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Ann Thorac Surg 2008;85:135-146. doi:10.1016/j.athoracsur.2007.04.101
© 2008 The Society of Thoracic Surgeons
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Nishant D. Patel
Lois U. Nwakanma
Jason A. Williams
John V. Conte
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Right arrow Myocardial infarction

Original Articles: Cardiovascular

Impact of Septal Myocardial Infarction on Outcomes After Surgical Ventricular Restoration

Nishant D. Patel, BA, Lois U. Nwakanma, MD, Eric S. Weiss, MD, Jason A. Williams, MD, John V. Conte, MD*

Division of Cardiac Surgery, The Johns Hopkins Medical Institutions, Baltimore, Maryland

Accepted for publication April 13, 2007.

Abbreviations and Acronyms AICD = automated internal cardoversion defibrillator; CHF = congestive heart failure; EF = ejection fraction; LVEDVI = left ventricular end-diastolic volume index; LVESVI = left ventricular end-systolic volume index; MRI = magnetic resonance imaging; SMI = septal myocardial infarction; SVR = surgical ventricular restoration

* Address correspondence to Dr Conte, Division of Cardiac Surgery, Heart and Lung Transplantation, Johns Hopkins Medical Institutions, Blalock 618, 600 North Wolfe St, Baltimore, MD 21287 (Email: jconte{at}csurg.jhmi.jhu.edu).

Presented at the Forty-third Annual Meeting of The Society of Thoracic Surgeons, San Diego, CA, Jan 29–31, 2007.


Dr Conte discloses that he has a financial relationship with Chase Medical Corporation.

 

   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Comment
 Discussion
 Acknowledgments
 References
 
Background: Surgical ventricular restoration (SVR) is classically performed in heart failure patients with anteroseptal infarction. It is unknown how the extent of septal myocardial infarction (SMI) affects prognosis. We reviewed our experience to evaluate the impact of the extent of SMI on outcomes after SVR.

Methods: We retrospectively reviewed SVR patients from January 2002 to December 2005. Patients were stratified based on the extent of SMI assessed by magnetic resonance imaging and intraoperative findings; SMI was graded as less than 50%, 50% to 74%, and 75% or greater of the length or height, or both, of the septum. Follow-up was 100%.

Results: Seventy-eight patients underwent SVR. Twenty-eight patients had less than 50%, 30 patients had 50% to 74%, and 20 patients had 75% or greater involvement of the length or height, or both, of the septum. Patients with 75% or greater involvement had a significantly lower ejection fraction and larger left ventricular volumes preoperatively by magnetic resonance imaging. All patients with 75% or greater involvement were New York Heart Association (NYHA) class III/IV preoperatively, and 50% (10 of 20) had significant mitral regurgitation requiring a concomitant mitral valve procedure. Operative mortality was similar between groups. Cardiac function improved and was similar among the three groups postoperatively. The PR intervals on electrocardiography were similar among the three groups, but did show trends toward longer duration for those with more extensive SMI. Preoperative mean QRS duration was significantly longer for patients with 75% or greater SMI. Three-year Kaplan-Meier survival was also similar among groups; 75% or greater involvement was not a predictor of mortality on Cox regression (odds ratio = 1.4; 95% confidence interval: 0.3 to 7.0; p = 0.6). Three quarters (15 of 20) of patients with 75% or greater involvement of the septum improved to NYHA class I/II at follow-up.

Conclusions: This study has evaluated the impact of the extent of SMI on SVR outcomes. These data demonstrate similar survival and significant functional and clinical improvement after SVR regardless of the extent of SMI.

Congestive heart failure (CHF) is a significant public health burden, with a prevalence of 5 million patients in the United States alone [1]. The majority of these patients have CHF secondary to ischemic cardiomyopathy. Despite optimal medical management, patients with CHF have a poor 2-year survival of approximately 50% [2, 3]. Limitations in medical therapy and the paucity of surgical alternatives demand innovative strategies to improve survival and functional outcomes for CHF patients.

Surgical ventricular restoration (SVR) is an alternative therapy for some CHF patients with ischemic cardiomyopathy. Surgical ventricular restoration attempts to reverse the maladaptive shape changes of postinfarction ventricular remodeling by reducing left ventricular size and restoring a more elliptical shape to the cavity to reduce myocardial wall stress and improve ventricular function. Surgical ventricular restoration is performed in conjunction with myocardial revascularization and mitral valve repair or replacement, as needed. Indications for SVR include anterior wall myocardial infarction (MI) with subsequent left ventricular dilatation, akinetic or dyskinetic segments, and reconstructable coronary artery and valvular disease [4–8].

The interventricular septum plays an important role in left ventricular function. Septal infarction has many deleterious effects, among which are the loss of contractile function, impairment of electrical conduction, and loss of ventricular synchrony. The major arterial blood supply to the ventricular septum is from the septal branches off the left anterior descending artery whereas the uppermost, posterior portion of the septum receives blood from branches off the posterior descending artery [9]. As a result, many patients with left anterior descending artery territory infarction may have MI of the ventricular septum in addition to the anterior wall of the left ventricle. The septum plays a pivotal role in all of the reconstruction techniques used currently for SVR. Despite this, no investigator has studied the impact of the extent of septal MI (SMI) on outcomes after SVR. Owing to the central role of the ventricular septum on cardiac function, we sought to evaluate the impact of the extent of SMI on outcomes after SVR.


