- Email: [email protected]
Ventricular reconstruction for ischemic cardiomyopathy
Ventricular Reconstruction for Ischemic Cardiomyopathy Lynda L. Mickleborough, MD, Naeem Merchant, MD, Yves Provost, MD, Susan Carson, AHT, and Joan Ivanov, PhD Divisions of Cardiovascular Surgery and Radiology, Toronto General Hospital, University of Toronto, Toronto, Ontario, Canada
Left ventricular surgical reconstruction has been advocated for patients with coronary artery disease, prior myocardial infarction, and poor left ventricular function. The objective of the approach is to resect or exclude all akinetic or dyskinetic nonfunctioning portions of the ventricular cavity and to restore the left ventricle size and shape toward normal as much as possible. We review the pathophysiology of ischemic cardiomyopathy and suggest guidelines for preoperative assessment and patient selection for ventricular reconstruction. Because of the prevalence and prognostic significance of ventricular arrhythmias in this patient population we include in our operative approach a visually directed ablation procedure in those with significant septal scarring. We describe our operative technique and review results
achieved with this approach. The procedure results in a significant decrease in ventricular volume, increase in ejection fraction and improvement in apical geometry. We conclude that in selected patients with ischemic cardiomyopathy, left ventricular reconstruction can be accomplished with low operative mortality and results in significant improvement in left ventricular function. During follow up symptom class is decreased in most patients and overall survival at 5 years is 84% and freedom from sudden death is 96%. Ventricular reconstruction should be considered in all patients with coronary artery disease and akinetic or dyskinetic scar.
T
surgery, ventricular surgical remodeling, or surgical anterior ventricular endocardial restoration the basic priniciples are the same.
he treatment of ischemic heart disease continues to be a challenge with an ever-increasing patient population presenting with congestive failure. In patients with coronary disease and a previous infarct the goal of surgery should be not only to prevent ongoing ischemia but also to minimize the negative effects of the infarct on ventricular structure and function. In valvular disease, surgery is often recommended early to prevent adverse ventricular remodeling. Similarly in ischemic heart disease when significant ventricular scarring has occurred surgical reconstruction should be done to prevent progressive deterioration of heart function over time. For years we and others [1, 2] have advocated the removal of akinetic or dyskinetic scar. The goals of the procedure are to revascularize wherever possible, to resect or exclude all nonfunctioning portions of the ventricular cavity, and to restore size and shape toward normal as much as possible. This results in decreased ventricular volume and decreased wall tension and wall stress that decreases ischemia in the remaining viable myocardium, improves heart failure symptoms, and decreases the incidence of ventricular arrhythmias or the severity of associated mitral insufficiency. Whether such a procedure is called aneurysm resection, heart reduction Presented at the Heart Failure & Circulatory Support Summit, Cleveland, OH, Aug 22–25, 2002. Address reprint requests to Dr Mickleborough, Toronto General Hospital, 200 Elizabeth St, Toronto, Ontario, Canada M5G 2C4; e-mail: [email protected].
© 2003 by The Society of Thoracic Surgeons Published by Elsevier Inc
(Ann Thorac Surg 2003;75:S6 –12) © 2003 by The Society of Thoracic Surgeons
Pathophysiology After myocardial infarction necrotic muscle is replaced by fibrous tissue. When significant scarring occurs an area of relative thinning often results along the distribution of the culprit vessel (elliptical in shape). The amount of thinning and whether a classic dyskinetic aneurysm occurs depends on many factors including speed of development and extent of collateral circulation as well as healing properties of the heart that may be influenced by advanced age, sex, or corticosteroid use. To compensate for loss of contractile function of the infarcted segment the ventricular chamber dilates. That results in increased wall tension, decreased systolic shortening, and increased oxygen consumption in areas remote from the original infarct. In some cases the infarcted area shows little infarct expansion and it may take many years for adverse ventricular remodeling to occur. In other cases there is rapid development of an obvious dyskinetic aneurysm and heart failure symptoms. Expansion and thinning of the infarct may produce additional work because of paradoxic motion of the thinned segment and may result in malalignment of muscle fibers in surrounding contractile segments leading to further decrease in efficiency of contraction. Scarring and dilatation associated with aneurysm formation 0003-4975/03/$30.00 PII S0003-4975(03)00464-8
Ann Thorac Surg 2003;75:S6 –12
CIRCULATORY SUPPORT MICKLEBOROUGH ET AL VENTRICULAR RECONSTRUCTION
S7
akinesis or dyskinesis. We believe these are the very patients who will benefit from ventricular reconstruction. To summarize our approach in patients with poor LV function, if regional wall motion abnormalities associated with thinning can be identified we believe these areas should be considered for possible resection. On the other hand even in dilated hearts we have not resected akinetic areas where thinning has not occurred as advocated by Buckberg and coworkers [11]. Rather we have revascularized these areas hoping to recruit hibernating myocardium and improve ventricular function. Using this approach we have achieved good results in patients with poor LV function either with revascularization alone (operating room mortality 4%, 5-year survival 72%) [5] or with revascularization and LV reconstruction (operating room mortality 3%, 5-year survival 84%) [12]. Fig 1. Magnetic resonance image in a patient with prior anteroapical infarct. There is thinning at the apex. The septum is still well preserved and of normal thickness. The left ventricular cavity is dilated. The end diastolic volume index (EDVI) is 112 mL/m2 and end systolic volume index (ESVI) is 77 mL/m2.
may provide a subtrate for ventricular arrhythmias. If papillary muscles are involved in the original infarct or if changes in ventricular geometry interfere with function of the subvalvular apparatus, mitral regurgitation may occur. We believe that whenever an infarct results in an area of akinesia or dyskinesia surgery has something to offer.
Revascularization With or Without Surgical Remodeling In patients with coronary artery disease the benefits of surgical revascularization in terms of increased longevity and decreased symptoms are most obvious in those with poor ventricular function. Because the risks of surgery are slightly increased in these cases there may be reluctance to operate if there is less than ideal distal coronary anatomy [3]. In many patients with anteroapical akinesis and no significant thinning the left anterior descending artery (LAD) is totally occluded proximally and not well visualized on the angiogram. That raises concern over the possibility of incomplete revascularization and such patients may be considered poor candidates for surgery. In our experience, in such patients revascularization of the LAD is almost always possible even though the distal vessel may be 1 mm in size or diffusely diseased [4]. Using an aggressive approach to revascularization we have reported excellent results even in patients with an ejection fraction less than 20% [5]. In many centers great effort is made to identify a subset of patients who would most benefit from revascularization [6 – 8]. Patients with reversible ischemia are most likely to show significant improvement in ventricular function with revascularization alone. However recent studies have pointed out that the benefits of revascularization may be limited if left ventricular (LV) volumes are grossly increased [9] or if there is evidence of asymmetry of ventricular motion [10], namely localized areas of
Ventricular Reconstruction: Patient Selection and Preoperative Assessment Ventriculography can identify areas of wall motion abnormality (akinesia or dyskinesia). Biplane views are essential to assess involvement of the septum. Angiography however provides no information with regard to extent or distribution of wall thinning. Using echocardiographic techniques in dilated poorly functioning hearts it is often difficult to accurately assess size and function at the apex. In the past in patients with low ejection fraction we evaluated the extent of wall thinning intraoperatively using needle aspiration [13]. Since 1998 we have used magnetic resonance imaging (MRI) to obtain preoperative assessment of ventricular shape and volume (Fig 1). Magnetic resonance imaging also provides information about regional wall function and thinning which has allowed us to decide preoperatively whether a patient with poor LV function is a candidate for revascularization alone (no thinning) or in combination with surgical reconstruction.
