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European Journal of Heart Failure 2005 7(5):704-709; doi:10.1016/j.ejheart.2005.07.005
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© 2005 European Society of Cardiology

Surgical left ventricular remodeling in heart failure

Theis Tønnessena,* and Cathrine Wold Knudsenb

a Department of Cardiothoracic Surgery, Heart and Lung Center Ullevål University Hospital, 0407 Oslo, Norway
b Department of Cardiology, Heart and Lung Center Ullevål University Hospital, 0407 Oslo, Norway

* Corresponding author. Tel.: +47 230 15268 E-mail address: thto{at}uus.no


   Abstract
Top
 Abstract
1. Introduction
 2. Surgical treatment of...
 3. Partial left ventriculectomy...
 4. Other methods of...
 5. Summary
 References
 
The high mortality and morbidity of patients in terminal heart failure are a therapeutic challenge to modern medicine. Surgically, cardiac transplantation is an excellent treatment for many patients. However, lack of donors combined with an increasing number of patients has led to the search for other surgical strategies. Patients with symptomatic large left ventricular aneurysms have been treated with resection of the aneurysm and closure of the left ventricle either directly (linear closure, first reported by Cooley) or by implantation of a patch (endoventricular patch plasty or Dor procedure). Akinetic areas of the left ventricle have also been successfully treated by the latter method. According to the law of Laplace, large dilated ventricles have increased wall tension and thus increased oxygen consumption. Based on this fact, Batista and coworkers have reduced the volume of enlarged left ventricles in patients in terminal heart failure by removing a wedge of myocardium from the apex of the heart towards the base of the left ventricular free wall. Although a favorable outcome has been reported in selected patients, this method is currently not recommended for treatment of heart failure because of high surgical failure rates.

The present paper reviews some of the relevant literature regarding surgical left ventricular remodeling in heart failure. Two new techniques (Myosplint and CorCap cardiac support device) are also briefly described.

Key Words: Left ventricular aneurysm • Dor procedure • Batista procedure • Endoventricular patch plasty • Surgical left ventricular remodeling

Received April 5, 2005; Revised May 22, 2005; Accepted July 11, 2005


   1. Introduction
Top
 Abstract
 1. Introduction
2. Surgical treatment of...
 3. Partial left ventriculectomy...
 4. Other methods of...
 5. Summary
 References
 
Heart failure is a major cause of death in the western population. Five-year survival of patients in heart failure is below 50% and patients in NYHA class III and IV have a 1-year survival below 50% [1]. Besides reduced quality of life, medical treatment and recurrent hospitalization of this group of patients represent a big economic burden to society. The results from several clinical trials have led to improved medical treatment of patients in heart failure. Moreover, surgical treatments such as revascularization of hibernating myocardium in coronary artery disease, as well as correction of valvular disease, are well established treatments which might be crucial to maintain or improve cardiac function. Despite this therapeutic armamentarium, some patients will continue to be in terminal heart failure. The "gold standard" treatment of these patients is heart transplantation. However, lack of donors combined with an increasing number of patients has resulted in the search for other therapies. Some patients might achieve additional benefit from surgical left ventricular remodeling.

If contractility of the left ventricle decreases, stroke volume will be reduced. Trying to compensate for an insufficient stroke volume, the left ventricle dilates. While this might seem a "smart" way of solving the problem in the beginning, the result will in the end turn out to be increased wall stress according to the law of Laplace, and thus increased energy consumption. Moreover, the disorganization of left ventricular architecture taking place as the dilating left ventricle changes from an elliptical towards a spherical form contributes further to the dysfunction. Theoretically, it seems logical to reduce the diameter of the left ventricle in order to reduce wall stress and restore left ventricular function, especially if reducing the diameter can be done by removing non-viable tissue. These theoretical considerations have resulted in various surgical methods trying to help the numerous patients in terminal heart failure.

This review will focus on the most common surgical techniques used in restoring left ventricular shape and function. Among these are resections of aneurysms and non-viable left ventricular tissues (endoventricular patch plasty, Dor procedure, linear closure), and remodeling of viable left ventricular tissues without defined aneurysms (Batista operation). In addition, two new techniques (Myosplint, CorCap cardiac support device) will be briefly presented.