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Comment
 Discussion
 Acknowledgments
 References
 
Study Design
Retrospective review of all patients who underwent SVR between January 2002 and December 2005 was conducted after Institutional Review Board approval; individual waiver for consent was granted. The extent of SMI was based on preoperative magnetic resonance imaging (MRI) studies with delayed enhancement using gadolinium contrast and intraoperative inspection of the opened left ventricle by a single surgeon (J.V.C.). When MRI was available, our routine preoperative work-up included careful delineation of viable myocardium using gadolinium contrast to help plan the left ventricular reconstruction. Magnetic resonance imaging findings were then used to guide the surgeon’s inspection of the left ventricular chamber and estimation of height and length of the septum involved. Some patients with automated internal cardoversion defibrillators (AICD) either were not able to have MRIs done or they were of insufficient quality to use for septal measurements. A detailed map demonstrating the extent of infarction was prospectively filled out for each patient (Fig 1). These observational data were then used to estimate the height and length as less than 50%, 50% to 74%, or 75% or greater. Patients were divided into three groups based on the extent of septal involvement with MI: group A, less than 50% of the height or length, or both; group B, 50% to 74% of the height or length, or both; and group C, 75% or greater of the height or length, or both (Fig 2).


Figure 1
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  		Fig 1. Magnetic resonance imaging (MRI) and operative map detailing the extent of infarction. (A) First-pass perfusion MRI images after 0.1 mmol/kg gadolinium. Delayed T1-weighted after additional 0.1 mmol/kg gadolinium. The MRI short- and long-axis cine images showing marked dilatation of the left ventricle, thinning in the apex, and anteroseptal and inferolateral akinesis. (Ejection fraction = 20.7%; left ventricular end-systolic volume index = 97.9 mL/m2, left ventricular end-diastolic volume index = 123.4 mL/m2.) (B) Operative map based on intraoperative inspection of the opened left ventricle.

 

Figure 2
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  		Fig 2. Extent of septal myocardial infarction.

 
Our SVR exclusion criteria included the presence of hypokinesis without akinetic or dyskinetic segments, and poor basilar function. We did not exclude patients with multiterritory MI [10], preoperative pulmonary hypertension [11], severely depressed left ventricular function [12], or patients who were candidates for transplantation (n = 39).

Patient Variables
Data collection included demographics, New York Heart Association (NYHA) functional status, clinical and electrocardiographic characteristics, cardiac function determinants, and postoperative complications and procedures. Magnetic resonance imaging and echocardiography were used to measure cardiac function parameters: Left ventricular ejection fraction (EF), left ventricular end-systolic volume index (LVESVI), and left ventricular end-diastolic volume index (LVEDVI).

Operative Technique
Our surgical technique has been previously described [10–13]. Surgical ventricular restoration was performed after coronary artery bypass grafting and mitral valve repair/replacement, if necessary. Our method of anteroseptal reconstruction excludes no more than half of the height of the septum, whether a patch is used or a primary closure is performed [10]. An interventricular sizing device was used in most patients to aid in the ventricular reconstruction. The size of the device was selected based on an optimal LVEDVI of 50 to 60 mL/m2 body surface area. When necessary, lateral wall or inferior wall MI was addressed with linear plication, as previously described [10].

Statistical Analysis
Statistical analyses were performed with SPSS 12.0 software (SPSS, Chicago, Illinois). Chi-square and analysis of variance (ANOVA) were used to compare preoperative clinical characteristics, operative data, and MRI/echocardiography data among the three groups, as appropriate. A Student t test was used to compare preoperative versus postoperative cardiac function data on MRI and echocardiograms. Cox regression analysis was used to determine if extent of SMI was a predictor of mortality among patients undergoing SVR. Kaplan-Meier and log-rank analysis were used to compare survival and freedom from adverse outcomes between groups.


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Comment
 Discussion
 Acknowledgments
 References
 
Clinical Characteristics
Seventy-eight patients underwent SVR within the study period. All patients had anterior wall MI. Based on the intraoperative mapping, 12 patients had 75% or greater, 23 patients had 50% to 74%, and 43 had less than 50% of the height of the septum involved with infarction. Similarly, 20 patients had 75% or greater, 30 patients had 50% to 74%, and 28 had less than 50% of the length of the septum involved with infarction. Based on these findings, there were 20 patients with 75% or greater (group C), 30 patients with 50% to 74% (group B), and 28 patients with less than 50% (group A) of the height or length, or both, of septum involved with MI (Fig 3). Clinical characteristics of patients in the three groups are presented in Table 1. Ninety-seven percent of patients in this study had advanced CHF with NYHA class III or class IV status; 65% and 35% of patients in group C were in preoperative NYHA class III and IV, respectively. Twenty percent (4 of 20) of group C, 23.3% (7 of 30) of group B, and 28.6% (8 of 28) of group A had angina ({chi}2 p = 0.78) at presentation. The presence of a concomitant inferior wall MI (along with anteroseptal MI) was similar between the groups, with 45.0% (9 of 20) of group C, 56.7% (17 of 30) of group B, and 50.0% (14 of 28) of group A demonstrating evidence of inferior wall infarction on intraoperative inspection of the left ventricle ({chi}2 p = 0.71). The presence of a concomitant lateral wall MI was also similar among the three groups, with 32.1% (9 of 28), 53.3% (16 of 30), and 35.0% (7 of 20) of patients in groups A, B, and C demonstrating a lateral MI, respectively ({chi}2 p = 0.21).


