methods of revascularization followed by afterload reduction and ß-blocker therapy has played a highly successful role in the prevention of LV aneurysm formation and remodeling.16

The intracavitary repair of LV aneurysm is a technique that has evolved as the result of the observation of a thin-walled cardiac septum that could not be resected and was frequently associated with a patent anterior descending artery suitable for bypass grafting.17-20 Few reports have been published that compare the late survival results (>5 years) with various methods of LV volume reduction.18,21 The early results have shown similar survival among the patient groups. No randomized trials have been performed.

A survey of changes in cardiac function and volume after the 3 types of repair, as discussed here, has been reported and is beyond the intent of this work.1,2,7,8,21 The incidence of preoperative congestive heart failure, angina, and recent MI in our study was similar in the 3 groups of patients and matches the reports by other investigators.5,13,14 The larger number of patients with VT in our study was possibly the result of referrals to our Sudden Death Center during the 1980s when catheter ablative therapy was not available. In recent years, the incidence of ventricular aneurysm surgery in general and the referral rate for surgical treatment of VT in particular have substantially declined.1,15

In this study, a comparison of preoperative hemodynamic factors shows a difference in EF, cardiac index, and end-diastolic pressure in the 3 patient groups. The difference was significant in group III who had lower EF (22%) and higher pulmonary occlusive pressure (20 mm Hg) and end-diastolic pressure (23 mm Hg) values compared with groups I and II (Table 3). This difference may have negatively influenced the operative mortality (13%) and long-term survival of patients in group III. Despite a more depressed cardiac function, group III patients had a higher survival at 5 and 7 years compared with group II patients (67% vs 47% P = .04) (Figure 4). However, other factors, such as newer therapeutic regimen (eg, angiotensin-converting enzyme inhibitors and ß blockers), may have contributed to the improved survival in group III as well.

A significant decrease in pulmonary occlusive (wedge) pressure after aneurysm resection has been reported by a number of investigators.15,17,21 Similarly, an elevated LV end-diastolic pressure markedly decreases postoperatively.4,13,14 For these reasons, we considered an elevated preoperative PAO pressure as a possible factor that may prognosticate long-term survival after the operation. The accepted maximum normal value of 18 mm Hg was considered to be the cutoff point. There was a significant difference in survival (P = .05) among hospital survivors with preoperative PAO pressure of 17 mm Hg or less and those with PAO pressure of 18 mm Hg or greater. This finding is not supported by previous reports, probably because of the lack of survival analysis considering this factor or use of mean pulmonary artery pressure readings.5,21,22 Mickleborough and colleagues15 have considered severe pulmonary hypertension as a contraindication to this procedure. We believe that patients with a high intracardiac diastolic pressure and congestive failure in association with preserved LV systolic function have diastolic dysfunction.23 This condition may not improve with LV volume reduction surgery, especially in patients with a mostly akinetic LV aneurysm. Instead, these patients may benefit from circulatory assist devices aiming for cardiac transplantation.

The incidence of cardiogenic shock and the use of an IABP were higher in this study compared with other reports.14,15,21 As shown in Table 4, the use of an IABP was associated with a high probability of poor early and late outcomes. Factors that showed no significant effect on long-term survival, if the initial operative mortality was excluded, were congestive heart failure, preoperative VT, the use of arterial grafts for coronary bypass, and whether the operation was urgent, emergency, or elective (Figure 6). In this regard, the results of our study do not conform to some of the previous reports that involved follow-up times of 2 to 5 years.3,15,24 A longer follow-up may be necessary to clarify these points.

In the past, the goals of surgical management of patients with a large anteroseptal LV aneurysm involved the elimination of the dyskinetic segment with little regard to the restoration of LV cavity size and shape. In recent years, the functional significance and the effects on long-term survival of LV configuration have been realized.19,24-26 Our study shows that if these concerns are met, the survival results of surgical management of LV aneurysm will be satisfactory, especially with the endoventricular patch technique.