Effects of LV Reconstruction: Limitations of Studies to Date In an attempt to understand the pathophysiology of abnormal ventricular function, to aid in the choice of patients for surgery and to determine which of several available reconstruction techniques should yield optimal results, various computer models have been used [14, 15]. However these analyses make assumptions about the physical properties of the tissue excised and about function of the surrounding myocardium. In our experience the physical properties of the excised tissue varies widely depending on whether the resected wall is akinetic or dyskinetic and whether it is calcified or not. Furthermore resection may have different effects on the size and function of the remaining chamber depending on the techniques of myocardial preservation and ventricular reconstruction used and the completeness of revascularization achieved. Many groups using a variety of repair techniques have reported decreased volume and increased ejection frac-
S8
CIRCULATORY SUPPORT MICKLEBOROUGH ET AL VENTRICULAR RECONSTRUCTION
Ann Thorac Surg 2003;75:S6 –12
Fig 2. Preoperative (left) and postoperative (right) magnetic resonance imaging. Preoperatively an anteroapical aneurysm involves the distal portion of the septum; the apex is globular in shape. Postoperatively a septal patch has excluded the aneurysmal septum and is incorporated anteriorly into the modified linear closure. The space between the patch and the septal aneurysm has been filled with clot. Ventricular volume is decreased and the shape of the apex has been restored toward normal, namely more conical.
tion after repair [2, 11, 12]. Dor and coworkers [16] who advocate the endoventricular patch technique have reported extensively on postoperative changes in ventricular function and shape. That group reported increased sphericity after repair which seems counterintuative given their excellent clinical results. We have used a different technique (modified linear closure with patch septoplasty when indicated) and have demonstrated with preoperative and postoperative MRI a more conical shape after the repair (Fig 2). Clearly further studies are needed to document effects of these procedures on ventricular geometry, shape, and function.
Anteroapical Location of Scar Most patients in whom ventricular reconstruction is indicated have anteroapical scarring which often extends over the apex to involve the distal inferior wall. There is a great deal of variability in size and extent of thinning of the area involved. In particular the extent of septal scarring and thinning is extremely variable (Fig 1) [12]. Whenever significant septal thinning and dyskinesis occur the reconstruction technique should exclude this part of the dysfunctional ventricle.
Mitral Regurgitation In patients with ischemic cardiomyopathy, mitral regurgitation may be related to several possible mechanisms. Papillary muscle ischemia may contribute to mitral regurgitation. Adverse ventricular remodeling with regional displacement of the ventriclar wall or chamber dilatation may lead to mitral regurgitation, which may not respond to revascularization alone. Resection of akinetic or dyskinetic scar with restoration of ventricular size and geometry toward normal may improve valve function or annuloplasty as advocated by Bolling and coworkers [17] may partially compensate for malfunction of the subvalvular apparatus. In our experience resection
of akinetic or dykinetic scar and revascularization often significantly improve valve function [12]. In selected cases we have added mitral valvoplasty to the repair [18]. After ventricular reconstruction when significant mitral regurgitation persists on intraoperative echocardiography, mitral valve replacement may be required.
Ventricular Arrhythmias In patients with ischemic cardiomyopathy, ventricular arrhythmias are a major source of morbidity and mortality. In these patients the value of complete revascularization in reducing arrhythmia recurrence should not be underestimated. For example the Coronary Artery Bypass Graft (CABG) Patch trial [19] compared arrhythmia occurrence and long-term survival in patients with poor ejection fraction (⬍ 35%) and an abnormal signalaveraged electrocardiogram who underwent revascularization. This important trial showed that patients undergoing revascularization did not benefit from implantable cardiac defibrillator (ICD) implantation, presumably owing to the positive effect of grafting on the arrhythmia substrate (relief of ischemia or improvement of ventricular function). In contrast the MADIT study [20] showed a survival benefit after ICD implantation in patients with low ejection fraction (⬍ 35%), nonsustained ventricular tachycardia, and inducible ventricular tachycardia. Patients were excluded from this trial if they were candidates for concurrent revascularization (within 3 months). Clearly the patient populations in these two studies are not comparable. It seems obvious from the CABG Patch trial results, that revascularization alone using contemporary surgical techniques is of significant benefit in preventing recurrence of ventricular arrhythmias in patients with poor ventricular function. When revascularization is combined with ventricular reconstruction the potential benefits of the surgical approach in controlling arrhythmias is even more striking.
Ann Thorac Surg 2003;75:S6 –12
In the past in patients with recurrent sustained ventricular tachycardia, intraoperative mapping and surgical ablation of ventricular tachycardia foci (popular in the early 1990s) taught us important lessons about the pathophysiology of the arrhythmias [21]. These patients usually had large dilated hearts with akinetic or dyskinetic scar. Use of an intraventricular mapping balloon demonstrated very graphically that ease of induction of arrhythmias was critically related to mechanical loading conditions of the heart [22]. As the balloon was inflated ventricular arrhythmias were easily induced. Therefore any procedure that restores ventricular volume and size toward normal (such as ventricular construction) is likely to reduce the inducibility or occurrence of ventricular arrhythmias. Mapping studies in patients with anteroapical scarring showed that the anatomic substrate for ventricular arrhythmias was located in the borderzone between scar and surrounding normal endocardium on the ventricular septum [23]. Ablation using endocardial excision often combined with cryoablation or creation of homogeneous scar after attachment of a septal patch controlled the arrhythmia. In our series of map-directed surgery freedom from sudden death was excellent 97% at 5 years and overall survival was 79% [21]. For patients with ischemic cardiomyopathy, because ventricular arrhythmias have an important effect on prognosis in those with significant septal scarring, we have included in our approach to ventricular reconstruction a visually directed endocardial excision with cryoablation at the periphery. Our left ventricular reconstruction series includes 86 patients who had recurrent ventricular tachycardia preoperatively and inducible ventricular tachycardia at electrophysiologic study. Clearly these patients are at increased risk for arrhythmias during follow-up. After revascularization and ventricular reconstruction, patients with a history of ventricular tachycardia undergo electrophysiologic testing. Those with inducible or spontaneous tachycardia postoperatively are discharged on a regimen of amiodarone. During follow-up arrhythmia recurrence was only rarely a problem. Only 1 patient in the entire series required an ICD and freedom from sudden death or recurrent ventricular tachycardia was 99% at 1 year and 96% at 5 years. The combination of revascularization and ventricular reconstruction appears to be very effective in preventing arrhythmia recurrence in these patients.
Modified Linear Closure Technique for Ventricular Reconstruction Since 1983 in patients with ischemic cardiomyopathy and akinetic or dyskinetic scar we have used a modified linear closure technique combined with patch septoplasty when indicated [12]. This approach can be compared with more complex techniques such as the purse string technique of Jatene [24], the endoventricular circuloplasty of Dor [2], or the endoaneurysmorrhaphy of Cooley [25]. In most cases in our series the area of resection was anteroapical in location (90%). Major indi-
CIRCULATORY SUPPORT MICKLEBOROUGH ET AL VENTRICULAR RECONSTRUCTION
S9
Fig 3. With the patient on cardiopulmonary bypass the heart is opened through the thinned area and the surrounding edges are palpated to assess contractility and wall thickening. Areas that do not contract in the unloaded state are considered for excision. (Reprinted with permission from Mickleborough LL. Left ventricular aneurysm: modified linear closure. In: Cox JL, Sundt TM, eds. Operative techniques in cardiac and thoracic surgery: a comparative atlas. Philadelphia: WB Saunders, 1997;2:118 –31.)
cations for surgery were often multiple and included angina in 56%, heart failure in 60%, and ventricular arrhythmias in 45%. In these patients it was often difficult to determine whether shortness of breath was a reflection of ischemia (anginal equivolent) or heart failure. Most of our patients were in symptom class III or IV preoperatively (83%). The mean ejection fraction was 25% ⫾ 8%. Significant mitral regurgitation was present in 45% (3 to 4⫹ in 14%).