Figure 3
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  		Fig 3. Distribution of patients based on height and length of septum involved in myocardial infarction.

 

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  		Table 1 Clinical Characteristics and Operative Data
 
Operative Data
Operative data are presented in Table 1 and are similar between groups. Fifty percent of patients in group C had a concomitant mitral valve procedure for significant mitral regurgitation; 7 underwent mitral valve annuloplasty and 3 underwent replacement. A greater number of patients also required intra-aortic balloon pump counterpulsation in group C versus groups A and B. All patients in group C were left with residual infarcted septum that was not excluded by SVR given our method of excluding no more than half the height of the septum. No patients in groups A or B were left with residual septal scar.

Ejection Fraction and Left Ventricular Volumes
Magnetic resonance imaging and echocardiography demonstrated that patients in group C had a lower preoperative EF and larger preoperative LVESVI and LVEDVI when compared with patients who had less extensive SMI. Surgical ventricular restoration improved EF, LVESVI, and LVEDVI for all three groups (Table 2). When comparing EF and left ventricular volumes postoperatively, there were no significant differences in EF, LVESVI, or LVEDVI.


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  		Table 2 Preoperative and Postoperative Cardiac Function
 
Pulmonary Pressures and Pulmonary Vascular Resistance Index
We also assessed preoperative pulmonary pressures and the pulmonary vascular resistance index of the three groups, when available. Preoperatively, there were no statistically significant differences between average preoperative mean pulmonary artery pressures (32.8 versus 33.2 versus 42.3 mm Hg; ANOVA p = 0.24), or systolic pulmonary artery pressure (40.7 versus 46.6 versus 53.3 mm Hg; ANOVA p = 0.32), for groups A, B, and C, respectively. Data were also not statistically significant when comparing mean pulmonary artery pressures for group C versus B (t test p = 0.19) and group C versus A (t test p = 0.15) and when comparing systolic pulmonary artery pressures for group C versus B (t test p = 0.46) and group C versus A (t test p = 0.14). Diastolic pulmonary artery pressure trended higher among patients with more extensive SMI (21.2 versus 29.8 versus 32.4 mm Hg; ANOVA p = 0.07). Preoperative pulmonary vascular resistance index also did not demonstrate statistically significant differences among the three groups (3.7 versus 5.4 versus 6.0 Woods units; ANOVA p = 0.19) for groups A, B, and C, respectively. These results were not statistically significant when comparing group C versus B (t test p = 0.75) and group C versus A (t test p = 0.18).

Electrocardiogram Data
When comparing PR intervals on electrocardiogram, there were no differences among the three groups preoperatively (ANOVA p = 0.92). Immediately after surgery, postoperative electrocardiograms revealed a statistically significant difference among the three groups (166 ms versus 176 ms versus 266 ms; ANOVA p = 0.048). Group C patients showed trends toward longer PR intervals immediately after SVR when compared with patients in group B (266 ms versus 176 ms; t test p = 0.10) and group A (266 ms versus 166 ms; t test p = 0.055). Electrocardiograms obtained closest to the time of discharge revealed no significant difference in PR intervals among the three groups (ANOVA p = 0.34). Patients in group C did trend toward longer PR intervals when compared with group A (187 ms versus 170 ms; t test p = 0.077).

Preoperative QRS duration was significantly different among the three groups (109 ms versus 108 ms versus 124 ms; ANOVA p = 0.03). Group C patients demonstrated a longer preoperative QRS duration versus group A (124 ms versus 109 ms; t test p = 0.04) and versus group B (124 ms versus 108 ms; t test p = 0.02). The QRS duration obtained closest to the time of discharge did not reveal statistically significant differences among the three groups (118 ms versus 107 ms versus 123 ms; ANOVA p = 0.10). Results were also not statistically significant when comparing group C and A (123 ms versus 118 ms; t test p = 0.57), but trended toward significance when comparing group C and B (123 ms versus 107 ms; t test p = 0.055).

Preoperative and postoperative need for biventricular pacemakers and AICDs are shown in Table 3. No patient required a pacemaker for intrinsic or induced rhythm disturbances postoperatively. Preoperatively, 1 patient in group A, 2 patients in group B, and 2 patients in group C required a biventricular pacemaker ({chi}2 p = 0.66). Postoperatively, no patient in group A, 3 patients in group B, and 2 patients in group C required a biventricular pacemaker ({chi}2 p = 0.22) for dysynchrony and functional considerations based on the referring cardiologist’s preference.


