A computational study of post-infarct mechanical effects of injected biomaterial into ischaemic myocardium

Includes abstract.Includes bibliographical references.Cardiovascular diseases account for one third of all deaths worldwide, more than 33% of which are related to ischaemic heart disease, involving a myocardial infarction (MI). Emerging MI therapies involving biomaterial injections have shown some benefits; the underlying mechanisms of which remain unclear. Computational models offer considerable potential to study the biomechanics of a myocardial infarction and novel therapies. Geometrical data of a healthy human left ventricle (LV) obtained from magnetic resonance images (MRI) was used to create a finite element (FE) mesh of the LV at the end-systolic time point using Continuity® 6.3 (University of California in San Diego, US). A mesh of 96 hexahedral elements with high order basis functions was employed to adequately describe the geometry of the LV. Simulations of diastolic filling and systolic contraction were performed using a transversely isotropic exponential strain energy function and a model for active stress based on contraction at the cellular level. An anterior apical, transmural MI was modelled in the LV encompassing 16% of the LV wall volume. The infarct was modelled at acute and fibrotic stages of post-infarct LV remodelling by altering the constitutive and active stress models to best describe passive and active behaviour of the ischaemic myocardium at each time point. The geometry of the LV with the fibrotic infarct was adjusted to represent the wall thinning that occurs during LV post-MI remodelling. Hydrogel injection was modelled as layers with material properties differing from those of the surrounding myocardium while accounting for thickening of the LV wall at the injection site. The study design comprised a healthy case and two infarcted cases with and without hydrogel injection. The end-diastolic volume (EDV) increased in the acute infarct model compared to the healthy case due to the reduced stiffness in the infarct wall. An EDV increase was not observed in the fibrotic infarct model compared to the healthy case. This was partially attributed to the increase in infarct stiffness and partially due to the fact that remodelling-related dilation of the LV was not implemented in the model. Inclusion of hydrogel lowered EDV in both the acute and fibrotic models. The predicted ejection fraction (EF) decreased from 41.2% for the healthy case to 28.5% and 33.0% for the acute and fibrotic infarct models, respectively. Inclusion of hydrogel layers caused an improvement in EF in the acute model only