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Ann Thorac Surg 2003;75:S13-S19
© 2003 The Society of Thoracic Surgeons

Supplement

The cardiac support device and the Myosplint: treating heart failure by targeting left ventricular size and shape

Hani N. Sabbah, PhDa*

a Department of Medicine, Division of Cardiovascular Medicine, Henry Ford Heart and Vascular Institute, Henry Ford Health System, Detroit, Michigan, USA

* Address reprint requests to Dr Sabbah, Cardiovascular Research, Henry Ford Hospital, 2799 West Grand Blvd., Detroit, MI 48202, USA
e-mail: hsabbah1{at}hfhs.org

Presented at the Heart Failure & Circulatory Support Summit, Cleveland, OH, Aug 22–25, 2002.

Abstract

Left ventricular (LV) remodeling occurs in patients with heart failure and is associated with poor long-term outcome. Two important components of this remodeling process are progressive LV dilation and LV shape changes, the latter manifested by increased LV chamber sphericity. This brief review describes two passive mechanical devices that were developed to prevent the progressive LV dilation and shape changes that occur during the evolution of heart failure. One such device is the Cardiac Support Device ([CSD] CorCap; Acorn Cardiovascular, St Paul, MN) and the other is the Myosplint (Myocor, Maple Grove, MN). Studies in dogs with coronary microembolization-induced heart failure have shown that the CSD prevents progressive LV dilation, increases LV ejection fraction, lowers LV wall stress, and attenuates LV chamber sphericity. Safety and feasibility studies in patients with heart failure have shown that the CSD is safe. The same studies have provided strong efficacy trends that are consistent with those seen in experimental animals. Studies in dogs with rapid pacing induced heart failure showed that the Myosplint device can reshape the LV leading to reduced LV volumes, increased ejection fraction, and reduced wall stress. Safety and feasibility studies of the Myosplint device in humans are limited and trends are not as yet easily discerned. Final conclusions on the clinical effectiveness of these devices must await completion of randomized clinical trials. These trials should provide the first tests in humans of the hypothesis that limiting LV remodeling alone can improve long-term outcome and quality of life in patients with heart failure.


Doctor Sabbah discloses that he has a financial relationship with Acorn Cardiovascular.

 

Heart failure is a progressive disorder whereby the hemodynamic and symptomatic status of the affected patient deteriorates over time despite the absence of any apparent intercurrent clinical adverse events. Hemodynamically the progressive deterioration of left ventricular (LV) function is accompanied by LV chamber remodeling both globally and at the cellular level [1–3]. Globally the remodeling process is characterized by progressive LV dilation, progressive increase in LV chamber sphericity, and progressive decline in LV ejection fraction. Left ventricle size and shape have long been recognized as strong predictors of mortality and morbidity in patients with heart failure [4–6]. In addition to being a hallmark of poor prognosis in heart failure progressive LV dilation leads to increased LV wall stress and consequently to increased myocardial oxygen consumption, an undesirable development in the setting of heart failure. Progressive LV dilation can also lead to increased myocyte stretch and upregulation of stretch response proteins that can lead to the induction of pathologic cardiomyocyte hypertrophy [7–11]. The latter is invariably associated with abnormalities of calcium cycling within the sarcoplasmic reticulum that can lead to further exacerbation of intrinsic contractile dysfunction [12–14]. As with LV size, LV chamber shape in the form of increased sphericity is also associated with poor prognosis in patients with heart failure [4]. Increased LV sphericity is also associated with increased LV wall stress [15, 16] and correlates strongly with exercise intolerance in patients with heart failure [17, 18]. Left ventricular shape changes, again in the form of increased LV chamber sphericity during the evolution of heart failure, have also been shown to play an important role in the development of functional mitral regurgitation [19–22]. We have convincing evidence at present that in the setting of heart failure progressive LV dilation and progressive LV chamber sphericity can lead to biochemical, cellular, and molecular maladaptation that ultimately culminate in intractable heart failure. Accordingly that intervention that target LV size and shape can offer a therapeutic advantage in the treatment of heart failure.