   2. Surgical treatment of left ventricular aneurysms and post-ischemic tissues
Top
 Abstract
 1. Introduction
 2. Surgical treatment of...
3. Partial left ventriculectomy...
 4. Other methods of...
 5. Summary
 References
 
Following acute myocardial infarction, necrotic tissue will be replaced by scar tissue within a few weeks. Before the era of acute revascularization with thrombolytic treatment or percutaneous coronary intervention, large transmural infarctions with subsequent development of left ventricular aneurysms were seen frequently. Today, the acute revascularization procedures make the development of large aneurysms much less likely. Endocardial necrotic tissue combined with variable degrees of viable myocardium towards the epicardium results in akinetic (non-contracting) myocardium rather than dyskinetic (paradoxically contracting or bulging) myocardium. However, there is obviously a continuum between akinetic and dyskinetic myocardium and there is yet no consensus on how to treat these patients correctly.

Surgical treatment of symptomatic large dyskinetic areas of the left ventricle (true aneurysms) has been practiced for 50 years. Cooley and coworkers reported the first surgical treatment of a large left ventricular aneurysm on cardiopulmonary bypass [2,3]. They resected the aneurysm with subsequent direct linear closure of the ventricle. This method was the "gold standard" for treating dyskinetic aneurysms up to the mid-eighties. However, besides the fact that this method is not developed to deal with septal aneurysms, there is a risk that the configuration and volume of the remaining left ventricular cavity might become suboptimal for restoring left ventricular function. To circumvent the problem of leaving a left ventricular cavity which was too small, and to better restore left ventricular elliptical geometry, Dor reported a method [4,5] whereby he resected the aneurysm and placed a patch (normally 2.5–5 cm in diameter) to ensure that there was sufficient remaining left ventricular cavity (Fig. 1). The volume of the remaining left ventricle was determined by inserting a balloon with a known volume, usually about 60 mL/m2 into the cavity. This method has undergone some modifications over the years and is today usually named endoventricular circular patch plasty or the "Dor procedure." Some authors recommend a somewhat larger left ventricular volume than 60 mL/m2 if peroperative left ventricular dilatation is very large [6]. Endoventricular patch plasty has today become the method of choice for most surgeons treating left ventricular aneurysms or dyskinetic left ventricular tissues. Although some studies have not been able to show any differences in survival between linear closure and endoventricular patch plasty [7,8], the most recent reports, although retrospective in design, seem to favor the endoventricular patch plasty method [9–11]. Lundblad and coworkers have identified linear repair of the aneurysm as a risk factor [10]. Overall 5-year cumulative survival was higher after endoventricular patch plasty (Fig. 2) in a retrospective study of 159 patients (91.4% and 70.1% after endoventricular patch plasty and linear repair, respectively) [11]. Recently, Mickleborough and coworkers [12] reported favorable long-term results of combining linear repair with septoplasty in cases of septal aneurysms. It is speculated that the less favorable result often achieved by linear repair compared to endoventricular patch plasty is partly due to the fact that in linear repair septal aneurysms are usually left untreated. This view is supported by the favorable results achieved by the combination of linear repair and septoplasty [12]. Which method to choose for patients with symptomatic left ventricular aneurysms is complicated by the lack of prospective, randomized trials. Although the majority of patients undergo coronary artery bypass grafting (CABG) associated with aneurysmectomy, there are major differences in the additional surgical procedures performed in patients from different studies, making comparison of data difficult. Surgery to the mitral valve varies widely between studies as does the frequency of concomitant preoperative cryoablation in patients prone to ventricular arrhythmias. Another problem with the retrospective studies is the change in surgical procedures over time. For example, linear repair is more often used in the earlier cohorts of patients. The need for prospective, randomized trials to finally decide what method to choose is obvious.


Figure 1
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  		Fig. 1 Surgical technique of endoventricular patch plasty (Dor procedure). (a) First, perform coronary revascularization. (b) If indicated—cryotherapy at the limits of endocardectomy. (c) Determination of left ventricular volume by tightening of the purse string suture. (d) Implantation of patch. (e) Plication of remaining scar tissue to secure hemostasis. Reprinted from Dor, Heart Fail Rev 2001; 6:187–193, with kind permission of Springer Science and Business Media.

 


Figure 2
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  		Fig. 2 Cumulative survival in patients receiving linear repair and endoventricular patch plasty (EVPP). Numbers on curves represent patients at risk. Reprinted from Lundblad et al., J Thorac Cardiovasc Surg 2004; 128:449–456, with permission from the American Association for Thoracic Surgery.