Operative Procedure With the patient on cardiopulmonary bypass at normothermia the heart is carefully examined. We avoid insertion of a ventricular vent, which may disrupt and embolize intraventricular clot. If the area of akinesis or dykinesis consists of a mixture of viable muscle and scar, relative thinning is confirmed by needle aspiration [13]. A small incision is made and any clot present is removed. With the unloaded heart open and beating the surrounding wall is palpated (Fig 3) and its ability to contract (regional wall thickening) is assessed. All thinned nonfunctioning portions of the wall are considered for resection. We preserve the LAD vessel whenever possible even if it is running in scar because we believe it may be important as a conduit for collateral circulation and intraoperative myocardial preservation.
S10
CIRCULATORY SUPPORT MICKLEBOROUGH ET AL VENTRICULAR RECONSTRUCTION
Ann Thorac Surg 2003;75:S6 –12
Fig 4. Technique of septal aneurysm patch exclusion. (A) Apical aneurysm with significant thinning and aneurysmal involvement of the distal septum. (B) Pericardial patch is sewn to preserved normal area of the septum on three sides. (C) Patch is pulled tight and the anterior edge incorporated into the modified linear closure effectively excluding the aneurysmal portion of the septum from the residual left ventricle cavity.
The extent of scarring, thinning, and bulging of the septum is evaluated. Whatever portion is significantly aneurysmal (concave toward the right ventricle) is excluded by attaching a patch of bovine preserved pericardium to the normal portion of the septum on three sides using a running 4-0 Prolene (Ethicon, Somerville, NJ) suture. The anterior edge of the patch is incorporated in the modified linear closure (Fig 4). The size and shape of the remaining ventricular cavity are evaluated in the open beating heart. Excision is planned to remove as much nonfunctioning wall as possible while restoring ventricular size and shape toward normal using a modified linear closure technique [13]. Felt strips are used and 2-0 Prolene mattress sutures are placed farther apart on the tissue edge than on the felt so that the length of the incision is plicated in the closure (Fig 5). That helps to restore the shape of the ventricle toward normal. Once ventricular repair has been completed bypass grafting is carried out including a graft to the proximal LAD whenever possible. Retrograde cardioplegia is used for protection of the left ventricle and antegrade cardioplegia or infusion down a graft is used to protect the right ventricle. In patients with extensive scarring of the septum visually directed endocardial excision and cryoablation at the periphery of the scar is carried out as previously described [12, 21]. Details of the operative procedure in our series of 193 patients are given in Table 1. All but 15 patients received aortocoronary bypass grafting. Most of the procedure was carried out on the open beating heart. Average cross-clamp time was only 60 ⫾ 24 minutes although average pump time was prolonged. All patients were successfully weaned from bypass but 56% required inotrope support and 18% required intraaortic balloon pump support.
Results Hospital mortality was 2.6%. Two deaths were due to adult respiratory distress syndrome in patients on amiodarone therapy [26]. Perioperative complications were
Fig 5. Principle of modified linear closure technique. (A) Thinned edges of the aneurysm are retracted with Babcock clamps. The thinned noncontractile area is excised. (B) The excision has been completed. The defect is closed with mattress sutures of 2-0 Prolene buttressed by felt strips. Mattress sutures are placed with wider bites on the tissue edge and narrower bites on the felt strips. (C) Tying the sutures leads to longitudinal plication of the incision, which helps restore the shape of distal left ventricle cavity toward normal. The closure is reenforced with a continuous over and over suture to ensure hemostasis. (Reprinted with permission from Mickleborough LL. Left ventricular aneurysm: modified linear closure. In: Cox JL, Sundt TM, eds. Operative techniques in cardiac and thoracic surgery: a comparative atlas. Philadelphia: WB Saunders, 1997;2:118 –31.)
rare: 1.6% myocardial infarction, 2.1% reoperation for bleeding, 1.0% sternal infection, 1.0% transient ischemic attack, and 0.5% stroke. These patients require careful follow-up postoperatively. In the first few months medical therapy for heart Table 1. Details of the Operative Procedure in 193 Patients Patch septoplasty Ventricular tachycardia ablation Removal of clot Coronary artery bypass graft (average 2.6 ⫾ 1.3 grafts per patient) No cross clamp Average cross clamp time Average pump time
24 (12%) 77 (40%) 55 (29%) 175 (91%)
15 (8%) 59 ⫾ 25 minutes 174 ⫾ 56 minutes
Ann Thorac Surg 2003;75:S6 –12
failure has to be frequently assessed as the patient adjusts to the effects of the ventricular reconstruction. At long-term follow-up symptoms improved in 78% of patients (41% in symptom class I and 38% in symptom class II). The average increase in symptom class was 1.4 ⫾ 1.0 class. Multigated acquisition nuclear scanning (MUGA) assessment preoperatively and postoperatively in patients with anterior resection showed a significant increase in ejection fraction of 8.9% ⫾ 9.6% (p ⬍ 0.001). In patients with significant mitral regurgitation (2⫹ or more) 57% showed improvement by at least 1 mitral regurgitation grade postoperatively [12]. During follow-up, which extends to 14 years (mean, 51 ⫾ 44 months), 7 patients required cardiac transplantation at a mean interval of 36 ⫾ 32 months. One patient required mitral valve replacement, 5 patients required pacemaker insertion for bradyarrhythmias, and 1 patient required an ICD for ventricular tachycardia. There have been 31 late deaths, most due to congestive heart failure with or without mitral insufficiency. Actuarial survival was 91% at 1 year, 89% at 2 years, and 84% at 5 years. Freedom from sudden death or recurrent ventricular tachycardia was 99%% at 1 and 2 years and 96% at 5 years.
Thoughts on the STICH Trial We are convinced that revascularization is of benefit in patients with coronary artery disease and poor left ventricular function whether or not they present with angina, congestive heart failure, or ventricular arrhythmias. We are also convinced that revascularization provides a survival benefit in asymptomatic patients with critical disease, namely triple vessel disease or left main stem stenosis. However some of our medical colleagues are still unconvinced and recommend medical treatment with or without an ICD for these patients. This is why the surgical treatment of ischemic heart failure (STICH) trial was designed to compare medical versus surgical treatment in patients with coronary artery disease and poor left ventricular function. Although we and many of my surgical colleagues are not comfortable randomizing patients to the medical arm of stratum A or B of the STICH trial, we hope that enough patients will be recruited for comparison of medical versus surgical therapy and that practice patterns may be altered accordingly. We are also convinced that ventricular reconstruction improves prognosis and controls ventricular arrhythmias and symptoms of ischemia and heart failure in patients with large areas of akinetic or dyskinetic scar. In these patients we will continue to perform ventricular reconstruction procedures excluding them from randomization in stratum C of the STICH trial. For us the point of equipoise is the patient with coronary artery disease, moderate dilatation of the heart, and an akinetic scar associated with a relatively small area of thinning. These are the patients we would be comfortable randomly assigning to the revascularization plus reconstruction versus revascularization alone arm of the STICH trial (stratum C). Doctor Buckberg and his associates have
CIRCULATORY SUPPORT MICKLEBOROUGH ET AL VENTRICULAR RECONSTRUCTION
S11
advocated ventricular reconstruction in patients who have no area of relative thinning. This approach involves making an incision through relatively thick myocardium. We believe these patients would have been better served with revascularization alone. Some centers will enroll these patients in the reconstruction arm of the STICH trial. At completion of the study we will be more able to choose appropriate surgical therapy for patients with ischemic cardiomyopathy.