It is clearly established that both angiotensin-converting enzyme inhibitors and ß-adrenergic receptor blockers significantly reduce mortality in heart failure and prevent or reverse LV remodeling at the global as well as the cellular level [23–25]. More recently LV assist devices (LVADs) have emerged as possible therapies that can inhibit or reverse LV remodeling in patients with advanced heart failure. There is an emerging school of thought that the failing LV if unloaded and the myocardium allowed to recover may be able to fully assume the task of providing adequate blood supply to meet the bodily demands without the need for cardiac transplantation [26]. Left ventricular assist devices profoundly unload the failing LV and accordingly studies using LVADs cannot determine the therapeutic effect of limiting chronic remodeling on the working heart nor can they easily differentiate unloading influences from changes during to systolic assist and neurohormonal deactivation [27]. The direct impact of remodeling the progression of heart failure was to some extent tested with dynamic cardiomyoplasty [28, 29] whereby a flat sheet of skeletal muscle is wrapped around the heart and then stimulated to assist the pumping action of the left ventricle. Of interest is that both studies in animal models of heart failure as well as in patients with heart failure demonstrated that the primary benefit of dynamic cardiomyoplasty on LV remodeling came from containment of the ventricle, a so-called "girdling effect," rather than from an active contraction of the skeletal muscle [30, 31]. These observations have led, albeit in part, to the emergence of at least two passive mechanical devices that are intended to directly influence LV size or shape with the intent of preventing the adverse consequences of progressive LV remodeling. As of this date both devices are in clinical trials in the United States. One such device is the Cardiac Support Device ([CSD] CorCap; Acorn Cardiovascular, St Paul, MN) and the other is the Myosplint (Myocor, Maple Grove, MN).

The Acorn Cardiac Support Device

The CSD is a passive mechanical device consisting of a preformed polyester polymer that is wrapped around the cardiac ventricles. Conceptually the CSD was initially developed as a device directed at preventing progressive LV enlargement. The technique for open-chest surgical implantation of the CSD is shown in Figure 1. The CSD is placed directly over the epicardial surface of the ventricles after opening the pericardium. The device is then anchored by stay sutures to the atrioventricular groove and is tailored anteriorly to fit "snugly" over the cardiac ventricles. The CSD is fitted to contain the left ventricle evidenced by the absence of significant changes in LV end-diastolic dimension after implantation compared with just before implantation. Studies in both animals as well as in patients with heart failure indicate that an acute reduction of as much as 5% is acceptable. The CSD can be readily implanted on the beating heart but has also been implanted in the patient on cardiopulmonary bypass. The CSD has built-in unique properties that are intended to allow it to accomplish its objectives. The CSD material shown in Figure 2 consists of multiple polyester fibers each of which consists of multiple filaments that allow the device to closely and evenly conform to the epicardial surface of the heart. Another property of the CSD is its compliance properties in both the circumferential and longitudinal direction. For a given load the CSD allows greater compliance in the longitudinal direction (apex to base) than in the circumferential direction. This property allows the CSD to over time restore the left ventricle to a shape that more closely approaches that of an ellipse rather than a sphere, more in line with the shape of the normal ventricle.



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  		Fig 1. The implantation procedure of the Acorn Cardiac Support Device (CSD). (1) The CSD is positioned and anchored to the atrioventricular groove with stay sutures. (2) The CSD is adjusted anteriorly with the help of a specifically designed clamp. (3) The longitudinal seam final adjustment is made to ensure a snug fit over the ventricles. (4) Excess fabric is trimmed with the clamp in place. (5) The CSD is sewn in place anteriorly. (6) The implantation is complete.

 


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  		Fig 2. (Top panel) A high magnification photograph illustrating the multiple small filaments that constitute the Cardiac Support Device (CSD) fabric fibers. The lower three panels illustrate the response of the CSD to load. (A) A segment of the CSD unloaded. (B) The same segment after application of a load of 0.8 lbs/in in the longitudinal direction (equivalent to the left ventricular base to apex direction). (C) The same segment after application of a load of 0.8 lbs/in in the circumferential direction. Note that for the same load the CSD allows for greater compliance or stretch in the longitudinal direction compared with the circumferential direction.