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  		Table 3 Preoperative and Postoperative Need for Biventricular Pacemakers and Defibrillators
 
The incidence of postoperative tachyarrhythmias was low, and the implantation of AICDs was done by standard functional criteria and not to treat observed or inducible arrhythmias. Automatic implantable cardioverter defibrillators were present in 6 patients in group A, 1 in group B, and 4 in group C preoperatively ({chi}2 p = 0.09). One patient in group A, 4 in group B, and 7 in group C underwent AICD placement after SVR ({chi}2 p = 0.01). Two of these patients had a single-chamber defibrillator preoperatively, which was replaced with a biventricular AICD after surgery.

Hospital Course
Length of stay data and postoperative complications are listed in Table 4. Mean total length of stay showed trends toward longer stays for patients with more extensive SMI; postoperative length of stay was significantly different among the three groups. Postoperative complication rates were similar when analyzing patients based on the extent of SMI. Seven patients in this study underwent left ventricular assist device implantation within the first 2 years after SVR: 3 in group C and 4 in group B. One patient in group C underwent cardiac transplantation.


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  		Table 4 Length of Stay and Postoperative Complications
 
Mortality
Operative mortality was similar among the three groups ({chi}2 p = 0.32). Operative mortality was 5.0% (1 of 20) for group C and was similar to that of patients in group B (13.3%; 4 of 30; p = 0.6) and group A (3.6%; 1 of 28; p = 1.00). Cause of death for the operative mortality in group C was cardiac related, as was the cause of death for the lone patient in group A. Causes of death for group B were CHF related (n = 1) and multisystem organ failure (n = 3).

Thirteen percent of patients (10 of 78) in this study died at late follow-up: 15.0% (3 of 20) in group C, 13.3% (4 of 30) in group B, and 10.7% (3 of 28) in group A. The late mortality rate among the three groups was not statistically significant ({chi}2 p = 0.90). Of the 3 group C patients who died at late follow-up, causes of death were cardiac related (n = 1), rectal cancer (n = 1), and unknown cause (n = 1). Causes of late mortality in group B were sepsis (n = 2), renal failure (n = 1), and massive gastrointestinal bleeding (n = 1). The causes of death for the 3 late mortalities among group A patients were cardiac related (n = 1), sepsis (n = 1), and unknown cause (n = 1).

Total follow-up for our entire series is 1,372 patient-months (range, 0.5 to 45). Three-year Kaplan-Meier survival (including hospital deaths) for all patients undergoing SVR was 76.7% ± 5.2%. Kaplan-Meier survival (including hospital deaths) for SVR patients based on the extent of SMI is shown in Figure 4. Three-year Kaplan-Meier survival for patients in groups A, B, and C were 85.0% ± 6.9%, 69.4% ± 9.3%, and 76.8% ± 10.4%, respectively. The difference in survival among the three groups was not statistically significant on log-rank analysis (p = 0.43), although patients with less extensive SMI showed trends toward improved 3-year survival.


Figure 4
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  		Fig 4. Kaplan-Meier survival based on height and length of septum involved in myocardial infarction. (Dashed line = group A; dash-dotted line = group B; solid line = group C.)

 
Functional Outcomes
Surgical ventricular restoration significantly improved functional outcomes for patients irrespective of the extent of SMI. Preoperatively, 100% of patients in groups C and B and 92.9% (26 of 28) of those in group A were in NYHA class III or class IV. Seventy-five percent of group C (15 of 20), 66.7% of group B (20 of 30), and 88.5% of group A (23 of 26) improved to NYHA class I or II at follow-up. The improvement in NYHA class was significant for each group, but when compared with each other did not reach statistical significance ({chi}2 p = 0.15). However, patients in group A showed trends toward more patients in NYHA class I or II postoperatively when compared with those in group B (p = 0.07).

Septal Myocardial Infarction With Inferior Wall Involvement
We also assessed the impact of inferior wall MI on outcomes based on the extent of SMI. Of the 20 patients in group C, 9 had concomitant inferior infarction. Four of these patients were in NYHA class IV preoperatively, 4 had pulmonary hypertension preoperatively, 6 required perioperative intra-aortic balloon pump counterpulsation, and 3 required a mitral valve procedure at the time of SVR. Among these 9 patients, there were no operative deaths; there were 2 late deaths, and 5 patients are in NYHA class I or II at follow-up.

When comparing preoperative and postoperative cardiac function between group C patients with versus without concomitant inferior MI, there were no statistically significant differences in EF, LVESVI, or LVEDVI. Similarly, when comparing preoperative and postoperative EF, LVESVI, and LVEDVI for group B patients with versus without inferior MI, there were no statistically significant differences. However, group B patients with inferior MI did trend toward a lower postoperative EF (t test p = 0.07) and larger postoperative LVESVI (t test p = 0.09) when compared with group B patients without inferior MI. We extended this analysis to group B and group C patients (≥50% of height and the length) grouped together, and then divided into those with and without inferior wall MI. This analysis also revealed no statistically significant differences in preoperative and postoperative EF, LVESVI, and LVEDVI.