Comment Based on our current experience as outlined in this report, we recommend an aggressive approach to revascularization and ventricular reconstruction in patients with coronary artery disease and poor ventricular function. In such patients we believe that areas of akinesis or dyskinesis associated with relative thinning should be excised to restore ventricular size and shape toward normal and to prevent progressive adverse ventricular remodeling. If repair is delayed, contractile function of the residual viable muscle may deteriorate with progressive decrease in ejection fraction, chamber dilatation, and increasing mitral insufficiency, all of which are associated with a less satisfactory surgical result [12]. The tendency for ventricular arrhythmias increases with ventricular dilatation and increased wall stress. Like Dor and colleagues [27] we recommend early repair because surgical risks in these patients are low [12]. We differ from Dor’s approach in our choice of reconstruction technique. We believe that septoplasty should be employed only when a septal aneurysm has occurred. We suggest that the modified linear repair technique is technically easier to perform than the Dor procedure. The repair is performed in the open beating ventricle, which makes it easier to identify areas of nonfunctioning myocardium for resection or exclusion. It also is easier in the beating heart to estimate the volume and shape of the residual reconstructed cavity in order to avoid rare cases of decreased cardiac output due to insufficient cavity size after repair. We believe our technique restores a more normal conical shape to the apex of the ventricle, which may be important in optimizing long-term results. We suggest that patients in whom akinetic or dyskinetic areas develop after infarction should be followed up closely and considered for surgical treatment when signs of decompensation such as increasing symptoms with optimal medical management first occur or in asymptomatic patients if there is evidence of increasing ventricular volume or mitral insufficiency. The salutary effects of revascularization and ventricular reconstruction on the occurrence of ventricular arrhythmias in these patients should not be underestimated. Operation should be considered before these patients reach the stage of gross ventricular dilatation and severe mitral insufficiency when transplantation may be the only reasonable option.
S12
CIRCULATORY SUPPORT MICKLEBOROUGH ET AL VENTRICULAR RECONSTRUCTION
Ann Thorac Surg 2003;75:S6 –12
References 1. Mickleborough LL, Maruyama H, Liu P, Mohammed S. Results of left ventricular aneurysmectomy with a tailored scar excision and primary closure technique. J Thorac Cardiovasc Surg 1994;107:690 –8. 2. 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 –9. 3. Langenburg SE, Buchanan SA, Blackbourne LH, et al. Predicting survival after coronary revascularization for ischemic cardiomyopathy. Ann Thorac Surg 1995;60:1193–7. 4. Mickleborough LL, Carson S, Ivanov J. Gender differences in quality of distal vessels: effect on results of coronary artery bypass grafting. J Thorac Cardiovasc Surg. 2002. In press. 5. Mickleborough LL, Carson S, Tamariz M, Ivanov J. Results of revascularization in patients with severe left ventricular dysfunction. J Thorac Cardiovasc Surg 2000;119:550 –7. 6. DiCarli MF, Asgarzadie F, Schelbert HR, et al. Quantitative relation between myocardial viability and improvement in heart failure symptoms after revascularization in patients with ischemic cardiomyopathy. Circulation 1995;92:3436 –44. 7. DiCarli MF, Maddahi J, Rokhsar S, et al. Long-term survival of patients with coronary artery disease, and left ventricular dysfunction. Implications for the role of myocardial viability assessment in management decisions. J Thorac Cardiovasc Surg 1999;116:997–1004. 8. Afridi I, Grayburn PA, Panza JA, Oh JK, Zoghbi WA, Marwick TH. Myocardial viability during dobutamine echocardiography predicts survival in patients with coronary artery disease and severe left ventricular systolic dysfunction. J Am Coll Cardiol 1998;32:921–6. 9. Yamaguchi A, Takashi I, Adachi H, et al. Left ventricular volume predicts postoperative course in patients with ischemic cardiomyopathy. Ann Thorac Surg 1998;65:434 –8. 10. Salati M, Lemma M, Di Mattia DG, et al. Myocardial revascularization in patients with ischemic cardiomyopathy: functional observations. Ann Thorac Surg 1997;64:1728 –34. 11. Athanasuleas CL, Stanley AWH Jr, Buckberg GD, et al. Surgical anterior ventricular endocardial restoration (SAVER) in the dilated remodeled ventricle after anterior myocardial infarction. J Am Coll Cardiol 2001;37:1199 –209. 12. 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: 675–82. 13. Mickleborough LL. Left ventricular aneurysm: modified linear closure technique. In: Cox JL, Sundt TM, eds. Operative techniques in cardiac and thoracic surgery. Philadelphia: WB Saunders 1997;2:118 –31. 14. Dickstein ML, Spotnitz HM, Rose EA, Burkhoff D. Heart
15.
16.
17. 18.
19.
20.
21. 22.
23.
24. 25. 26. 27.
reduction surgery: an analysis of the impact on cardiac function. J Thorac Cardiovasc Surg 1997;113:1032–41. Ratcliffe MB, Hong J, Salahieh A, Ruch S, Wallace AW. The effect of ventricular volume reduction surgery in the dilated, poorly contractile left ventricle: a simple finite element analysis. J Thorac Cardiovasc Surg 1998;116:566 –77. Di Donato M, Sabatier M, Dor V, et al. Effects of the Dor procedure on left ventricular dimension and shape and geometric correlates of mitral regurgitation one year after surgery. J. Thorac Cardiovas Surg 2001;121:91–6. Bolling SF, Pagani FD, Deals GM, Bash DS. Intermediate term outcome of mitral reconstruction in cardiomyopathy. J Thorac Cardiovasc Surg 1998;115:381–6. Konstantinov I, Mickleborough LL, Graba J, Merchant N. Intraventricular mitral annuloplasty technique for use with repair of posterior left ventricular aneurysm. J Thorac Cardiovasc Surg 2001;1221244 –7. Bigger JT, for the Coronary Artery Bypass Graft (CABG) Patch Trial Investigators. Prophylactic use of implanted cardiac defibrillators in patients at high risk for ventricular arrhythmias after coronary artery bypass graft surgery. N Engl J Med 1997;337:1569 –75. Moss AJ, Hall WJ, Cannom DS, et al, for the Multicenter Automatic Defibrillator Implantation Trial Investigators. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmias. N Engl J Med 1996;335:1933–40. Mickleborough LL, Mizuno S, Downar E, et al. Late results with surgery for ventricular tachycardia. Ann Thorac Surg 1992;54:832–9. Mickleborough LL, Usui A, Downar E, Harris L, Parson I, Gray G. Transatrial balloon technique for activation mapping during operations for recurrent ventricular tachycardia. J Thorac Cardiovasc Surg 1990;99:227–33. Downar E, Kimber S, Harris L, et al. Endocardial mapping of ventricular tachycardia in the intact human heart. II. Evidence for multiuse reentry in a functional sheet of surviving myocardium. J Am Coll Cardiol 1992;20:869 –78. Jatene AD. Left ventricular aneurysmectomy. J Thorac Cardiovasc Surg 1985;89:321–31. Cooley DA. Ventricular endoaneurysmorrhaphy; A simplified repair for extensive postinfarction aneurysm. J Card Surg 1989;4:200 –5. Mickleborough LL, Maruyama H, Mohammed S, et al. Are patients receiving amiodarone at increased risk for cardiac operations? Ann Thorac Surg 1994;58:622–9. Di Donato M, Sabatier M, Dor V, Toso A, Maioli M, Fantini F. Akinetic versus dyskinetic postinfarction scar: relation to surgical outcome in patients undergoing endoventricular circular patch plasty repair. J Am Coll Cardiol 1997;29:1569 – 75.