 
Preclinical studies with the CSD in dogs with heart failure
The efficacy of the CSD was studied in dogs with heart failure produced by intracoronary microembolizations [30, 32, 33] as well as in sheep with rapid-pacing–induced heart failure [34]. The findings reported in this review are those observed in dogs with microembolization-induced heart failure [35]. In this canine model chronic LV dysfunction and failure is induced by multiple sequential intracoronary embolizations with polystyrene Latex microspheres (70 to 102 µm in diameter). This results in loss of viable myocardium as seen in myocardial infarction. This model manifests most if not all of the sequelae of heart failure seen in humans including marked and sustained depression of LV systolic and diastolic function, ventricular dilation and hypertrophy, and LV shape changes [35]. Of particular importance to the exploration of the efficacy of the CSD is that the model manifests progressive LV dysfunction and dilation long after discontinuation of coronary microembolizations, a property that recapitulates the human disease phenotype [22, 24, 35].

Studies in dogs with heart failure (LV ejection fraction approximately 35%) in which the CSD was implanted showed that 3 months after implantation LV end-diastolic volume and LV end-systolic volume decreased significantly whereas in untreated dogs LV volumes increased significantly [32]. These initial findings argue in favor of the device design objective in that the CSD was able to prevent progressive LV dilation (Table 1). An unexpected finding was that the CSD also improved LV ejection fraction. In untreated control dogs LV ejection fraction decreased significantly but increased significantly in CSD-treated dogs [27, 36]. These positive remodeling findings were not associated with any evidence of constrictive or restrictive physiology [32, 33]. Improved diastolic function in CSD-treated dogs was further supported by a lack of deterioration of indices of diastolic function including deceleration time of mitral inflow velocity compared with control dogs [32]. Post mortem examination of the CSD-treated dogs after 3 months of implantation showed that the device was encapsulated in a translucent thin layer of (approximately 0.3 to 0.5 mm) connective tissue (Fig 3). Of particular interest was the finding of a clear demarcation between the CSD and the myocardium without encroachment of the connective tissue into the epicardial myocardium. This finding is a contradiction of what is typically observed in condition of constrictive pericarditis. The CSD had no effect on the integrity of the epicardial coronary arteries and veins. This was confirmed by both coronary arteriography as well as by histology (Fig 3). At the cellular level treatment with the CSD was associated with reduced cardiomyocyte hypertrophy, reduced volume fraction of interstitial fibrosis, increased capillary density, and reduced oxygen diffusion distance [32], all of which are directionally desirable remodeling indicators.


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  		Table 1. Change ({Delta}) in Hemodynamic, Angiographic, and Neurohormonal Parameters in Untreated Heart Failure Control Dogs and Heart Failure Dogs Treated With the Acorn Cardiac Support Device

 


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  		Fig 3. (A) Photograph of the appearance of the Cardiac Support Device (CSD) after 3 months of implantation in a dog with heart failure. (B) A trichrome stained section of myocardium from a dog with heart failure 3 months after implantation of the CSD. (C) A trichrome stained section of epicardial myocardium from a dog 3 months after implantation of the CSD showing a patent epicardial coronary artery and vein just beneath the CSD.

 
Dogs treated with the CSD also showed a benefit in the form of a reduction or elimination of functional mitral regurgitation. In effect in untreated dogs functional mitral regurgitation was sustained or worsened over the course of the 3-month follow-up whereas dogs in the CSD-treated group that manifested functional mitral regurgitation at the time of implantation had no evidence of mitral regurgitation at the end of 3 months of follow-up [32]. The absence of functional mitral regurgitation in CSD-treated dogs was associated with restoration of LV shape to one that more closely approximates that of an ellipse as opposed to that of a sphere [32].

In a separate study of the efficacy of the CSD in dogs with microembolization induced heart failure we showed that treatment with the CSD for 3 to 6 months can lead to reverse LV remodeling and enhanced adrenergic reserve [27]. Measurements of pressure volume relations by conductance micromanometer catheters demonstrated a significant shift in the end-systolic pressure-volume relation to the left that is compatible with reverse LV remodeling. In the same study the systolic response of the LV to dobutamine markedly improved after CSD implantation in conjunction with heightened adenylyl cyclase response to isoproterenol. These finding provided further support that reverse remodeling with improved adrenergic signaling can be achieved by long-term passive external support that does not generate diastolic constriction [27].