 
Surgical treatment of large dyskinetic aneurysms in patients with symptoms is generally accepted and also supported by the recent guidelines for the diagnosis and treatment of chronic heart failure given by the European Society of Cardiology (ESC) [13]. Treatment of akinetic myocardium without a defined aneurysm has, however, been more controversial. Dor and coworkers have reported favorable results by treating large ventricles with predominantly akinetic myocardium with endoventricular patch plasty [14]. In their study 100 patients with ejection fraction below 30% (51 with akinetic and 49 with dyskinetic scars) were treated with endoventricular patch plasty. CABG was performed in 98%, 10% had mitral valve repair or replacement and 47% of patients received cryotherapy due to preoperative ventricular arrhythmias. Overall in-hospital mortality was 12%. Up to 96 months, there was a tendency towards higher cumulative survival in the dyskinetic group (about 65% vs. 45% in the akinetic group) although statistical significance was not reached. Other authors report similar good results by surgical resection of akinetic myocardium. Di Donato demonstrated that the outcome of surgical remodeling of the left ventricle is more strongly linked to the extent of asynergy than to the presence or absence of dyskinesia, and patients with large akinetic scars and severely depressed pump function benefit to the same extent as patients with large dyskinetic scars [15]. A large multicenter trial (including 1198 patients) from the RESTORE group has also reported excellent 5-year outcome [16]. The inclusion criteria were previous anterior myocardial infarction, significant left ventricular dilatation (left ventricular end-systolic volume index ≥60 mL/m2) and a regional asynergic (non-contractile) left ventricular circumference of ≥35%. Akinesia was present in 66% of patients and dyskinesia in 34%. CABG was performed in 95%, mitral valve repair in 22% and mitral valve replacement in 1%. Before discharge from the hospital, ejection fraction increased from 29.6% preoperatively to 39.5% postoperatively. Thirty-day mortality was 5.3% and overall 5-year survival was almost 70% (65% and 80% in patients with akinesia and dyskinesia, respectively).

Although from theoretical considerations, most authors believe that surgical restoration of dilated left ventricles in terminal heart failure improves symptoms and life expectancy in properly selected patients, it is not yet proven that the surgical approach is better than medical therapy alone. Moreover, acceptable results can be achieved with CABG alone in patients with coronary artery disease with heart failure, and with dilated left ventricles [17–19]. However, concomitant ventricular restoration is advocated by most authors in dilated ischemic cardiomyopathy [20,21]. Which patients should be treated by which method might be answered by the ongoing STICH (Surgical Treatment for IschemiC Heart Failure) trial [22]. This prospectively, randomized trial tests two hypotheses: (1) CABG combined with intensive medical therapy improves long-term survival compared with medical therapy alone, (2) surgical ventricular restoration combined with CABG and medical therapy improves survival free of hospitalization compared with CABG and medical therapy without surgical ventricular restoration.


   3. Partial left ventriculectomy of viable tissues ("Batista operation")
Top
 Abstract
 1. Introduction
 2. Surgical treatment of...
 3. Partial left ventriculectomy...
4. Other methods of...
 5. Summary
 References
 
In patients with non-ischemic dilated cardiomyopathy, the same theoretical considerations based on the law of Laplace are valid, with a potential improvement in left ventricular dysfunction by reducing left ventricular diameter. On the basis of this, Batista and coworkers introduced partial left ventriculectomy in patients with end-stage dilated cardiomyopathies and poor ejection fraction (<20%) [23,24]. They removed a wedge of left ventricular muscle from the apex to the base of the heart. The mitral valve was either preserved, repaired or replaced. In 120 patients operated on in two different centers, they reported a 30-day mortality of 22% and a 2-year survival of 55% and concluded that this method can be used to treat end-stage dilated cardiomyopathy [24]. The Batista operation is also reported to have favorable immediate [25] and short-term (2–5 days) [26] effects, resulting in reduced left ventricular volume, increased ejection fraction, and reduced wall tension. Furthermore, the occurrence of systolic and diastolic paradoxical and asynchronous segmental LV volume motions decreased, increasing mechanical efficiency of ventricular ejection. Although the Batista operation improves left ventricular function and NYHA functional class in selected cases [27,28], a substantial number of surgical failures have been reported [29,30]. Two studies from the Cleveland clinic [29,30] conclude that early and late failures preclude the widespread use of partial left ventriculectomy. Between 1996 and 1998, they operated on 62 patients with partial left ventriculectomy and concomitant mitral valve surgery [30]. All but three patients were transplant candidates and all were in either NYHA class III or IV. Twenty-three patients were on preoperative inotropic support and all had a left ventricular end-diastolic dimension larger than 7.0 cm. Survival in 62 patients (59 with idiopathic dilated cardiomyopathy) was 80% and 60% at 1 and 3 years after surgery, respectively. These, at first sight, fairly good results were in part explained by an aggressive use of left ventricular assist devices (LVADs) and a high number of transplanted patients within the first postoperative year after partial left ventriculectomy. However, freedom from failure (failure was defined as death, implantation of LVAD, return to class IV heart failure (including relisting for transplantation), or the use of an internal defibrillator) was only 49% and 26% after 1 and 3 years, respectively. Risk factors for failure were increased left atrial and systolic pulmonary arterial pressures and decreased maximum exercise oxygen consumption. Although there was an overall modest improvement in left ventricular function, the authors concluded that the widespread use of partial left ventriculectomy is not recommended. Most hospitals have abandoned this operation which is also in accordance with the recently published guidelines for the diagnosis and treatment of chronic heart failure by ESC [13] which do not recommend use of the Batista operation for heart failure or as an alternative to transplantation.