Recently, Athanasuleas and colleagues4 reported for the RESTORE group of surgeons on 439 patients who were studied prospectively and had received anterior ventricular patch repair. There was an in-hospital mortality rate of 6.6%, a balloon pump was used in 7% of patients, and the preoperative EF was 29% ± 10% (SD). The overall early survival (at 18 months) was 84%. These early results are impressive and probably the result of proper patient selection and the experience of the entire group. In an elegant monograph, Buckberg and colleagues27 described in detail the basis for their concept in repairing the LV cavity considering the oblique anterior ventricular wall fiber orientation. The reconstruction of the anterior wall and the apex cone was accomplished with a 2 x 3-cm patch.28 We used a larger patch with an average size of 2 x 4 cm (in group III) that was cut to an ovoid shape to accommodate the LV outflow and construct the LV apex. It is possible that downsizing the patch would play a role in patient survival by decreasing the LV volume. The LV end-systolic volume index has been shown to significantly affect patient survival and freedom from cardiac morbidity.5

With recent improvement in medical and surgical treatment of ischemic heart disease, the indications for volume restoration surgery have expanded to include patients with small aneurysms and minimal symptoms.29 The variability of indications for this operation necessitates a prospective randomized trial to identify the method of treatment that consistently improves the long-term survival of these patients.


    Discussion
 Top
 Abstract
 Patients and methods
 Results
 Discussion
 Discussion
 References
 
Dr Gerald D. Buckberg (Los Angeles, Calif). I would like to compliment Dr Bolooki for an important review of the geometric changes after anterior infarction that link the evolution of corrective measures with early and late results. Improvement followed changing from a linear resection to include the septum, to plicating the dyskinetic septum with a triangular patch as described in 1986, to more recently excluding the septum with an oval patch to restore an elliptical shape. The composite results may lead to some confusion because different reasons can explain why high-risk components of EF, pulmonary artery pressure, and the need for a balloon will raise mortality. From a mechanical standpoint, patch exclusion of the septum is a more complete procedure and was more successful in his presentation, despite the occurrence of the lowest EF of 22% and highest PA pressure of 21 mm Hg. Furthermore, adding patients with cardiogenic shock raises early mortality. Is their analysis without this data available?

Dr Bolooki. Yes. The article has more detailed data analysis. You are correct, patients with an intraventricular patch had overall higher survival results.

The composite slide (Figure 6) showed that by excluding the operative mortality, there is approximately a 10% better survivorship at 5 years, 7% at 10 years, and 4% at 15 years for the 3 patient groups. There were no statistically significant differences in overall survival among the 3 groups at 5 years. However, at 7 years of follow-up, the difference in survival was better for group III (patch exclusion of the septum) than for group II (septal inclusion). Preoperative use of a balloon pump, cardiogenic shock, and emergency operations had a significant effect on operative (in-hospital death) survival, but only balloon-pump use had an effect on long-term survival curves.

Dr Buckberg. I think that is correct, because a clearer picture emerges when you look at elective high-risk patients. We recently analyzed 662 patients, mostly in class III or IV heart failure, and the balloon was only needed in approximately 8%. Hospital mortality for restoration without repair was approximately 4%, so that goes along with what you are saying. I think that separating elective versus urgent operations will reduce the mortality as you describe, and you demonstrate that in your slide.

It seems that the consideration of methods of protection may suggest that the beating empty heart, rather than cardioplegia, may be useful for restoration when there is trabecular scar. This is because aneurysms are fairly rare today with the use of thrombolysis and percutaneous transluminal coronary angioplasty. However, the akinetic heart is relatively common. The thick akinetic heart is seen by echocardiography and ventriculography, and it does not collapse by venting. The junction between contracting and noncontracting muscle is found by palpation. I wonder how many thick akinetic hearts you see, because they are what we see most commonly.

Dr Bolooki. This operation involved infarcted, mostly dyskinetic anterior LV segments. I agree that the hearts with enlarged LV with an akinetic trabeculated anterior wall are a surgical challenge. This is because of the absence of a clear demarcation line to identify the contractile from the noncontractile parts. Finger palpation of the wall in a beating open LV cavity will help in delineating the contracting parts, but we have always believed that myocardial contraction, in thick-walled hibernating areas of the LV, may return after they are revascularized.

Dr Buckberg. Thickness is what I am getting at.