As alluded to earlier, treatment with the CSD is associated with an increase in LV ejection fraction. This beneficial effect may be the result of several factors. These include (1) down-regulation of stretch response proteins attenuation of cardiomyocyte hypertrophy and improvement in sarcoplasmic reticulum calcium that lead to improve calcium cycling [37]; and (2) reduction in end-diastolic circumferential wall stress that can lead to reduced myocardial oxygen consumption, reduced left ventricular sphericity with a complementary reduction of functional mitral regurgitation, and attenuation of activation of the sympathetic nervous system as evidenced by reduced levels of circulating plasma norepinephrine and enhanced cardiac adrenergic sensitivity (Table 1) [27].

Clinical safety and feasibility studies with the CSD in patients with heart failure
Safety studies of the CSD in patients with heart failure have been completed. The patient population was primarily a mixture of those who received the CSD alone and those who received the CSD in combination with mitral valve repair or replacement. A total of 48 patients were entered into the studies, the results of which showed that the CSD is safe. That observation was based on the absence of device related adverse events, no evidence of constriction based on LV pressure volume loop studies, no adverse impact on epicardial coronary vessels as evidenced by normal coronary arteriograms, and normal coronary vasodilation in response to adenosine infusion [38, 39]. The results of the safety study also provided some trends as to possible efficacy of the CSD. Table 2 depicts the changes in LV end-diastolic dimension and LV ejection fraction in patients who have been followed up for as long as 18 to 24 months post–CSD implantation. Consistent with studies in dogs with heart failure, trends in the safety trial showed the CSD was associated a significant reduction in LV end-diastolic dimension and a significant improvement in LV ejection fraction that persisted for as long as 2 years. This trend held true and was just as robust even when the group of patients with CSD-only intervention were evaluated. Clearly such data are only used to suggest trends and do not replace randomized efficacy trials. As eluded to earlier, randomized clinical efficacy trials of the CSD are under way in the United States, Europe, and Australia. Of the 300 patients to be entered into the United States trial, approximately 200 have been entered as of November 16, 2002. The patients are randomly assigned to either CSD-only arm versus optimal medical therapy or to mitral valve repair or replacement alone or in combination with CSD implantation (Fig 4). In trials in Europe and Australia coronary artery bypass surgery is also included with and without concomitant CSD implantation (Fig 4).


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  		Table 2. Change ({Delta}) From Preimplantation in Left Ventricular End-Diastolic Dimension and Ejection Fraction in Patients From the Acorn Safety Study Followed Up for 18 to 24 Months From the Time of Cardiac Support Device Implantation

 


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  		Fig 4. (Left panel) Implantation of the Cardiac Support Device (CSD) as the sole surgical procedure. (Middle) Surgical implantation of the CSD with concomitant mitral valve replacement. (Right) Surgical implantation of the CSD along with coronary artery bypass surgery.

 
The Myosplint device

The Myosplint device was conceived to directly address the increased LV sphericity that occurs frequently in patients with advanced heart failure. Accordingly the device was developed to change LV shape, decrease wall stress, and in doing so improve LV function. The Myosplint device consists of an implantable transventricular splint and two epicardial pads that are adjusted to draw the wall of the LV together and thereby reduce LV radius (Fig 5) [40]. Ventricular shape change is achieved by the placement of three Myosplints bisecting the LV with epicardial pads that disperse some of the force over the epicardium. The devices are adjusted to acutely reduce LV wall stress by approximately 20% [40]. The Myosplints are placed on the beating heart with a device [40] that precisely places the Myosplint to avoid epicardial vessels. A Myosplint has two components. The first is a 1.4 mm diameter polyethylene braided splint coated with expanded polytetrafluoroethylene. This tension member is connected to a second component, namely the epicardial pads. The pads are covered with polyester fabric. One pad is permanently fixed to the splint and the other is an adjustable pad threaded to the splint and fixed at the time of implantation (Fig 5).



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  		Fig 5. (Top) Three deployed transventricular splints that bisect the left ventricle. (Bottom) Photograph of a Myosplint consisting of a fixed pad (1), a tension member (2), and a deployable pad (3).