Septal Infarction and Anterior Wall Myocardial Infarction
We also compared the extent of septal involvement in relation to the extent of anterior wall infarction and, as expected, found that the extent of anterior wall MI correlated grossly with the extent of SMI. Of the 20 patients in group C, 16 had greater than 50% anterior wall infarction; the remaining 4 patients had less than 50% anterior wall infarction. Of the 30 patients in group B, 25 had greater than 50% anterior wall infarction and the remaining 5 patients had less than 50% anterior wall infarction.

Cox Regression Model
We ran three independent Cox regression analyses to see if increasing SMI predicted mortality and if less extensive SMI predicted improved survival. Greater than or equal to 75% involvement of the height and length of septum was not a predictor of mortality on Cox regression analysis (odds ratio [OR] = 1.4; 95% confidence interval [CI]: 0.3 to 7.0; p = 0.6); 50% to 74% SMI also did not predict mortality (OR = 2.5; 95% CI: 0.6 to 10.6; p = 0.2). Less than 50% SMI did not predict improved survival (OR = 0.2; 95% CI: 0.04 to 1.4; p = 0.1). Variables included in the Cox regression analysis included age, sex, NYHA class IV, smoking history, hypertension, hyperlipidemia, diabetes mellitus, three-vessel coronary artery disease, recent MI (<30 days), extent of SMI, anterior-inferior-lateral MI, mitral regurgitation requiring a mitral valve procedure, EF, LVESVI, and pulmonary hypertension.


   Comment
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
Discussion
 Acknowledgments
 References
 
Surgical ventricular restoration has become an established therapy for certain CHF patients after anterior wall MI. Outcomes after SVR have been excellent [4–8]. Many centers have demonstrated excellent survival among appropriate patients, with improvements in EF, left ventricular shape and volumes, and NYHA functional status after SVR [4–8, 10–12]. Others have shown that SVR reduces abnormal elevations in blood levels of neurohormones associated with CHF [14], and improves myocardial performance in nonischemic areas remote from scar [15]. In a recent study, Tulner and colleagues [16] showed that SVR normalized left ventricular volumes, improved measures of systolic function, reduced left ventricular wall stress, decreased mechanical dyssynchrony, and improved mechanical efficiency.

The interventricular septum has a unique role in cardiac structure and function. It is more than the wall of muscle between the two ventricles that carries the fibers of the cardiac conduction system. It plays a role in the independent function of the left and right ventricles as well as helping to maintain ventricular synchrony between the two ventricles, which impacts overall cardiac performance. The structure of the septum is still a subject of some controversy. There are two main schools of thought. One looks at the septum as a bilayered structure composed of left and right sided longitudinally oriented fibers. Evidence for this comes from echocardiographic studies that show the septum to be divided into right and left sides divided by a reproducible, bright signal with measurable differences in thickening and radial strain [17].

The other school of thought is that the heart consists of a single muscle band, which twists upon itself in a ropelike structure with two turns in a helical fashion. The septum consists of two parts: an ascending and a descending loop of the same muscle band [17]. A unifying concept applicable to both schools of thought is that the left and right sides of the septum have their own unique blood supply beginning with septal branches off both the left anterior descending and posterior descending vessels, which in turn give off secondary branches that supply the different sides of the septum separately and asymmetrically. Occlusion of a major vessel upstream from the septal perforators would affect both sides of the septum, which is exactly what is seen when we see a coronary occlusion. The extent of myocardial necrosis and scarring after coronary occlusion may be slightly different on both sides of the septum given the slightly different blood supply, but are undoubtedly closely related [18]. The impact of this differential on global cardiac function is probably negligible and it is reasonable to look at septal infarction as a singular event with a singular impact on cardiac function.

To date, no studies have focused on the extent of septal involvement in patients with anteroseptal MI who undergo SVR. Given the central role of the interventricular septum on left ventricular function and the paucity of data regarding SMI and its impact on SVR outcomes, we sought to determine the impact of the extent of septal infarction on outcomes. We concentrated our review on global function, electrocardiographic changes, survival and functional outcomes. The central anatomic findings were made by intraoperative observation by a single surgeon using a detailed anatomic map of each case. Magnetic resonance imaging and echocardiography are both tools capable of providing detailed anatomic and functional data as we have previously described and have used in many of the patients in this series [19]. In our series many patients received AICDs or biventricular pacemakers, which either prevented or significantly reduced the utility of MRI or high-resolution echocardiographic-derived data. Real-world insurance issues also impacted our ability to obtain MRI scans, so the postoperative MRI data set we had to work from was limited. This is why the observational data with all their limitations and imprecision were used. Although our data are largely observational, we believe that they provide a reasonably controlled data set adequate for the questions at hand.