   4. Other methods of left ventricular remodeling
Top
 Abstract
 1. Introduction
 2. Surgical treatment of...
 3. Partial left ventriculectomy...
 4. Other methods of...
5. Summary
 References
 
Myocardial remodeling in terminal heart failure changes the shape of the left ventricle from an elliptical towards spherical geometry and reduces the normal systolic torsion. The normal myofibril shortening of 15% generates a global ejection fraction of 30% in spherical ventricles compared to an ejection fraction of 60% in normally configured ventricles with natural torsion [31]. Since surgical left ventricular remodeling implying cutting and sewing in muscular tissue is associated with procedure-related mortality, the search for less invasive procedures continues.

The Acorn CorCap cardiac support device (Acorn Cardiovascular, St Paul, MN, USA) is a mesh-like device applied around the heart after opening the pericardium through a midline sternotomy (Fig. 3). The idea is that a passive ventricular constraint will improve left ventricular function and prevent further remodeling after myocardial infarction. Although it is too early to evaluate the long-term effects of this device, experimental studies [32,33] and the first clinical reports [34,35] are encouraging. Randomized clinical trials are underway.


Figure 3
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  		Fig. 3 Positioning of the Apicorn CorCap cardiac support device. Hemline is attached near atrioventricular groove with interrupted sutures. An anterior seam is applied to shape a proper device fit. Reprinted from Oz et al., J Thorac Cardiovasc Surg 2003; 126:983–991, with permission from the American Association for Thoracic Surgery.

 
Another concept is to reshape the spherical left ventricle into "two elliptical" left ventricles. A device named Myosplint (Myocor, Maple Grove, MN, USA) which consists of a transventricular splint with two epicardial pads has been constructed which when applied in triplicate bisect the left ventricle (Fig. 4). The few studies performed with this device show some hemodynamic improvement in animal experiments [36] and suggest that the placement of the device is safe in humans [37]. Further clinical studies are awaited.


Figure 4
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  		Fig. 4 Principle of Myosplint implantation. Three Myosplints are placed down the long axis of the left ventricle. When tightened, this device bisects the left ventricle and creates a bilobular configuration. Reprinted from Schenk et al., J Heart Lung Transplant 2002; 21:680–686, with permission from the International Society for Heart and Lung Transplantation.

 

   5. Summary
Top
 Abstract
 1. Introduction
 2. Surgical treatment of...
 3. Partial left ventriculectomy...
 4. Other methods of...
 5. Summary
References
 
In conclusion, surgical left ventricular remodeling for ischemic dilated cardiomyopathy is an established method, especially for large dyskinetic aneurysms. There are a growing number of reports favoring endoventricular patch plasty to linear repair, although modifications of the latter method with septoplasty might show equally good results. Proper revascularization is important, and severe mitral regurgitation should be corrected. Although, from a theoretical point of view, it seems logical to surgically reduce wall tension and thereby reduce oxygen consumption, the potentially better effect of surgery compared to medical treatment alone has yet to be proven. The vast majority of studies performed so far are retrospective. Hopefully, the prospective, randomized multicenter trial STICH will provide further information helping us to choose the best treatment for our patients.