Dr Bolooki. Many of the patients who have a thick akinetic anterior wall LV do have coronary artery disease. At the present time, we perform coronary bypass operation in these patients and do not rely on volume reduction surgery. This trend may change as time goes on, and we may perform volume reduction surgery and myocardial revascularization concomitantly in patients with a thick wall akinetic myocardium.

Dr Buckberg. You basically have not operated on the akinetic thick ventricles. You mainly revascularize those.

Dr Bolooki. That is correct. If there is obstructive disease coronary disease, we perform a coronary bypass operation and do not reduce the LV volume.

Dr Buckberg. Today, we usually operate on the akinetic thick-walled ventricles, and I believe that may make a difference in the future. We found a slightly lower mortality rate, despite lower EF and larger volumes, when we used the beating methods. This may have impact because the normal end-systolic volume index is approximately only 25 mL/m2. In a recent analysis, we found 10-year survival was greater than 80% if the systolic volume index was less than 120 mL/m2. This relatively flat trajectory, which you described and saw in group 3, may emphasize the importance of using a patch inside the ventricle for future restoration. Do you have any volume measurements to give us some insight about how this affected the future of the patients in your series?

Dr Bolooki. No, I do not have volume measurements in patients in this report. We are presently trying to estimate intraoperatively how much or to what extent the LV volume has been reduced. However, with the intraventricular patch, the LV shape changes, and the angle of the echocardiography beam does not always match the plane comparable to preoperative views. I believe that your group is performing this type of study and postoperative angiography. They are probably in a better position with their prospective studies to show the relation between a decrease in LV volume and long-term survival. No doubt if the end-systolic volume index of the LV is small, the patient will survive longer, according to your studies.

Dr Buckberg. We found 3 factors that may be critical to the decision and prognosis process. They include measuring the area of nonfunctioning muscle that is akinetic or dyskinetic and evaluating the function of the remote muscle and the septal muscle. This requires that we use a left anterior oblique view, either by ventriculogram or magnetic resonance imaging. We also measure end-systolic ventricular volume. These preoperative measurements may become a paradigm shift in our current analysis. What are your thoughts about making measurements of the muscle that is left in place to determine the impact of retained muscle on prognosis?

Dr Bolooki. I think that is an excellent question. We have known for some time that the EF of the remote areas and the basal segments is highly predictive of early and long-term survival. This point was emphasized by your group recently. We have not performed any wall motion studies to see whether the remaining LV segments retain the preoperative EF or show improvement after the operation. Also, myocardial revascularization may improve the function of the remote myocardial segments. Actually, postoperative cardiac function studies were beyond the aims of the present work. In this study, we tried to evaluate the relation of certain preoperative factors with long-term survival and all-cause mortality as an end point.

Dr Buckberg. The mitral valve was approached in only 3% of your patients. We have performed it in approximately 25%. Of course, functional mitral regurgitation relates to a high ventricular volume and may be a cause of the high PA pressures you found to adversely affect results. This can be corrected at the time of restoration by performing an annuloplasty and by narrowing the increased width between the papillary muscle heads with a circumferential suture. I believe that future mitral management will be defined by geometry and not by the grade of regurgitation. What are your thoughts about treating the mitral valve in this disease, and do you make this measurement preoperatively or in the operating room?

Dr Bolooki. As you indicated, only 3% of these patients underwent mitral valve surgery. In those patients, the subvalvular apparatus was extensively damaged, and there was severe mitral regurgitation. I believe the technique of mitral valve repair that you presented last year before The American Association for Thoracic Surgery by using a limited circumferential suture is a good one. I have tried the method also, but not in patients after volume reduction surgery. I believe your suggestion of correcting the valve and the LV volume simultaneously is an important one. The combination of mitral valve incompetence and ischemic heart disease has been a challenge for all of us, and we do not always know the correct answer to its management. I try to decide on the management of mitral valve preoperatively, as well as in the operating room, on the basis of clinical and echocardiography findings. We extensively use echocardiography in the operating room to evaluate the valve before and after repair.

Dr Buckberg. In conclusion, your goals and management are really similar to ours. We also deal with what we call the VVV—the vessels, the valve, and the ventricle. These components of heart failure cannot be separated, but they can change surgically and may reflect the pioneering frontier Dr Doty described in his presidential address.

