Infarct Size Reduction and Attenuation of Global Left Ventricular Remodeling with the CorCapTM Cardiac Support Device Following Acute Myocardial Infarction in Sheep

Blom, Aaron S.; Pilla, James J.; Gorman, Robert C.; Gorman, Joseph H.; Mukherjee, Rupak; Spinale, Francis G.; Acker, Michael A.

doi:10.1007/s10741-005-4640-2

Cited by 27 publications

(19 citation statements)

References 44 publications

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“…This concept has been tested by injecting polymer based hydrogels into the infarct site to prevent dilation [38]. Other techniques such as attaching patches of support material to the exterior of the LV have also been investigated with promising results [39, 40]. A more pharmacological approach could be in delivering activated lysyl oxidase or bone morphogenetic protein-1 to the infarct site.…”

Section: Discussionmentioning

confidence: 99%

Building a better infarct: Modulation of collagen cross-linking to increase infarct stiffness and reduce left ventricular dilation post-myocardial infarction

Voorhees

DeLeon‐Pennell

et al. 2015

Journal of Molecular and Cellular Cardiology

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Matrix metalloproteinase-9 (MMP-9) deletion attenuates collagen accumulation and dilation of the left ventricle (LV) post-myocardial infarction (MI); however the biomechanical mechanisms underlying the improved outcome are poorly understood. The aim of this study was to determine the mechanisms whereby MMP-9 deletion alters collagen network composition and assembly in the LV post-MI to modulate the mechanical properties of myocardial scar tissue. Adult C57BL/6J wild-type (WT; n=88) and MMP-9 null (MMP-9−/−; n=92) mice of both sexes underwent permanent coronary artery ligation and were compared to day 0 controls (n=42). At day 7 post-MI, WT LVs displayed a 3-fold increase in end-diastolic volume, while MMP-9−/− showed only a 2-fold increase (p<0.05). Biaxial mechanical testing revealed that MMP-9−/− infarcts were stiffer than WT infarcts, as indicated by a 1.3-fold reduction in predicted in vivo circumferential stretch (p<0.05). Paradoxically, MMP-9−/− infarcts had a 1.8-fold reduction in collagen deposition (p<0.05). This apparent contradiction was explained by a 3.1-fold increase in lysyl oxidase (p<0.05) in MMP-9−/− infarcts, indicating that MMP-9 deletion increased collagen cross-linking activity. Furthermore, MMP-9 deletion led to a 3.0-fold increase in bone morphogenetic protein-1, the metalloproteinase that cleaves pro-collagen and pro-lysyl oxidase (p<0.05) and reduced fibronectin fragmentation by 49% (p<0.05) to enhance lysyl oxidase activity. We conclude that MMP-9 deletion increases infarct stiffness and prevents LV dilation by reducing collagen degradation and facilitating collagen assembly and cross-linking through preservation of the fibronectin network and activation of lysyl oxidase.

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Section: Discussionmentioning

confidence: 99%

Building a better infarct: Modulation of collagen cross-linking to increase infarct stiffness and reduce left ventricular dilation post-myocardial infarction

Voorhees

DeLeon‐Pennell

et al. 2015

Journal of Molecular and Cellular Cardiology

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“…[18] Cardiac restraint devices such as the CorCap (Acorn Cardiovascular Inc) and Heart Net (Paracor Medical Inc) employ Dacron and nitinol wraps, respectively, to provide physical support for the failing ventricular wall – Figure 2. [19–22] Experimental devices such as the Myosplint (Myocor Inc) and CardioClasp (CardioClasp Inc) force a dilated ventricle into two smaller lobes to reduce the intraventricular radius and thereby decrease wall stress. [23, 24] Advanced surgical procedures such as endoventricular patch plasty (the Dor procedure) and partial left ventriculectomy (the Batista procedure) physically restructure a spherical, dilated ventricle into a more natural elongated shape.…”

Section: Mechanical Approaches To Heart Diseasementioning

confidence: 99%

“…The CorCap device (A) uses a Dacron woven mesh to maintain ventricular dimensions whereas the Heart Net (B) surrounds the ventricle in an elastic nitinol metal wrap. ((A) from [22], (B) from[20])…”