Left ventricular surgical reconstruction has been advocated for patients with coronary artery disease, prior myocardial infarction, and poor left ventricular function. The objective of the approach is to resect or exclude all akinetic or dyskinetic nonfunctioning portions of the ventricular cavity and to restore the left ventricle size and shape toward normal as much as possible. We review the pathophysiology of ischemic cardiomyopathy and suggest guidelines for preoperative assessment and patient selection for ventricular reconstruction. Because of the prevalence and prognostic significance of ventricular arrhythmias in this patient population we include in our operative approach a visually directed ablation procedure in those with significant septal scarring. We describe our operative technique and review results
achieved with this approach. The procedure results in a significant decrease in ventricular volume, increase in ejection fraction and improvement in apical geometry. We conclude that in selected patients with ischemic cardiomyopathy, left ventricular reconstruction can be accomplished with low operative mortality and results in significant improvement in left ventricular function. During follow up symptom class is decreased in most patients and overall survival at 5 years is 84% and freedom from sudden death is 96%. Ventricular reconstruction should be considered in all patients with coronary artery disease and akinetic or dyskinetic scar.
T
surgery, ventricular surgical remodeling, or surgical anterior ventricular endocardial restoration the basic priniciples are the same.
he treatment of ischemic heart disease continues to be a challenge with an ever-increasing patient population presenting with congestive failure. In patients with coronary disease and a previous infarct the goal of surgery should be not only to prevent ongoing ischemia but also to minimize the negative effects of the infarct on ventricular structure and function. In valvular disease, surgery is often recommended early to prevent adverse ventricular remodeling. Similarly in ischemic heart disease when significant ventricular scarring has occurred surgical reconstruction should be done to prevent progressive deterioration of heart function over time. For years we and others [1, 2] have advocated the removal of akinetic or dyskinetic scar. The goals of the procedure are to revascularize wherever possible, to resect or exclude all nonfunctioning portions of the ventricular cavity, and to restore size and shape toward normal as much as possible. This results in decreased ventricular volume and decreased wall tension and wall stress that decreases ischemia in the remaining viable myocardium, improves heart failure symptoms, and decreases the incidence of ventricular arrhythmias or the severity of associated mitral insufficiency. Whether such a procedure is called aneurysm resection, heart reduction Presented at the Heart Failure & Circulatory Support Summit, Cleveland, OH, Aug 22–25, 2002. Address reprint requests to Dr Mickleborough, Toronto General Hospital, 200 Elizabeth St, Toronto, Ontario, Canada M5G 2C4; e-mail: [email protected].
© 2003 by The Society of Thoracic Surgeons Published by Elsevier Inc
(Ann Thorac Surg 2003;75:S6 –12) © 2003 by The Society of Thoracic Surgeons
Pathophysiology After myocardial infarction necrotic muscle is replaced by fibrous tissue. When significant scarring occurs an area of relative thinning often results along the distribution of the culprit vessel (elliptical in shape). The amount of thinning and whether a classic dyskinetic aneurysm occurs depends on many factors including speed of development and extent of collateral circulation as well as healing properties of the heart that may be influenced by advanced age, sex, or corticosteroid use. To compensate for loss of contractile function of the infarcted segment the ventricular chamber dilates. That results in increased wall tension, decreased systolic shortening, and increased oxygen consumption in areas remote from the original infarct. In some cases the infarcted area shows little infarct expansion and it may take many years for adverse ventricular remodeling to occur. In other cases there is rapid development of an obvious dyskinetic aneurysm and heart failure symptoms. Expansion and thinning of the infarct may produce additional work because of paradoxic motion of the thinned segment and may result in malalignment of muscle fibers in surrounding contractile segments leading to further decrease in efficiency of contraction. Scarring and dilatation associated with aneurysm formation 0003-4975/03/$30.00 PII S0003-4975(03)00464-8
Ann Thorac Surg 2003;75:S6 –12
CIRCULATORY SUPPORT MICKLEBOROUGH ET AL VENTRICULAR RECONSTRUCTION
S7
akinesis or dyskinesis. We believe these are the very patients who will benefit from ventricular reconstruction. To summarize our approach in patients with poor LV function, if regional wall motion abnormalities associated with thinning can be identified we believe these areas should be considered for possible resection. On the other hand even in dilated hearts we have not resected akinetic areas where thinning has not occurred as advocated by Buckberg and coworkers [11]. Rather we have revascularized these areas hoping to recruit hibernating myocardium and improve ventricular function. Using this approach we have achieved good results in patients with poor LV function either with revascularization alone (operating room mortality 4%, 5-year survival 72%) [5] or with revascularization and LV reconstruction (operating room mortality 3%, 5-year survival 84%) [12]. Fig 1. Magnetic resonance image in a patient with prior anteroapical infarct. There is thinning at the apex. The septum is still well preserved and of normal thickness. The left ventricular cavity is dilated. The end diastolic volume index (EDVI) is 112 mL/m2 and end systolic volume index (ESVI) is 77 mL/m2.
may provide a subtrate for ventricular arrhythmias. If papillary muscles are involved in the original infarct or if changes in ventricular geometry interfere with function of the subvalvular apparatus, mitral regurgitation may occur. We believe that whenever an infarct results in an area of akinesia or dyskinesia surgery has something to offer.
Revascularization With or Without Surgical Remodeling In patients with coronary artery disease the benefits of surgical revascularization in terms of increased longevity and decreased symptoms are most obvious in those with poor ventricular function. Because the risks of surgery are slightly increased in these cases there may be reluctance to operate if there is less than ideal distal coronary anatomy [3]. In many patients with anteroapical akinesis and no significant thinning the left anterior descending artery (LAD) is totally occluded proximally and not well visualized on the angiogram. That raises concern over the possibility of incomplete revascularization and such patients may be considered poor candidates for surgery. In our experience, in such patients revascularization of the LAD is almost always possible even though the distal vessel may be 1 mm in size or diffusely diseased [4]. Using an aggressive approach to revascularization we have reported excellent results even in patients with an ejection fraction less than 20% [5]. In many centers great effort is made to identify a subset of patients who would most benefit from revascularization [6 – 8]. Patients with reversible ischemia are most likely to show significant improvement in ventricular function with revascularization alone. However recent studies have pointed out that the benefits of revascularization may be limited if left ventricular (LV) volumes are grossly increased [9] or if there is evidence of asymmetry of ventricular motion [10], namely localized areas of
Ventricular Reconstruction: Patient Selection and Preoperative Assessment Ventriculography can identify areas of wall motion abnormality (akinesia or dyskinesia). Biplane views are essential to assess involvement of the septum. Angiography however provides no information with regard to extent or distribution of wall thinning. Using echocardiographic techniques in dilated poorly functioning hearts it is often difficult to accurately assess size and function at the apex. In the past in patients with low ejection fraction we evaluated the extent of wall thinning intraoperatively using needle aspiration [13]. Since 1998 we have used magnetic resonance imaging (MRI) to obtain preoperative assessment of ventricular shape and volume (Fig 1). Magnetic resonance imaging also provides information about regional wall function and thinning which has allowed us to decide preoperatively whether a patient with poor LV function is a candidate for revascularization alone (no thinning) or in combination with surgical reconstruction.
