Modelling in vivo cardiac mechanics using MRI and FEM

Abstract

The role of myocardial mechanical properties in the progression of cardiovascular diseases such as heart failure (HF) remains poorly understood. In order to elucidate the mechanisms underlying cardiac dysfunction, mathematical modelling of ventricular mechanics is a useful tool. This thesis presents finite element modelling methods to estimate in vivo mechanical properties of the left ventricle (LV) by incorporating geometric and kinematic information derived from in vivo magnetic resonance image (MRI) tagging, ex vivo microstructural information extracted from diffusion tensor MRI (DTMRI), and LV cavity pressure data recorded during the MRI tagging experiments. This integrative LV modelling framework enabled in vivo characterisation of LV muscle properties and performance on a subject specific basis, and investigation of mechanisms of HF. In order to investigate passive ventricular mechanics, LV FE models were customised to geometric data segmented from in vivo tagged MRI, and myofibre orientation data derived from ex vivo DTMRI of five canine hearts using nonlinear FE fitting techniques. Simulation of diastolic LV mechanics allowed estimation of the passive myocardial mechanical properties, which were tuned to provide the best match between the end diastolic model predictions and the MRI tagging data. Contractile function and regional myocardial work of the LV were then examined by simulating systolic mechanics and estimating the associated contractile properties during the ventricular cycle. Based on these data, the LV efficiency throughout the cardiac cycle was quantified. The FE modelling framework was applied to study HF by investigating the effects of ventricular dilation, loss of anisotropy, and reduced myocardial contractility on LV mechanical performance. By comparing the mechanical function of normal and abnormal LVs, it was found that cardiac performance was most sensitive to the combination of ventricular dilation and compromised muscle contractility. Integrated physiological modelling of this kind enables mechanistic investigations into the pumping function of the LV on an individualised basis. As demonstrated in this thesis, this type of quantitative modelling can be used to analyse the functional implications of changes to the geometry, structure or mechanical properties of normal hearts, and thus can provide insight into mechanisms underlying mechanical dysfunction in the diseased or failing heart.