Section: Figurementioning

confidence: 99%

Intra-myocardial biomaterial injection therapy in the treatment of heart failure: Materials, outcomes and challenges

et al. 2011

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Heart failure initiated by coronary artery disease and myocardial infarction (MI) is a widespread, debilitating condition for which there are a limited number of options to prevent disease progression. Intramyocardial biomaterial injection following MI theoretically provides a means to reduce the stresses experienced by the infarcted ventricular wall, which may alter the pathological remodeling process in a positive manner. Furthermore, biomaterial injection provides an opportunity to concurrently introduce cellular components and depots of bioactive agents. Biologically-derived, synthetic and hybrid materials have been applied, as well as designed expressly for this purpose, although optimal design parameters, including degradation rate and profile, injectability, elastic modulus, and various possible bioactivities largely remain to be elucidated. This review seeks to summarize the current body of growing literature where biomaterial injection, with and without concurrent pharmaceutical or cellular delivery, has been pursued to improve functional outcomes following MI. The literature to date generally demonstrates acute functional benefits associated with biomaterial injection therapy across a broad variety of animal models and material compositions. Further functional improvements have been reported when cellular or pharmaceutical agents have been incorporated into the delivery system. Despite these encouraging early results, the specific mechanisms behind the observed functional improvements remain to be fully explored and future studies employing hypothesis-driven material design and selection may increase the potential for this approach to alleviate the morbidity and mortality of heart failure.

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“…Previous work has demonstrated that the use of ventricular restraints, such as polymeric meshes wrapped around the heart or sutured to the surface of the infarcted myocardium, reduces infarct expansion by mechanically stabilizing the heart and forcing it to maintain its original shape, thus limiting long-term global LV remodeling in large animal models [10,[14][15][16][17]. However, these approaches are limited by the invasive procedure in which they are applied, and clinical adoption has not occurred.…”

Section: Introductionmentioning

confidence: 99%

Injectable Acellular Hydrogels for Cardiac Repair

Tous

Purcell

Ifkovits

et al. 2011

J. of Cardiovasc. Trans. Res.

147

136

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Injectable hydrogels are being developed as potential translatable materials to influence the cascade of events that occur after myocardial infarction. These hydrogels, consisting of both synthetic and natural materials, form through numerous chemical crosslinking and assembly mechanisms and can be used as bulking agents or for the delivery of biological molecules. Specifically, a range of materials are being applied that alter the resulting mechanical and biological signals after infarction and have shown success in reducing stresses in the myocardium and limiting the resulting adverse left ventricular (LV) remodeling. Additionally, the delivery of molecules from injectable hydrogels can influence cellular processes such as apoptosis and angiogenesis in cardiac tissue or can be used to recruit stem cells for repair. There is still considerable work to be performed to elucidate the mechanisms of these injectable hydrogels and to optimize their various properties (e.g., mechanics and degradation profiles). Furthermore, although the experimental findings completed to date in small animals are promising, future work needs to focus on the use of large animal models in clinically relevant scenarios. Interest in this therapeutic approach is high due to the potential for developing percutaneous therapies to limit LV remodeling and to prevent the onset of congestive heart failure that occurs with loss of global LV function. This review focuses on recent efforts to develop these injectable and acellular hydrogels to aid in cardiac repair.

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Infarct Size Reduction and Attenuation of Global Left Ventricular Remodeling with the CorCapTM Cardiac Support Device Following Acute Myocardial Infarction in Sheep

Abstract: The CorCap cardiac support device retarded infarct expansion, improved global and regional cardiac function and beneficially modified LV and myocyte remodeling post-MI. These findings provide evidence that non-pharmacological strategies can interrupt adverse LV remodeling post-MI.

Cited by 27 publications

References 44 publications

Building a better infarct: Modulation of collagen cross-linking to increase infarct stiffness and reduce left ventricular dilation post-myocardial infarction

Building a better infarct: Modulation of collagen cross-linking to increase infarct stiffness and reduce left ventricular dilation post-myocardial infarction

Intra-myocardial biomaterial injection therapy in the treatment of heart failure: Materials, outcomes and challenges

Injectable Acellular Hydrogels for Cardiac Repair

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