Dr Bolooki. Thank you very much Dr Buckberg. I agree with the VVV (ventricle, vessels, and valve) repair that you brought up, which is one more innovation from you. I also enjoyed President Doty’s presentation and admire his pioneering contributions to cardiac surgery.

Dr Roger Baskett (Halifax, Nova Scotia, Canada). If you are comparing groups of patients from very different eras over a long period of time, an essential piece is how many patients are receiving optimal medical heart failure therapy. Specifically, who is receiving angiotensin-converting enzyme inhibitors or ß-blockers, and how many patients in each group have automatic internal cardioverter-defibrillators in place?

Dr Bolooki. You are correct that patients in the early 1980s did not receive angiotensin-converting enzyme inhibitors and ß-blockers as freely as today. The optimal medical therapy of heart failure as we know it today was used in these patients beginning in the early 1990s and probably contributed a great deal to patient survival.

Cardioverter-defibrillators were used in approximately 10% of the surviving patients. During the 1980s, recurrent malignant VTs that were unresponsive to pharmacologic therapy or ablative surgery were managed with the implantation of patches on the ventricles according to a sudden-death protocol. We believe that the patients in this study who had preoperative VT were managed very effectively. In fact, the long-term survival curves in this group were similar to patients who did not have preoperative VT.


    Acknowledgments
 
Drs Gerald Kaiser, Richard Perryman, Michael Horowitz, Kenneth Herskowitz, and George Palatianos (presently director of Cardiac Surgery Service at Onassis Cardiac Center in Athens, Greece) collaborated in the early part of this study. I am grateful to Mrs Joanne Bolooki for typing and editing this manuscript.


    Footnotes
 
Supported in part by the Thomas Curtis Research Grant.


    References
 Top
 Abstract
 Patients and methods
 Results
 Discussion
 Discussion
 References
 

