Does Time Heal All Wounds? Predicting acute and long-term damage in blood vessels In an effort to minimize the number of complications following cardiovascular surgery, research is directed at decreasing unnecessary intraoperative trauma. A frequent side effect of surgical intervention is mechanical overloading of the affected or surrounding tissue. This can lead to acute damage and, if not immediately problematic, trigger longer term remodeling that will necessitate re-intervention. Therefore, optimizing surgical techniques and instrument design is imperative. The effectiveness of these techniques and designs depends on how well injury mechanisms in cardiovascular tissue are understood and how they can be translated into objective engineering design criteria. The ultimate goal of this collaborative project is therefore to define reliable models to quantify the long-term effects of mechanically-induced damage to cardiovascular tissue, a unique and novel concept. This knowledge can then be used to virtually test surgical interventions, in casu balloon angioplasty, such that the can be optimized to minimize acute and long term damage. Three objectives can be identified, each separately innovative and relevant to the field of cardiovascular biomechanics. The first objective of this project is to understand and haracterize the microstructural organization of collagen fibers and other extracellular matrix structures through innovative imaging and image processing techniques. This information will subsequently be used in a mechanical model for arterial tissue, where collagen fibers are represented in a biofidelic and microstructurally validated way, including acute and longterm damage and healing capability. The second objective aims at understanding how smooth muscle cells, in both their contractile and synthetic phenotype, are organized in arterial tissue and how they react to cellular and tissue level mechanical loading. This will lead to a novel, experimentally validated, constitutive model for arterial tissue where the active energy contribution of the SMCs are taken into account due to changes in wall shear stress and mechanical stretching. The occurring reaction cascades resulting in contraction, relaxation, phenotype switching and extracellular matrix production, will be modeled, where also acute and long-term damage capability will be included, leading to a unique biomechanical and mechanobiological model for arterial smooth muscle cells. Using the results of above objectives, the third objective aims at predicting acute damage and vascular remodeling after balloon angioplasty through finite element modeling. We hypothesize that, given accurate modeling of collagen and smooth muscle damage behavior, a computational model is a strong predictive tool for cardiovascular intervention outcomes.
|Effective start/end date||1/10/20 → 30/09/24|
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