   References
Top
 Abstract
 1. Introduction
 2. Surgical treatment of...
 3. Partial left ventriculectomy...
 4. Other methods of...
 5. Summary
 References
 

  1. Schocken D.D., Arietta M.I., Leaverton P.E., Ross E.A. Prevalence and mortality rate of congestive heart failure in the United States. J Am Coll Cardiol (1992) 20:301–306.[Abstract]
  2. Cooley D.A., Collins H.A., Morris GC. Jr., Chapman D.W. Ventricular aneurysm after myocardial infarction: surgical excision with use of temporary cardiopulmonary bypass. J Am Med Assoc (1958) 167:557–560.[Abstract/Free Full Text]
  3. Cooley D.A., Hallman G.L. Surgical treatment of left ventricular aneurysm: experience with excision of postinfarction lesions in 80 patients. Prog Cardiovasc Dis (1968) 11:222–228.[CrossRef][Medline]
  4. Dor V., Saab M., Coste P., Kornaszewska M., Montiglio F. Left ventricular aneurysm: a new surgical approach. Thorac Cardiovasc Surg (1989) 37:11–19.[Web of Science][Medline]
  5. Dor V. The endoventricular circular patch plasty ("Dor Procedure") in ischemic akinetic dilated ventricles. Heart Fail Rev (2001) 6:187–193.[CrossRef][Medline]
  6. Menicanti L., Di Donato M. The Dor procedure: what has changed after fifteen years of clinical practice? J Thorac Cardiovasc Surg (2002) 124:886–890.[Free Full Text]
  7. Tavakoli R., Bettex D., Weber A., et al. Repair of postinfarction dyskinetic LV aneurysm with either linear or patch technique. Eur J Cardiothorac Surg (2002) 22:129–134.[Abstract/Free Full Text]
  8. Doss M., Martens S., Sayour S., Hemmer W. Long term follow up of left ventricular function after repair of left ventricular aneurysm. A comparison of linear closure versus patch plasty. Eur J Cardiothorac Surg (2001) 20:783–785.[Abstract/Free Full Text]
  9. Sinatra R., Macrina F., Braccio M., Melina G., Luzi G., Ruvolo G., et al. Left ventricular aneurysmectomy; comparison between two techniques; early and late results. Eur J Cardiothorac Surg (1997) 12:291–297.[Abstract]
  10. Lundblad R., Abdelnoor M., Svennevig J.L. Repair of left ventricular aneurysm: surgical risk and long-term survival. Ann Thorac Surg (2003) 76:719–725.[Abstract/Free Full Text]
  11. Lundblad R., Abdelnoor M., Svennevig J.L. Surgery for left ventricular aneurysm: early and late survival after simple linear repair and endoventricular patch plasty. J Thorac Cardiovasc Surg (2004) 128:449–456.[Abstract/Free Full Text]
  12. Mickleborough L.L., Merchant N., Ivanov J., Rao V., Carson S. Left ventricular reconstruction: early and late results. J Thorac Cardiovasc Surg (2004) 128:27–37.[Abstract/Free Full Text]
  13. Swedberg K., Chairperson, et al. Guidelines for the diagnosis and treatment of chronic heart failure: executive summary (update 2005): the task force for the diagnosis and treatment of chronic heart failure of the European Society of Cardiology. Eur Heart J (2005) 26:1115–1140.[Free Full Text]
  14. Dor V., Sabatier M., Di Donato M., Montiglio F., Toso A., Maioli M. Efficacy of endoventricular patch plasty in large postinfarction akinetic scar and severe left ventricular dysfunction: comparison with a series of large dyskinetic scars. J Thorac Cardiovasc Surg (1998) 116:50–59.[Abstract/Free Full Text]
  15. 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) 29:1569–1575.[Abstract]
  16. Athanasuleas C.L., Buckberg G.D., Stanley A.W.H., et al. Surgical ventricular restoration in the treatment of congestive heart failure due to post-infarction ventricular dilation. J Am Coll Cardiol (2004) 44:1439–1445.[Abstract/Free Full Text]
  17. Kron I.L., Flanagan T.L., Blackbourne L.H., Schroeder R.A., Nolan S.P. Coronary revascularization rather than cardiac transplant for chronic ischemic cardiomyopathy. Ann Surg (1989) 210:348–352.[Web of Science][Medline]
  18. Samady H., Elefteriades J.A., Abbott B.G., Mattera J.A., McPherson C.A., Wackers F.J.T. Failure to improve left ventricular function after coronary revascularization for ischemic cardiomyopathy is not associated with worse outcome. Circulation (1999) 100:1298–1304.[Abstract/Free Full Text]