Effects of LV Reconstruction: Limitations of Studies to Date In an attempt to understand the pathophysiology of abnormal ventricular function, to aid in the choice of patients for surgery and to determine which of several available reconstruction techniques should yield optimal results, various computer models have been used [14, 15]. However these analyses make assumptions about the physical properties of the tissue excised and about function of the surrounding myocardium. In our experience the physical properties of the excised tissue varies widely depending on whether the resected wall is akinetic or dyskinetic and whether it is calcified or not. Furthermore resection may have different effects on the size and function of the remaining chamber depending on the techniques of myocardial preservation and ventricular reconstruction used and the completeness of revascularization achieved. Many groups using a variety of repair techniques have reported decreased volume and increased ejection frac-
S8
CIRCULATORY SUPPORT MICKLEBOROUGH ET AL VENTRICULAR RECONSTRUCTION
Ann Thorac Surg 2003;75:S6 –12
Fig 2. Preoperative (left) and postoperative (right) magnetic resonance imaging. Preoperatively an anteroapical aneurysm involves the distal portion of the septum; the apex is globular in shape. Postoperatively a septal patch has excluded the aneurysmal septum and is incorporated anteriorly into the modified linear closure. The space between the patch and the septal aneurysm has been filled with clot. Ventricular volume is decreased and the shape of the apex has been restored toward normal, namely more conical.
tion after repair [2, 11, 12]. Dor and coworkers [16] who advocate the endoventricular patch technique have reported extensively on postoperative changes in ventricular function and shape. That group reported increased sphericity after repair which seems counterintuative given their excellent clinical results. We have used a different technique (modified linear closure with patch septoplasty when indicated) and have demonstrated with preoperative and postoperative MRI a more conical shape after the repair (Fig 2). Clearly further studies are needed to document effects of these procedures on ventricular geometry, shape, and function.
Anteroapical Location of Scar Most patients in whom ventricular reconstruction is indicated have anteroapical scarring which often extends over the apex to involve the distal inferior wall. There is a great deal of variability in size and extent of thinning of the area involved. In particular the extent of septal scarring and thinning is extremely variable (Fig 1) [12]. Whenever significant septal thinning and dyskinesis occur the reconstruction technique should exclude this part of the dysfunctional ventricle.
Mitral Regurgitation In patients with ischemic cardiomyopathy, mitral regurgitation may be related to several possible mechanisms. Papillary muscle ischemia may contribute to mitral regurgitation. Adverse ventricular remodeling with regional displacement of the ventriclar wall or chamber dilatation may lead to mitral regurgitation, which may not respond to revascularization alone. Resection of akinetic or dyskinetic scar with restoration of ventricular size and geometry toward normal may improve valve function or annuloplasty as advocated by Bolling and coworkers [17] may partially compensate for malfunction of the subvalvular apparatus. In our experience resection
of akinetic or dykinetic scar and revascularization often significantly improve valve function [12]. In selected cases we have added mitral valvoplasty to the repair [18]. After ventricular reconstruction when significant mitral regurgitation persists on intraoperative echocardiography, mitral valve replacement may be required.
Ventricular Arrhythmias In patients with ischemic cardiomyopathy, ventricular arrhythmias are a major source of morbidity and mortality. In these patients the value of complete revascularization in reducing arrhythmia recurrence should not be underestimated. For example the Coronary Artery Bypass Graft (CABG) Patch trial [19] compared arrhythmia occurrence and long-term survival in patients with poor ejection fraction (⬍ 35%) and an abnormal signalaveraged electrocardiogram who underwent revascularization. This important trial showed that patients undergoing revascularization did not benefit from implantable cardiac defibrillator (ICD) implantation, presumably owing to the positive effect of grafting on the arrhythmia substrate (relief of ischemia or improvement of ventricular function). In contrast the MADIT study [20] showed a survival benefit after ICD implantation in patients with low ejection fraction (⬍ 35%), nonsustained ventricular tachycardia, and inducible ventricular tachycardia. Patients were excluded from this trial if they were candidates for concurrent revascularization (within 3 months). Clearly the patient populations in these two studies are not comparable. It seems obvious from the CABG Patch trial results, that revascularization alone using contemporary surgical techniques is of significant benefit in preventing recurrence of ventricular arrhythmias in patients with poor ventricular function. When revascularization is combined with ventricular reconstruction the potential benefits of the surgical approach in controlling arrhythmias is even more striking.
Ann Thorac Surg 2003;75:S6 –12
In the past in patients with recurrent sustained ventricular tachycardia, intraoperative mapping and surgical ablation of ventricular tachycardia foci (popular in the early 1990s) taught us important lessons about the pathophysiology of the arrhythmias [21]. These patients usually had large dilated hearts with akinetic or dyskinetic scar. Use of an intraventricular mapping balloon demonstrated very graphically that ease of induction of arrhythmias was critically related to mechanical loading conditions of the heart [22]. As the balloon was inflated ventricular arrhythmias were easily induced. Therefore any procedure that restores ventricular volume and size toward normal (such as ventricular construction) is likely to reduce the inducibility or occurrence of ventricular arrhythmias. Mapping studies in patients with anteroapical scarring showed that the anatomic substrate for ventricular arrhythmias was located in the borderzone between scar and surrounding normal endocardium on the ventricular septum [23]. Ablation using endocardial excision often combined with cryoablation or creation of homogeneous scar after attachment of a septal patch controlled the arrhythmia. In our series of map-directed surgery freedom from sudden death was excellent 97% at 5 years and overall survival was 79% [21]. For patients with ischemic cardiomyopathy, because ventricular arrhythmias have an important effect on prognosis in those with significant septal scarring, we have included in our approach to ventricular reconstruction a visually directed endocardial excision with cryoablation at the periphery. Our left ventricular reconstruction series includes 86 patients who had recurrent ventricular tachycardia preoperatively and inducible ventricular tachycardia at electrophysiologic study. Clearly these patients are at increased risk for arrhythmias during follow-up. After revascularization and ventricular reconstruction, patients with a history of ventricular tachycardia undergo electrophysiologic testing. Those with inducible or spontaneous tachycardia postoperatively are discharged on a regimen of amiodarone. During follow-up arrhythmia recurrence was only rarely a problem. Only 1 patient in the entire series required an ICD and freedom from sudden death or recurrent ventricular tachycardia was 99% at 1 year and 96% at 5 years. The combination of revascularization and ventricular reconstruction appears to be very effective in preventing arrhythmia recurrence in these patients.
Modified Linear Closure Technique for Ventricular Reconstruction Since 1983 in patients with ischemic cardiomyopathy and akinetic or dyskinetic scar we have used a modified linear closure technique combined with patch septoplasty when indicated [12]. This approach can be compared with more complex techniques such as the purse string technique of Jatene [24], the endoventricular circuloplasty of Dor [2], or the endoaneurysmorrhaphy of Cooley [25]. In most cases in our series the area of resection was anteroapical in location (90%). Major indi-
CIRCULATORY SUPPORT MICKLEBOROUGH ET AL VENTRICULAR RECONSTRUCTION
S9
Fig 3. With the patient on cardiopulmonary bypass the heart is opened through the thinned area and the surrounding edges are palpated to assess contractility and wall thickening. Areas that do not contract in the unloaded state are considered for excision. (Reprinted with permission from Mickleborough LL. Left ventricular aneurysm: modified linear closure. In: Cox JL, Sundt TM, eds. Operative techniques in cardiac and thoracic surgery: a comparative atlas. Philadelphia: WB Saunders, 1997;2:118 –31.)
cations for surgery were often multiple and included angina in 56%, heart failure in 60%, and ventricular arrhythmias in 45%. In these patients it was often difficult to determine whether shortness of breath was a reflection of ischemia (anginal equivolent) or heart failure. Most of our patients were in symptom class III or IV preoperatively (83%). The mean ejection fraction was 25% ⫾ 8%. Significant mitral regurgitation was present in 45% (3 to 4⫹ in 14%).