  1. Dor V, Sabatier M, Di Donato M, Montiglio F, Toso A, Maioli M. Efficacy of endoventricular patch plasty in large postinfarction akinetic scar and severe left ventricular dysfunction: comparison with a series of large dyskinetic scars. J Thorac Cardiovasc Surg. 1998;116:50–59[Abstract/Free Full Text]
  2. Elefteriades JA, Solomon LW, Salazar AM, Batsford WP, Baldwin JC, Kopf GS. Linear left ventricular aneurysmectomy: modern imaging studies reveal improved morphology and function. Ann Thorac Surg. 1993;56:242–252[Abstract]
  3. Kawata T, Kitamura S, Kawachi K, Morita R, Yoshida Y, Hasegawa J. Systolic and diastolic function after patch reconstruction of left ventricular aneurysms. Ann Thorac Surg. 1995;59:403–407[Abstract/Free Full Text]
  4. Athanasuleas CL, Stanley AWH Jr, Buckberg GD, Dor V, Di Donato M, Blackstone EHRESTORE group. Surgical anterior ventricular endocardial restoration (SAVER) in dilated remodeled ventricle after anterior myocardial infarction. J Am Coll Cardiol. 2001;37:1199–1209[Abstract/Free Full Text]
  5. Di Donato M, Toso A, Maioli M, Sabatier M, Stanley AWH Jr, Dor VRESTORE group. Intermediate survival and predictors of death after surgical ventricular restoration. Semin Thorac Cardiovasc Surg. 2001;13:468–475[Medline]
  6. Palatianos GM, Bolooki H, Horowitz MD, Lowery MH, Rosenthal SP, Chandarlapaty SKC, et al. Sequential internal mammary artery grafts for coronary artery bypass. Ann Thorac Surg. 1993;56:1136–1140[Abstract]
  7. Palatianos GM, Craythorne CB, Schor JS, Bolooki H. Hemodynamic effects of radical left ventricular scar resection in patients with and without congestive failure. J Surg Res. 1988;44:690–695[Medline]
  8. Bolooki H, Palatianos GM, Zaman L, Thurer RJ, Luceri RM, Myerburg RJ. Surgical management of post–myocardial infarction ventricular tachyarrhythmia by myocardial debulking, septal isolation, and myocardial revascularization. J Thorac Cardiovasc Surg. 1986;92:716–725[Abstract]
  9. Bolooki H, Horowitz MD, Interian A, Thurer RJ, Palatianos GM, De Marchena EJ, et al. Long-term surgical results in sudden death syndrome associated with cardiac dysfunction after myocardial infarction. Ann Surg. 1992;216:333–343[Medline]
  10. McKay RG, Pfeffer MA, Posternak RC, Markis JE, Come PC, Nakao S, et al. Left ventricular remodeling after myocardial infarction: a corollary to infarct expansion. Circulation. 1986;74:693–702[Abstract/Free Full Text]
  11. Pfeffer MA, Braunwald E. Ventricular remodeling after myocardial infarction. Experimental observations and clinical implications. Circulation. 1990;81:1161–1172[Abstract/Free Full Text]
  12. Cooley DA, Henly WS, Ahmad KH, Chapman DW. Ventricular aneurysm following myocardial infarction: results of surgical treatment. Ann Surg. 1959;150:595–612[Medline]
  13. Pasini S, Gagliardotto P, Punta G, Del Ponte S, Serra M, Parisi F, et al. Early and late results after surgical therapy of post infarction left ventricular aneurysm. J Cardiovasc Surg. 1998;39:209–215[Medline]
  14. Couper GS, Bunton RW, Birjiniuk V, Disesa VJ, Fallon MP, Collins JJ Jr, et al. Relative risks of left ventricular aneurysmectomy in patients with akinetic scars versus true dyskinetic aneurysms. Circulation. 1990;82(Suppl IV):IV248–256
  15. Mickleborough LL, Carson S, Ivanov J. Repair of dyskinetic or akinetic left ventricular aneurysm: results obtained with a modified linear closure. J Thorac Cardiovasc Surg. 2001;121:675–682[Abstract/Free Full Text]
  16. Pfeffer MA, Lamas GA, Vaughan DE, Parisi AF, Braunwald E. Effect of captopril on progressive ventricular dilatation after anterior myocardial infarction. N Engl J Med. 1988;319:80–86[Abstract]
  17. Dor V, Bourlon DF, Sabatier M, Grinneiser D, Montiglio F, Coste P, et al. La reconstruction du ventricule gauche par plastie circulaire endoventriculaire avec exclusion septale. Arch Mal Coeur. 1990;83:1687–1694
  18. Buckberg GD. Congestive heart failure: treat the disease, not the symptom—return to normalcy. J Thorac Cardiovasc Surg. 2001;121:628–637[Free Full Text]
  19. Cooley DA. Ventricular endoaneurysmorrhaphy: simplified repair for extensive postinfarction aneurysm. J Card Surg. 1989;4:200–205[Medline]
  20. Cosgrove DM, Lytle BW, Taylor PC, Stewart RW, Golding LAR, Mahfood S, et al. Ventricular aneurysm resection. Trends in surgical risk. Circulation. 1989;79(Suppl I):I97–101
  21. Shapira OM, Davidoff R, Hilkert RJ, Aldea GS, Fitzgerald CA, Shemin RJ. Repair of left ventricular aneurysm: long-term results of linear repair versus endoaneurysmorrhaphy. Ann Thorac Surg. 1997;63:701–705[Abstract/Free Full Text]
  22. Grossi EA, Chinitz LA, Galloway AC, Delianides J, Schwartz DS, McLoughlin DE, et al. Endoventricular remodeling of left ventricular aneurysm. Functional, clinical and electrophysiological results. Circulation. 1995;(Suppl II):II98-100
  23. Vasan RS, Levy D. Defining diastolic heart failure. A call for standardized diagnostic criteria. Circulation. 2000;101:2118–2121[Free Full Text]
  24. White HD, Norris RM, Brown MA, Brandt PWT, Whitlock RML, Wild CJ. Left ventricular end-systolic volume as the major determinant of survival after recovery from myocardial infarction. Circulation. 1987;76:44–51[Abstract/Free Full Text]
  25. Jatene AD. Left ventricular aneurysmectomy: resection or reconstruction. J Thorac Cardiovasc Surg. 1985;89:321–331[Medline]
  26. Mills NL, Everson CT, Hockmuth DR. Technical advances in the treatment of left ventricular aneurysm. Ann Thorac Surg. 1993;55:792–800[Abstract]
  27. Buckberg GD, Coghlan HC, Torrent-Guasp F. The structure and function of the helical heart and its buttress wrapping. VI. Geometric concepts of heart failure and use for structural corrections. Semin Thorac Cardiovasc Surg. 2001;13:386–401[Medline]
  28. Anthanasuleas CL, Buckberg GD, Menicanti L, Gharib MRESTORE Group. Optimizing ventricular shape in anterior restoration. Semin Thorac Cardiovasc Surg. 2001;13:459–467[Medline]
  29. Jones RH. Is it time for a randomized trial of surgical treatment of ischemic heart failure? J Am Coll Cardiol. 2001;37:1210–1213[Free Full Text]