Surgical ventricular restoration has been used as a treatment of congestive heart failure in patients with ischemic cardiomyopathy for many years. The surgical techniques utilized are different but the guiding surgical principles are the same, namely, to reduce the volume in the akinetic anteroseptal region by exclusion of the nonviable scar tissue, reduce the volume of the ventricle, and restore the elliptical shape. Surgical ventricular restoration is performed in conjunction with coronary artery bypass grafting and repair of any valvular problems. The treatment of the septum is different in each of the main surgical techniques. The most popular technique is endoventricular circular patch plasty, popularized by Dr Vincent Dor; it utilizes a pursestring suture to outline the new borders of the anterior wall, followed by direct or patch closure over this pursestring [20, 21] (Fig 5). This has been called the Fontan stitch by many authors because of a similar description by Dr Fontan [22]. The septum is reduced in length by tying the pursestring suture, and the height of the septal exclusion, and ultimately the size of the reconstructed ventricle, is determined by the placement of the pursestring suture across the septum and the lateral wall. A concentric pursestring technique described by McCarthy and associates [23] is a modification of this technique (Fig 5). The Jatene technique uses imbricating sutures in the septum to reduce the length of the septum, followed by patch or primary closure to reduce the height of the septum (Fig 5) [24]. A linear closure technique described by Mickleborough [25] utilizes direct reapproximation of the anterolateral scar to the septum with a vertical septal exclusion patch in a small number of patients with large septal volumes (Fig 5). There is no evidence that any technique is better than the other, and given the same guiding principles utilized for all techniques, it is unlikely that any technique is superior.


Figure 5
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  		Fig 5. Surgical ventricular restoration operative techniques. (A) Dor endoventricular circular patch plasty (Reprinted from Dor V [21], with permission from Elsevier). (B) Jatene technique (Reprinted from Cox [24], with permission from Elsevier). (C) McCarthy concentric pursestrings technique (Reprinted from Caldeira and McCarthy [23], with permission from Elsevier). (D) Mickleborough linear closure with septoplasty (Reprinted from Mickleborough LL. Left ventricular aneurysm: modified linear closure technique. In: Operative techniques in thoracic and cardiovascular surgery: a comparative atlas. Vol 2. Philadelphia: WB Saunders, 1997:118–31; with permission from Elsevier).

 
The placement of the pursestring suture laterally and across the septum, or where the lateral wall is sewn to the septum, determines the volume of the reconstructed ventricle. Where this is placed is important. Some centers use the transition zone between contractile and noncontractile myocardium, among other factors, to determine the placement of the pursestring stitch for anterior wall reconstruction; others use the base of the papillary muscles as a guide. Doctor Dor began using simple balloons to size the ventricle to avoid making the reconstructed ventricle too small. This concept led to the development of commercially available sizing devices. We have routinely deployed an interventricular sizing device (Chase Medical, Richardson, Texas; Bioventrix, Danville, California) into the left ventricular cavity to guide reconstruction. We have found these sizing devices to be helpful in patients with larger left ventricles, in those with multiterritory myocardial infarction, and in those with a mosaic pattern of infarction in which a clear transition zone is difficult to identify. The size of the intraventricular sizing device is based on patient body surface area in an effort to approach an optimal LVEDVI of 50 to 60 mL/m2. We have found the interventricular sizing device to be very useful in delineating the placement of the pursestring suture, optimizing left ventricular volume, and preventing the reconstruction of a left ventricular chamber that is too small. Furthermore, the sizing device addresses shape by acting as an elliptical reference to help guide the reconstruction of an elliptical chamber.

We routinely exclude no more than half of the height of the septum, whether a patch is used for reconstruction or a linear plication is performed. The optimal amount of septum that should be excluded is unknown. In patients with SMI extending more than half of the height of the septum, inevitably some infarcted myocardium is not excluded. The impact of the nonexcluded infarcted septum on left ventricular function remains unclear. We have found no significant differences in outcome among patients having more extensive SMI compared with patients having less than 50% SMI, which is completely excluded with anteroseptal reconstruction. There is no evidence that residual infarcted septum has had any impact on function or survival; however, our suspicion is that sophisticated functional assessment with high-fidelity instrumentation might show a detrimental effect of infarcted septum that is not addressed. Our current strategy to exclude no more than 50% of the septum stems from our concern about making the left ventricle too small after reconstruction.

Importantly, the different techniques discussed above, as well as our own approach, focus on excluding diseased myocardium. Recently, Isomura and colleagues [26] reported their results with septal anterior ventricular exclusion pacopexy where the focus of restoration was form and not disease as the endpoint for oblique patch placement. In the technique described by the authors, placement of the patch followed an oblique trajectory between the apex and septum below the aortic valve to produce an elliptical shape. The authors excluded any amount of septum necessary to create an ellipsoid, as their focus was correcting shape and not excluding disease. Their results were good, but there is no evidence that outcomes after this technique are better than those of any other technique in the long term.

Mitral regurgitation is common in CHF patients owing to postinfarction remodeling and tethering of the mitral valve chords. That leads to restricted mitral leaflet motion, reduced leaflet coaptation, and mitral regurgitation [27]. In this study, the rate of concomitant mitral procedures was higher among patients with 75% or greater SMI compared with patients having less extensive SMI. Although patients with 75% or greater SMI had more mitral regurgitation preoperatively, the operative mortality rate remained low and was similar to that of patients with less extensive SMI. Although others have shown that preoperative mitral regurgitation and addition of a mitral valve procedure increases mortality [28], we could not make this association based on our analysis.