Operative Procedure With the patient on cardiopulmonary bypass at normothermia the heart is carefully examined. We avoid insertion of a ventricular vent, which may disrupt and embolize intraventricular clot. If the area of akinesis or dykinesis consists of a mixture of viable muscle and scar, relative thinning is confirmed by needle aspiration [13]. A small incision is made and any clot present is removed. With the unloaded heart open and beating the surrounding wall is palpated (Fig 3) and its ability to contract (regional wall thickening) is assessed. All thinned nonfunctioning portions of the wall are considered for resection. We preserve the LAD vessel whenever possible even if it is running in scar because we believe it may be important as a conduit for collateral circulation and intraoperative myocardial preservation.
S10
CIRCULATORY SUPPORT MICKLEBOROUGH ET AL VENTRICULAR RECONSTRUCTION
Ann Thorac Surg 2003;75:S6 –12
Fig 4. Technique of septal aneurysm patch exclusion. (A) Apical aneurysm with significant thinning and aneurysmal involvement of the distal septum. (B) Pericardial patch is sewn to preserved normal area of the septum on three sides. (C) Patch is pulled tight and the anterior edge incorporated into the modified linear closure effectively excluding the aneurysmal portion of the septum from the residual left ventricle cavity.
The extent of scarring, thinning, and bulging of the septum is evaluated. Whatever portion is significantly aneurysmal (concave toward the right ventricle) is excluded by attaching a patch of bovine preserved pericardium to the normal portion of the septum on three sides using a running 4-0 Prolene (Ethicon, Somerville, NJ) suture. The anterior edge of the patch is incorporated in the modified linear closure (Fig 4). The size and shape of the remaining ventricular cavity are evaluated in the open beating heart. Excision is planned to remove as much nonfunctioning wall as possible while restoring ventricular size and shape toward normal using a modified linear closure technique [13]. Felt strips are used and 2-0 Prolene mattress sutures are placed farther apart on the tissue edge than on the felt so that the length of the incision is plicated in the closure (Fig 5). That helps to restore the shape of the ventricle toward normal. Once ventricular repair has been completed bypass grafting is carried out including a graft to the proximal LAD whenever possible. Retrograde cardioplegia is used for protection of the left ventricle and antegrade cardioplegia or infusion down a graft is used to protect the right ventricle. In patients with extensive scarring of the septum visually directed endocardial excision and cryoablation at the periphery of the scar is carried out as previously described [12, 21]. Details of the operative procedure in our series of 193 patients are given in Table 1. All but 15 patients received aortocoronary bypass grafting. Most of the procedure was carried out on the open beating heart. Average cross-clamp time was only 60 ⫾ 24 minutes although average pump time was prolonged. All patients were successfully weaned from bypass but 56% required inotrope support and 18% required intraaortic balloon pump support.
Results Hospital mortality was 2.6%. Two deaths were due to adult respiratory distress syndrome in patients on amiodarone therapy [26]. Perioperative complications were
Fig 5. Principle of modified linear closure technique. (A) Thinned edges of the aneurysm are retracted with Babcock clamps. The thinned noncontractile area is excised. (B) The excision has been completed. The defect is closed with mattress sutures of 2-0 Prolene buttressed by felt strips. Mattress sutures are placed with wider bites on the tissue edge and narrower bites on the felt strips. (C) Tying the sutures leads to longitudinal plication of the incision, which helps restore the shape of distal left ventricle cavity toward normal. The closure is reenforced with a continuous over and over suture to ensure hemostasis. (Reprinted with permission from Mickleborough LL. Left ventricular aneurysm: modified linear closure. In: Cox JL, Sundt TM, eds. Operative techniques in cardiac and thoracic surgery: a comparative atlas. Philadelphia: WB Saunders, 1997;2:118 –31.)
rare: 1.6% myocardial infarction, 2.1% reoperation for bleeding, 1.0% sternal infection, 1.0% transient ischemic attack, and 0.5% stroke. These patients require careful follow-up postoperatively. In the first few months medical therapy for heart Table 1. Details of the Operative Procedure in 193 Patients Patch septoplasty Ventricular tachycardia ablation Removal of clot Coronary artery bypass graft (average 2.6 ⫾ 1.3 grafts per patient) No cross clamp Average cross clamp time Average pump time
24 (12%) 77 (40%) 55 (29%) 175 (91%)
15 (8%) 59 ⫾ 25 minutes 174 ⫾ 56 minutes
Ann Thorac Surg 2003;75:S6 –12
failure has to be frequently assessed as the patient adjusts to the effects of the ventricular reconstruction. At long-term follow-up symptoms improved in 78% of patients (41% in symptom class I and 38% in symptom class II). The average increase in symptom class was 1.4 ⫾ 1.0 class. Multigated acquisition nuclear scanning (MUGA) assessment preoperatively and postoperatively in patients with anterior resection showed a significant increase in ejection fraction of 8.9% ⫾ 9.6% (p ⬍ 0.001). In patients with significant mitral regurgitation (2⫹ or more) 57% showed improvement by at least 1 mitral regurgitation grade postoperatively [12]. During follow-up, which extends to 14 years (mean, 51 ⫾ 44 months), 7 patients required cardiac transplantation at a mean interval of 36 ⫾ 32 months. One patient required mitral valve replacement, 5 patients required pacemaker insertion for bradyarrhythmias, and 1 patient required an ICD for ventricular tachycardia. There have been 31 late deaths, most due to congestive heart failure with or without mitral insufficiency. Actuarial survival was 91% at 1 year, 89% at 2 years, and 84% at 5 years. Freedom from sudden death or recurrent ventricular tachycardia was 99%% at 1 and 2 years and 96% at 5 years.
Thoughts on the STICH Trial We are convinced that revascularization is of benefit in patients with coronary artery disease and poor left ventricular function whether or not they present with angina, congestive heart failure, or ventricular arrhythmias. We are also convinced that revascularization provides a survival benefit in asymptomatic patients with critical disease, namely triple vessel disease or left main stem stenosis. However some of our medical colleagues are still unconvinced and recommend medical treatment with or without an ICD for these patients. This is why the surgical treatment of ischemic heart failure (STICH) trial was designed to compare medical versus surgical treatment in patients with coronary artery disease and poor left ventricular function. Although we and many of my surgical colleagues are not comfortable randomizing patients to the medical arm of stratum A or B of the STICH trial, we hope that enough patients will be recruited for comparison of medical versus surgical therapy and that practice patterns may be altered accordingly. We are also convinced that ventricular reconstruction improves prognosis and controls ventricular arrhythmias and symptoms of ischemia and heart failure in patients with large areas of akinetic or dyskinetic scar. In these patients we will continue to perform ventricular reconstruction procedures excluding them from randomization in stratum C of the STICH trial. For us the point of equipoise is the patient with coronary artery disease, moderate dilatation of the heart, and an akinetic scar associated with a relatively small area of thinning. These are the patients we would be comfortable randomly assigning to the revascularization plus reconstruction versus revascularization alone arm of the STICH trial (stratum C). Doctor Buckberg and his associates have
CIRCULATORY SUPPORT MICKLEBOROUGH ET AL VENTRICULAR RECONSTRUCTION
S11
advocated ventricular reconstruction in patients who have no area of relative thinning. This approach involves making an incision through relatively thick myocardium. We believe these patients would have been better served with revascularization alone. Some centers will enroll these patients in the reconstruction arm of the STICH trial. At completion of the study we will be more able to choose appropriate surgical therapy for patients with ischemic cardiomyopathy.
