|
|
||||||||
J Thorac Cardiovasc Surg 2003;126:374-385
© 2003 The American Association for Thoracic Surgery
Surgery for acquired cardiovascular disease |
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 |
|---|
|
|
|---|
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
|
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 |
|---|
|
|
|---|
|
|
|
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).
|
|
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
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 |
|---|
|
|
|---|
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).
|
|
|
|
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).
|
|
|
|
| Discussion |
|---|
|
|
|---|
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 |
|---|
|
|
|---|
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 VVVthe 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 Dotys 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 |
|---|
| Footnotes |
|---|
| References |
|---|
|
|
|---|
This article has been cited by other articles:
![]() |
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] |
||||
![]() |
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] |
||||
![]() |
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] |
||||
![]() |
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] |
||||
![]() |
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] |
||||
![]() |
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] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| 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 |