Patients with left ventricular dilatation have increased wall stress and stretch, which may contribute to arrhythmia development [29, 30]. Surgical ventricular restoration has been shown to decrease arrhythmia development [31, 32], which results from reducing ventricular volume, and therefore tension and stretch, and excluding scar tissue that may act as a nidus for arrhythmia generation. Also important, revascularization relieves ischemia and may contribute to lowering the incidence of arrhythmias after SVR. We analyzed electrocardiographic data to see whether the degree of SMI affected the conduction system. There were no statistically significant differences in PR intervals preoperatively or postoperatively. Preoperatively, those with more extensive SMI did demonstrate a longer mean QRS duration, but postoperative QRS duration was similar regardless of the extent of SMI. That finding may be due to decreased wall tension, but the exact reason is not known. There were no AICDs or biventricular pacemakers implanted for purely rhythm disturbances, but rather to optimize function and prevent sudden death. With most referrals coming from outside cardiologists who made the AICD and biventricular pacemaker decisions, no real statements can be made regarding the significance of their insertion.

Coronary artery bypass grafting is an important component of SVR. Myocardial revascularization of viable and stunned muscle may play a significant role in the functional improvement seen in these patients. We did observe improved myocardial contractility and cardiac function in a small number of patients in our study who did not undergo revascularization at the time of SVR. Because of this, we believe that some of the benefits of SVR are independent of revascularization. We await the results of the Surgical Treatment for Ischemic Heart Failure (STITCH) trial to help elucidate the role of SVR in the management of these patients.

Kaplan-Meier survival for all SVR patients at our institution is 76% at 3 years. This outcome is significantly better compared with class III and IV CHF patients treated with optimal medical therapy [33, 34] and similar to the SVR survival of class III or IV patients reported by the RESTORE registry [6, 7] and others despite being used exclusively as a heart failure therapy in the sickest group of SVR patients yet reported in the literature. In this series, the 3-year Kaplan-Meier survival was similar regardless of the extent of SMI. Additionally, greater extent of SMI was not a significant predictor of mortality on Cox regression analysis. However, patients with less than 50% SMI did show trends toward a survival advantage over patients with more extensive SMI. This is not surprising given the importance of the septum on left and right ventricular function and is consistent with our previous findings. Our belief is that there is a critical quantity of viable myocardium necessary for a successful outcome after SVR. With this in mind, we expect that a larger MI with greater septal involvement signifies less viable myocardium and a decrease in the functioning mass of the left ventricle, which will lead to inferior outcomes. At present, this critical amount of myocardium is unknown. We are actively working with our MRI and echocardiography colleagues to try to quantify exactly how much and where the critical muscle is required.

The retrospective design of our study limited the amount of MRI data available. Many patients in our study had defibrillators or biventricular pacers present at the time of MRI, which created artifact and limited our ability to apply appropriate measuring algorithms. Some patients had imaging studies at other institutions, which we were unable to repeat; we were able to obtain volumetric data, but not specific morphologic data. We attempted to control for this by prospectively filling out a detailed intraoperative map of infarct size and location for each case based on a single surgeon’s inspection of the opened left ventricle. As a result, for patients who did not have MRI preoperatively, or had MRI at outside institutions or with artifact, we were unable to precisely quantify the extent of septal infarction. Instead, for these patients, we relied on intraoperative inspection alone. Given this limitation and for the ease of statistical comparison we considered it was appropriate to categorize patients in this study into one of three groups based on extent of septal infarction.

We have shown that SVR significantly improves cardiac function, functional status, and survival for CHF patients regardless of the extent of SMI. Patients with more extensive SMI, despite having larger left ventricular volumes and lower EF preoperatively, show significant improvement after SVR with postoperative EF and volumes similar to patients with less extensive SMI at midterm follow-up. Surgical ventricular restoration remains a safe procedure for selected CHF patients regardless of the extent of SMI, but longer follow-up is necessary to draw definitive conclusions.


   Discussion
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Discussion
Acknowledgments
 References
 
DR JOSEPH CLEVELAND, JR (Denver, CO): Has it been your center’s policy to revascularize the anteroseptal wall regardless of viability? In other words, do all these people get LIMAs, or do you do it based on whether you think the septum is alive or dead? Do you revascularize the anterior wall at the time of their SVR?

DR NWAKANMA: Yes.

DR CLEVELAND: All patients?

DR NWAKANMA: Most patients.

DR CHARLES T. KLODELL (Gainesville, FL): I’d like to congratulate you on an outstanding presentation.

I wonder if you or Dr Conte could comment. I think your presentation shows us that maybe the extent of the infarction shouldn’t be what determines whether or not somebody is a candidate to go to the operating room. I think we all have a little bit of fear sometimes of the people that have the extensive septal infarctions. When you went back and looked at these patients, did the extent of infarctions impact the technique you used in the operating room? In other words, were the ones with more infarction more likely to have received a patch, or was the use of a patch consistent across all patient groups? Is there anything that that preoperative knowledge of the MRI allowed you to predict about the intraoperative course that we could take away as a clinical pearl?

DR NWAKANMA: Thank you for those questions and your comments.

In terms of the use of the patch, it was the standard procedure for all patients. Usually the method we use is if it is more than a 3-cm defect, then in that case, most of the time, we use a patch regardless of the extent of infarction.