This article has been cited by other articles:


Home page
Eur. J. Cardiothorac. Surg.Home page
S. Castelvecchio, M. Ranucci, and L. A. Menicanti
The role of surgical technique in determining the outcome of left ventricular reconstruction: a difficult assessment
Eur. J. Cardiothorac. Surg., June 1, 2009; 35(6): 1111 - 1111.
[Full Text] [PDF]


Home page
Eur. J. Cardiothorac. Surg.Home page
P. Klein, J. J. Bax, L. J. Shaw, H. H.H. Feringa, M. I.M. Versteegh, R. A.E. Dion, and R. J.M. Klautz
Early and late outcome of left ventricular reconstruction surgery in ischemic heart disease
Eur. J. Cardiothorac. Surg., December 1, 2008; 34(6): 1149 - 1157.
[Abstract] [Full Text] [PDF]


Home page
Ann. Thorac. Surg.Home page
K. Takeda, G. Matsumiya, H. Matsue, M. Sakaki, T. Sakaguchi, T. Fujita, and Y. Sawa
Left Ventricular Reconstructive Surgery in Ischemic Dilated Cardiomyopathy Complicated With Cardiogenic Shock
Ann. Thorac. Surg., April 1, 2008; 85(4): 1339 - 1343.
[Abstract] [Full Text] [PDF]


Home page
Ann. Thorac. Surg.Home page
A. Parolari, M. Naliato, C. Loardi, P. Denti, M. Trezzi, M. Zanobini, M. Porqueddu, M. Roberto, S. Kassem, F. Alamanni, et al.
Surgery of Left Ventricular Aneurysm: A Meta-Analysis of Early Outcomes Following Different Reconstruction Techniques
Ann. Thorac. Surg., June 1, 2007; 83(6): 2009 - 2016.
[Abstract] [Full Text] [PDF]


Home page
Asian Cardiovasc. Thorac. Ann.Home page
M. S Kalkat, U. Dandekar, C. Smallpeice, J. Parmar, C. Satur, and A. Levine
Left Ventricular Aneurysmectomy: Tailored Scar Excision and Linear Closure
Asian Cardiovasc Thorac Ann, June 1, 2006; 14(3): 231 - 234.
[Abstract] [Full Text] [PDF]


Home page
J. Thorac. Cardiovasc. Surg.Home page
G. Matsumiya, Y. Miyamoto, O. Monta, H. Takano, Y. Sawa, and H. Matsuda
Left ventricular restoration for ischemic cardiomyopathy and simultaneous implantation of left ventricular assist system actively aiming at bridge to recovery
J. Thorac. Cardiovasc. Surg., July 1, 2005; 130(1): 219 - 220.
[Full Text] [PDF]


Home page
Eur. J. Cardiothorac. Surg.Home page
M. Cotrufo, G. Romano, L. S. De Santo, A. D. Corte, C. Amarelli, G. Cafarella, C. Maiello, and M. Scardone
Treatment of extensive ischemic cardiomyopathy: quality of life following two different surgical strategies
Eur. J. Cardiothorac. Surg., March 1, 2005; 27(3): 481 - 487.
[Abstract] [Full Text] [PDF]


This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Hooshang Bolooki
Kushagra Katariya
Richard J. Thurer
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bolooki, H.
Right arrow Articles by Duncan, R. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bolooki, H.
Right arrow Articles by Duncan, R. C.
Related Collections
Right arrow Congestive Heart Failure
Right arrow Myocardial infarction


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS