Abstract
Detailed models of the biomechanics of the heart are important both for developing improved interventions for patients with heart disease and also for patient risk stratification and treatment planning. For instance, stress distributions in the heart affect cardiac remodelling, but such distributions are not presently accessible in patients. Biomechanical models of the heart offer detailed three-dimensional deformation, stress and strain fields that can supplement conventional clinical data. In this work, we introduce dynamic computational models of the human left ventricle (LV) that are derived from clinical imaging data obtained from a healthy subject and from a patient with a myocardial infarction (MI). Both models incorporate a detailed invariant-based orthotropic description of the passive elasticity of the ventricular myocardium along with a detailed biophysical model of active tension generation in the ventricular muscle. These constitutive models are employed within a dynamic simulation framework that accounts for the inertia of the ventricular muscle and the blood that is based on an immersed boundary (IB) method with a finite element description of the structural mechanics. The geometry of the models is based on data obtained non-invasively by cardiac magnetic resonance (CMR). CMR imaging data are also used to estimate the parameters of the passive and active constitutive models, which are determined so that the simulated end-diastolic and end-systolic volumes agree with the corresponding volumes determined from the CMR imaging studies. Using these models, we simulate LV dynamics from enddiastole to end-systole. The results of our simulations are shown to be in good agreement with subject-specific CMR-derived strain measurements and also with earlier clinical studies on human LV strain distributions.
Highlights
Cardiovascular diseases are the leading causes of death worldwide and account for ~17 million deaths annually, or ~30% of all deaths worldwide (WHO, 2011)
We develop dynamic models of left ventricle (LV) function in health and disease using a version of the immersed boundary (IB) method (Griffith & Luo) that uses Lagrangian finite element (FE) methods to describe the passive and active response of the ventricular myocardium
For the myocardial infarction (MI) patient, who suffers from minor mitral valve regurgitation, we choose a slightly higher end-diastolic pressure of 16 mmHg (Mielniczuk et al, 2007), and as in the healthy model, the end-systolic pressure is estimated from the brachial arterial pressure of the patient, which in this case is 110 mmHg
Summary
Cardiovascular diseases are the leading causes of death worldwide and account for ~17 million deaths annually, or ~30% of all deaths worldwide (WHO, 2011). One of the most common outcomes of coronary heart disease is myocardial infarction (MI). Untreated or unsuccessfully treated MIs can cause extensive fibrous scarring and the expansion of the infarct region, hypertrophy of the remote myocardium and ventricular dilatation. These adverse remodelling processes can impair cardiac pump function and can lead to lethal arrhythmias such as ventricular fibrillation. There is a clear need for integrative mathematical and computational models of the heart that can help to understand the interplay of physiological and pathophysiological mechanisms at the molecular, cellular, tissue and organ scales in both the ischaemic region and in the remote healthy myocardium
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