And your second question about whether the MRI could predict which patients would be the best candidates for surgical ventricular restoration, we are working with our radiology colleagues to find out which predictors on MRI perioperatively can tell us about the outcomes in SVR.

In terms of the amount of septum that is excluded, all the patients who had less than 50% septal infarction had their scar excluded. Our policy is not to exclude more than 50%. So some of the patients in group C who had more than 75% septal infarction may have had some retained scar, because we do not exclude more than 50 percent of infarction involvement.

DR GERALD D. BUCKBERG (Los Angeles, CA): I congratulate you on a very nice study. You have nicely shown how cardiac enlargement is linked to septal involvement, since the septum occupies 35% of the myocardial mass. Consequently, the ventricular chamber attains a bigger volume, as a larger amount of septum becomes scarred.

Why did you select 50% of the septum as the site of cutoff of your patch placement, since this choice leaves some disease in place when more septum is involved. Consequently, there is impairment of the potential of rebuilding a more conical ventricle. In contrast, we make another choice in larger ventricles, and place the patch at a higher septal site. When a large chamber is encountered this region may sometimes be beyond the disease. Have you studied the post operative ventricular shape to determine if a conical form has been restored?

This issue is raised by your data, since the table shows similar end systolic volumes in each of the three group categories. Perhaps the marked decrease in volume in patients with 75% or greater septum disease suggests that you may have misjudged the 50% site of patch placement, and have selected a higher level that was closer to the aortic annulus. If this did not happen, there must be another explanation for similar post operative end systolic volumes.

DR NWAKANMA: Well, your first question was why did we use 50% as the cutoff. It is not very clear the effect of retained scar of the septal infarction like I explained in the answer to the previous question. It’s actually an arbitrary cutoff. It is not very clear what effect the retained scar tissue has.

However, we did look at other outcome measures such as the incidence of biventricular pacer or defibrillator placement and there was no difference among the groups.

DR BUCKBERG: We have looked at the change in shape by selecting a higher patch site in larger hearts. Dr Isomura is a member of the RESTORE Group, and his team observed that a more conical ventricle results from higher patch site selection, so that both size and shape are changed by restoration. For this reason, I am interested in learning if the larger ventricles reconstructed at >75% septum involvement were more conical.

DR NWAKANMA: You mean postoperatively?

DR BUCKBERG: Yes, postoperatively.

DR NWAKANMA: We don’t have data on all MRI results for postoperative. And also, it would be an interesting thing to go back and look at. But like I mentioned, we do not have any data to support that 50% cutoff.

DR EDWARD B. SAVAGE (St. Louis, MO): I have two questions.

First is, how are you defining the infarction? When you read the literature on this, people are using akinetic areas, thinned-out areas, et cetera. What’s your definition of infarction?

Number two, have you done any analysis in this patient group comparing them to similar patients who did not have discrete aneurysmal areas though similar levels of function and compared their mortality? I ask this because in your graph, the 1-year survival is about 85%, that’s a significant drop-off after 1 year, have you done any comparisons to nonrepair coronary bypass groups?

DR NWAKANMA: That’s an excellent question. We did have that question in our mind as well. We have been able to only do that retrospectively at this time whereby we looked at the outcome of CHF patients who are potential candidates for SVR, who did not receive SVR, and tried to compare their outcomes to the patients who were candidates for SVR and received SVR. And we found no difference in survival. However, there were better improvements in EF and NYHA class, and fewer re-hospitalizations among the combined SVR and CABG group. The data has not been published yet but is in the process.

Hopefully the STITCH trial, which is a prospective randomized trial, will help to answer that question.

DR SAVAGE: I hope to see that data soon because this is an important question that we need to answer if we’re going to continue to do this operation.

DR NWAKANMA: Another question you asked was how do we identify the infarcted areas. I mentioned about our technique of carefully studying the MRI based on gadolinium contrast and the surgeon’s careful inspection. One of the best criteria we always use is to make sure that the basilar function of the heart is intact. That appears to be a very good predictor of good outcome.

Also, we look at only akinetic scar area. Hypokinesis does not seem to be a good option. So if the scar is akinetic on MRI, no areas of hypokinesis and has good basilar function, those patients tend to do well with SVR. Again, STITCH trial will tell us how patients who are potential candidates for SVR, who do not receive SVR, how they fare compared with those who do receive SVR. But many work by our group and others have shown that this is a feasible procedure that can be performed with acceptable outcomes, even in high-risk patients.

And talking about mortality, 2-year survival for CHF patients is only 50%. Our 3-year survival was 76%, which is a reasonable and better outcome, than patients who receive maximal medical treatment.

DR SAVAGE: (Inaudible.)

DR NWAKANMA: Yes, we can do it that way, comparison. Again, STITCH trial has an arm that also looks at those who are maximally medically treated.

I hope that answers your question.


   Acknowledgments
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Discussion
 Acknowledgments
References
 
Nishant Patel is the 2005 Chase Medical Research Scholar for Surgical Ventricular Restoration, Jason Williams and Eric Weiss are Irene Piccinini Research Fellows, and Lois Nwakanma is a Hugh R. Sharp Jr Research Fellow.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Discussion
 Acknowledgments
 References
 

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