 
Preclinical studies with the Myosplint in dogs with heart failure
In an acute bovine model of heart failure secondary to volume overload implantation of the Myosplint was shown to improve mean pulmonary artery wedge pressure and cardiac output [40]. Pivotal preclinical studies were conducted in dogs with heart failure produced by rapid ventricular pacing. Hemodynamic two-dimensional and three-dimensional echocardiographic studies were performed at base line before Myosplint implantation and repeated at 4 weeks postimplantation [41]. Four weeks of treatment with the Myosplint device was associated with a significant reduction of LV end-diastolic volume and LV end-systolic volume evaluated from three-dimensional echocardiograms (Table 3) [41]. Along with LV volume reduction there was an increase in LV ejection fraction and a significant decrease of LV end-diastolic and end-systolic circumferential wall stress (Table 3) [40]. From a safety standpoint animal studies with follow-up ranging from 28 to 180 days showed no pad pull through or chronic migration, no evidence of embolic events, and no thrombus in the LV cavity. Tension members were found to be covered with fibrous tissue and surface cells consistent with endothelium (Fig 6). (Safety data provided courtesy of Myocor.)


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  		Table 3. Hemodynamic and Echocardiographic Measurements in Dogs With Heart Failure Before (PRE) and 4 Weeks After (POST) Treatment With the Myosplint

 


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  		Fig 6. (Left) Gross photograph of a Myosplint tension member across the left ventricle 12 weeks after implantation in a pig showing no evidence of thrombosis. (Right) Section from a Myosplint tension member stained with factor VIII showing endothelial cell (brown) coverage along the member’s surface.

 
Clinical safety and feasibility studies with the Myosplint in patients with heart failure
Clinical and safety and feasibility studies are under way in Europe and the United States with the Myosplint but lag behind the Acorn CSD. A recent study by Schenk and colleagues [42] reported on patients with dilated cardiomyopathy in whom the Myosplint device was deployed. Of these patients, 4 received the Myosplint device as the only therapy and 4 received the Myosplint in combination with mitral valve repair. At 90 days postimplantation there were no device-related complications such as thromboembolism, bleeding device instability, or vascular damage, suggesting that placement of the Myosplint device is safe [42]. Assessment of clinical status based on a 6-minute walk and Minnesota Living With Heart Failure Questionnaire (MLHFQ) score was somewhat variable. At 90 days the 6-minute walk improved in 3 patients, was unchanged in 2, and worsened in 2 patients. With respect to the MLHFQ score, 4 patients improved and 3 worsened [42]. One must bear in mind that this is a very small series of patients and no conclusion can be drawn from it with respect to even trends for device efficacy.

Final conclusions on the clinical effectiveness of both the Acorn CSD and the Myosplint device must await completion of randomized clinical trials that are under way. These trials should provide the first tests in humans of the hypothesis that limiting LV remodeling alone can improve long-term outcome and quality of life in patients with heart failure.

Acknowledgments

These studies were supported in part by grants from Acorn Cardiovascular, Inc, and by National Heart, Lung, and Blood Institute Grant HL 49090-08.

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Preservation of Cardiac Extracellular Matrix by Passive Myocardial Restraint: An Emerging New Therapeutic Paradigm in the Prevention of Adverse Remodeling and Progressive Heart Failure
Circulation, August 30, 2005; 112(9): 1245 - 1247.
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A. S. Blom, R. Mukherjee, J. J. Pilla, A. S. Lowry, W. M. Yarbrough, J. T. Mingoia, J. W. Hendrick, R. E. Stroud, J. E. McLean, J. Affuso, et al.
Cardiac Support Device Modifies Left Ventricular Geometry and Myocardial Structure After Myocardial Infarction
Circulation, August 30, 2005; 112(9): 1274 - 1283.
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 CirculationHome page
D. L. Mann and M. R. Bristow
Mechanisms and Models in Heart Failure: The Biomechanical Model and Beyond
Circulation, May 31, 2005; 111(21): 2837 - 2849.
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 J. Thorac. Cardiovasc. Surg.Home page
H.-Y. Yu, M.-Y. Su, T.-Y. Liao, H.-H. Peng, F.-Y. Lin, and W.-Y. I. Tseng
Functional mitral regurgitation in chronic ischemic coronary artery disease: Analysis of geometric alterations of mitral apparatus with magnetic resonance imaging
J. Thorac. Cardiovasc. Surg., October 1, 2004; 128(4): 543 - 551.
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