The role of regional myocardial topography post-myocardial infarction on infarct extension.

Infarct extension involves necrosis of healthy myocardium in the border zone (BZ), progressively enlarging the infarct zone (IZ) and recruiting the remote zone (RZ) into the BZ, eventually leading to heart failure. The mechanisms underlying infarct extension remain unclear, but myocyte stretching has been suggested as the most likely cause. Using human patient-specific left-ventricular (LV) numerical simulations established from cardiac magnetic resonance imaging (MRI) of myocardial infarction (MI) patients, the correlation between infarct extension and regional mechanics abnormality was investigated by analysing the fibre stress-strain loops (FSSLs).

Computational Modelling of the Effect of Infarct Stiffness on Regional Myocardial Mechanics.

Ventricular remodeling after myocardial infarction increases the rate of mortality and is highly associated with the extent of infarct transmurality. It is hypothesized that infarct stiffness alters regional mechanics and affects the likelihood of human ventricular remodeling. However, this is yet to be studied in detail.

The role of end-diastolic myocardial fibre stretch on infarct extension.

Myocardial infarct extension, a process involving the enlargement of infarct and border zone, leads to progressive degeneration of left ventricular (LV) function and eventually gives rise to heart failure. Despite carrying a high risk, the causation of infarct extension is still a subject of much speculation. In this study, patient-specific LV models were developed to investigate the correlation between infarct extension and impaired regional mechanics.

Impact of myocardial infarction on intraventricular vortex and flow energetics assessed using computational simulations.

Flow energetics have been proposed as early indicators of progressive left ventricular (LV) functional impairment in patients with myocardial infarction (MI), but its correlation with individual MI parameters has not been fully explored. Using electro-fluid-structure interaction LV models, this study investigated the correlation between four MI parameters: infarct size, infarct multiplicity, regional enhancement of contractility at the viable myocardium area (RECVM), and LV mechanical dyssynchrony (LVMD) with intraventricular vortex and flow energetics. In LV with small infarcts, our results showed that infarct appearance amplified the energy dissipation index (DI), where substantial viscous energy loss was observed in areas with high flow velocity and near the infarct-vortex interface.

The role of infarct transmural extent in infarct extension: A computational study.

Infarct extension, a process involving progressive extension of the infarct zone (IZ) into the normally perfused border zone (BZ), leads to continuous degradation of the myocardial function and adverse remodelling. Despite carrying a high risk of mortality, detailed understanding of the mechanisms leading to BZ hypoxia and infarct extension remains unexplored. In the present study, we developed a 3D truncated ellipsoidal left ventricular model incorporating realistic electromechanical properties and fibre orientation to examine the mechanical interaction among the remote, infarct and BZs in the presence of varying infarct transmural extent (TME).

Electromechanics modeling of the effects of myocardial infarction on left ventricular function.

Ventricular remodeling may occur following myocardial infarction of the left ventricle (LV) and such remodeling has been shown to be correlated with increased patient morbidity and mortality. It is thus important to estimate the likelihood of remodeling from the state of the infarcted LV. In this paper, we present simulations from an actively-contracting truncated ellipsoid LV model, incorporating realistic fiber orientation and electromechanical properties, to investigate the effects of infarct size and transmural extent (TME) on myofiber regional mechanics.