A bioresorbable biomaterial carrier and passive stabilization device to improve heart function post-myocardial infarction
Dolan, Eimear B.
de Vaal, M. Hamman
Monahan, David S.
Levey, Ruth E.
Monaghan, Michael G.
Murphy, Bruce P.
Kelly, Helena M.
Duffy, Garry P.
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Dolan, Eimear B., Hofmann, Björn, de Vaal, M. Hamman, Bellavia, Gabriella, Straino, Stefania, Kovarova, Lenka, Pravda, Martin, Velebny, Vladimir, Daro, Dorothee, Braun, Nathalie, Monahan, David S., Levey, Ruth E., O'Neill, Hugh, Hinderer, Svenja, Greensmith, Robert, Monaghan, Michael G., Schenke-Layland, Katja, Dockery, Peter, Murphy, Bruce P., Kelly,, Helena M., Wildhirt, Stephen, Duffy, Garry P. (2019). A bioresorbable biomaterial carrier and passive stabilization device to improve heart function post-myocardial infarction. Materials Science and Engineering: C, 103, 109751. doi: https://doi.org/10.1016/j.msec.2019.109751
The limited regenerative capacity of the heart after a myocardial infarct results in remodeling processes that can progress to congestive heart failure (CHF). Several strategies including mechanical stabilization of the weakened myocardium and regenerative approaches (specifically stem cell technologies) have evolved which aim to prevent CHF. However, their final performance remains limited motivating the need for an advanced strategy with enhanced efficacy and reduced deleterious effects. An epicardial carrier device enabling a targeted application of a biomaterial-based therapy to the infarcted ventricle wall could potentially overcome the therapy and application related issues. Such a device could play a synergistic role in heart regeneration, including the provision of mechanical support to the remodeling heart wall, as well as providing a suitable environment for in situ stem cell delivery potentially promoting heart regeneration. In this study, we have developed a novel, single-stage concept to support the weakened myocardial region post-MI by applying an elastic, biodegradable patch (SPREADS) via a minimal-invasive, closed chest intervention to the epicardial heart surface. We show a significant increase in %LVEF 14 days post-treatment when GS (clinical gold standard treatment) was compared to GS + SPREADS + Gel with and without cells (p ≤ 0.001). Furthermore, we did not find a significant difference in infarct quality or blood vessel density between any of the groups which suggests that neither infarct quality nor vascularization is the mechanism of action of SPREADS. The SPREADS device could potentially be used to deliver a range of new or previously developed biomaterial hydrogels, a remarkable potential to overcome the translational hurdles associated with hydrogel delivery to the heart.
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