  19. Elefteriades J., Edwards R. Coronary bypass in left heart failure. Semin Thorac Cardiovasc Surg (2002) 14:125–132.[CrossRef][Medline]
  20. Yamaguchi A., Ino T., Adachi H., Murata S., Kamio H., Okada M., et al. Left ventricular volume predicts postoperative course in patients with ischemic cardiomyopathy. Ann Thorac Surg (1998) 65:434–438.[Abstract/Free Full Text]
  21. Maxey T.S., Reece T.B., Ellman P.I., Butler P.D., Kern J.A., Tribble C.G., et al. Coronary artery bypass with ventricular restoration is superior to coronary artery bypass alone in patients with ischemic cardiomyopathy. J Thorac Cardiovasc Surg (2004) 127:428–434.[Abstract/Free Full Text]
  22. Doenst T., Velazquez E.J., Beyersdorf F., et al. To STICH or not to STICH: we know the answer, but do we understand the question? J Thorac Cardiovasc Surg (2005) 129:246–249.[Free Full Text]
  23. Batista R.J., Santos J.L., Takeshita N., Bocchino L., Lima P.N., Cunha M. Partial left ventriculectomy to improve left ventricular function in end-stage heart disease. J Card Surg (1996) 11:96–97.[Web of Science][Medline]
  24. Batista R.JV., Verde J., Nery P., et al. Partial left ventriculectomy to treat end-stage heart disease. Ann Thorac Surg (1997) 64:634–638.[Abstract/Free Full Text]
  25. Gorcsan J. III, Feldman A.M., Kormos R.L., Mandarino W.A., Demetris A.J., Batista R.JV. Heterogeneous immediate effects of partial left ventriculectomy on cardiac performance. Circulation (1998) 97:839–842.[Abstract/Free Full Text]
  26. Schreuder J.J., Steendijk P., van der Veen F.H., et al. Acute and short-term effects of partial left ventriculectomy in dilated cardiomyopathy. J Am Coll Cardiol (2000) 36:2104–2114.[Abstract/Free Full Text]
  27. McCarthy J.F., McCarthy P.M., Starling R.C., et al. Partial left ventriculectomy and mitral valve repair for end-stage congestive heart failure. Eur J Cardiothorac Surg (1998) 13:337–343.[CrossRef][Web of Science][Medline]
  28. Angelini G.D., Pryn S., Mehta D., Izzat M.B., Walsh C., Wilde P., et al. Left-ventricular-volume reduction for end-stage heart failure. Lancet (1997) 350:489.[CrossRef][Web of Science][Medline]
  29. McCarthy P.M., Starling R.C., Wong J., et al. Early results with partial left ventriculectomy. J Thorac Cardiovasc Surg (1997) 114:755–765.[Abstract/Free Full Text]
  30. Franco-Cereceda A., McCarthy P.M., Blackstone E.H., Hoercher K.J., White J.A., Young J.B., et al. Partial left ventriculectomy for dilated cardiomyopathy: is this an alternative to transplantation? J Thorac Cardiovasc Surg (2001) 121:879–893.[Abstract/Free Full Text]
  31. Ingels NB. Jr. Myocardial fiber architecture and left ventricular function. Technol Health Care (1997) 5:45–52.[Medline]
  32. Pilla J.J., Blom A.S., Brockman D.J., et al. Ventricular constraint using the Acorn Cardiac Support Device reduces myocardial akinetic area in an ovine model of acute infarction. Circulation (2002) 106:I-207–I-211.[Abstract/Free Full Text]
  33. Pilla J.J., Blom A.S., Brockman D.J., Ferrari V.A., Yuan Q., Acker M.A. Passive ventricular constraint to improve left ventricular function and mechanics in an ovine model of heart failure secondary to acute myocardial infarction. J Thorac Cardiovasc Surg (2003) 126:1467–1476.[Abstract/Free Full Text]
  34. Oz M.C., Konertz W.F., Kleber F.X., et al. Global surgical experience with the Acorn cardiac support device. J Thorac Cardiovasc Surg (2002) 126:983–991.[CrossRef][Web of Science]
  35. Livi U., Alfieri O., Vitali E., et al. One-year clinical experience with the Acorn CorCap cardiac support device: results of a limited market release safety study in Italy and Sweden. Ital Heart J (2005) 6:59–65.[Medline]
  36. Mueller X.M., Tevaearai H., Boone Y., Augstburger M., von Segesser L.K. An alternative to left ventricular volume reduction. J Heart Lung Transplant (2002) 21:791–796.[CrossRef][Web of Science][Medline]
  37. Schenk S., Reichenspurner H., Boehm D.H., et al. Myosplint implant and shape-change procedure: intra- and peri-operative safety and feasibility. J Heart Lung Transplant (2002) 21:680–686.[CrossRef][Web of Science][Medline]

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