Comment Based on our current experience as outlined in this report, we recommend an aggressive approach to revascularization and ventricular reconstruction in patients with coronary artery disease and poor ventricular function. In such patients we believe that areas of akinesis or dyskinesis associated with relative thinning should be excised to restore ventricular size and shape toward normal and to prevent progressive adverse ventricular remodeling. If repair is delayed, contractile function of the residual viable muscle may deteriorate with progressive decrease in ejection fraction, chamber dilatation, and increasing mitral insufficiency, all of which are associated with a less satisfactory surgical result [12]. The tendency for ventricular arrhythmias increases with ventricular dilatation and increased wall stress. Like Dor and colleagues [27] we recommend early repair because surgical risks in these patients are low [12]. We differ from Dor’s approach in our choice of reconstruction technique. We believe that septoplasty should be employed only when a septal aneurysm has occurred. We suggest that the modified linear repair technique is technically easier to perform than the Dor procedure. The repair is performed in the open beating ventricle, which makes it easier to identify areas of nonfunctioning myocardium for resection or exclusion. It also is easier in the beating heart to estimate the volume and shape of the residual reconstructed cavity in order to avoid rare cases of decreased cardiac output due to insufficient cavity size after repair. We believe our technique restores a more normal conical shape to the apex of the ventricle, which may be important in optimizing long-term results. We suggest that patients in whom akinetic or dyskinetic areas develop after infarction should be followed up closely and considered for surgical treatment when signs of decompensation such as increasing symptoms with optimal medical management first occur or in asymptomatic patients if there is evidence of increasing ventricular volume or mitral insufficiency. The salutary effects of revascularization and ventricular reconstruction on the occurrence of ventricular arrhythmias in these patients should not be underestimated. Operation should be considered before these patients reach the stage of gross ventricular dilatation and severe mitral insufficiency when transplantation may be the only reasonable option.
S12
CIRCULATORY SUPPORT MICKLEBOROUGH ET AL VENTRICULAR RECONSTRUCTION
Ann Thorac Surg 2003;75:S6 –12
References 1. Mickleborough LL, Maruyama H, Liu P, Mohammed S. Results of left ventricular aneurysmectomy with a tailored scar excision and primary closure technique. J Thorac Cardiovasc Surg 1994;107:690 –8. 2. 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 –9. 3. Langenburg SE, Buchanan SA, Blackbourne LH, et al. Predicting survival after coronary revascularization for ischemic cardiomyopathy. Ann Thorac Surg 1995;60:1193–7. 4. Mickleborough LL, Carson S, Ivanov J. Gender differences in quality of distal vessels: effect on results of coronary artery bypass grafting. J Thorac Cardiovasc Surg. 2002. In press. 5. Mickleborough LL, Carson S, Tamariz M, Ivanov J. Results of revascularization in patients with severe left ventricular dysfunction. J Thorac Cardiovasc Surg 2000;119:550 –7. 6. DiCarli MF, Asgarzadie F, Schelbert HR, et al. Quantitative relation between myocardial viability and improvement in heart failure symptoms after revascularization in patients with ischemic cardiomyopathy. Circulation 1995;92:3436 –44. 7. DiCarli MF, Maddahi J, Rokhsar S, et al. Long-term survival of patients with coronary artery disease, and left ventricular dysfunction. Implications for the role of myocardial viability assessment in management decisions. J Thorac Cardiovasc Surg 1999;116:997–1004. 8. Afridi I, Grayburn PA, Panza JA, Oh JK, Zoghbi WA, Marwick TH. Myocardial viability during dobutamine echocardiography predicts survival in patients with coronary artery disease and severe left ventricular systolic dysfunction. J Am Coll Cardiol 1998;32:921–6. 9. Yamaguchi A, Takashi I, Adachi H, et al. Left ventricular volume predicts postoperative course in patients with ischemic cardiomyopathy. Ann Thorac Surg 1998;65:434 –8. 10. Salati M, Lemma M, Di Mattia DG, et al. Myocardial revascularization in patients with ischemic cardiomyopathy: functional observations. Ann Thorac Surg 1997;64:1728 –34. 11. Athanasuleas CL, Stanley AWH Jr, Buckberg GD, et al. Surgical anterior ventricular endocardial restoration (SAVER) in the dilated remodeled ventricle after anterior myocardial infarction. J Am Coll Cardiol 2001;37:1199 –209. 12. 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: 675–82. 13. Mickleborough LL. Left ventricular aneurysm: modified linear closure technique. In: Cox JL, Sundt TM, eds. Operative techniques in cardiac and thoracic surgery. Philadelphia: WB Saunders 1997;2:118 –31. 14. Dickstein ML, Spotnitz HM, Rose EA, Burkhoff D. Heart
15.
16.
17. 18.
19.
20.
21. 22.
23.
24. 25. 26. 27.
reduction surgery: an analysis of the impact on cardiac function. J Thorac Cardiovasc Surg 1997;113:1032–41. Ratcliffe MB, Hong J, Salahieh A, Ruch S, Wallace AW. The effect of ventricular volume reduction surgery in the dilated, poorly contractile left ventricle: a simple finite element analysis. J Thorac Cardiovasc Surg 1998;116:566 –77. Di Donato M, Sabatier M, Dor V, et al. Effects of the Dor procedure on left ventricular dimension and shape and geometric correlates of mitral regurgitation one year after surgery. J. Thorac Cardiovas Surg 2001;121:91–6. Bolling SF, Pagani FD, Deals GM, Bash DS. Intermediate term outcome of mitral reconstruction in cardiomyopathy. J Thorac Cardiovasc Surg 1998;115:381–6. Konstantinov I, Mickleborough LL, Graba J, Merchant N. Intraventricular mitral annuloplasty technique for use with repair of posterior left ventricular aneurysm. J Thorac Cardiovasc Surg 2001;1221244 –7. Bigger JT, for the Coronary Artery Bypass Graft (CABG) Patch Trial Investigators. Prophylactic use of implanted cardiac defibrillators in patients at high risk for ventricular arrhythmias after coronary artery bypass graft surgery. N Engl J Med 1997;337:1569 –75. Moss AJ, Hall WJ, Cannom DS, et al, for the Multicenter Automatic Defibrillator Implantation Trial Investigators. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmias. N Engl J Med 1996;335:1933–40. Mickleborough LL, Mizuno S, Downar E, et al. Late results with surgery for ventricular tachycardia. Ann Thorac Surg 1992;54:832–9. Mickleborough LL, Usui A, Downar E, Harris L, Parson I, Gray G. Transatrial balloon technique for activation mapping during operations for recurrent ventricular tachycardia. J Thorac Cardiovasc Surg 1990;99:227–33. Downar E, Kimber S, Harris L, et al. Endocardial mapping of ventricular tachycardia in the intact human heart. II. Evidence for multiuse reentry in a functional sheet of surviving myocardium. J Am Coll Cardiol 1992;20:869 –78. Jatene AD. Left ventricular aneurysmectomy. J Thorac Cardiovasc Surg 1985;89:321–31. Cooley DA. Ventricular endoaneurysmorrhaphy; A simplified repair for extensive postinfarction aneurysm. J Card Surg 1989;4:200 –5. Mickleborough LL, Maruyama H, Mohammed S, et al. Are patients receiving amiodarone at increased risk for cardiac operations? Ann Thorac Surg 1994;58:622–9. Di Donato M, Sabatier M, Dor V, Toso A, Maioli M, Fantini F. Akinetic versus dyskinetic postinfarction scar: relation to surgical outcome in patients undergoing endoventricular circular patch plasty repair. J Am Coll Cardiol 1997;29:1569 – 75.