Abstract
Understanding the healing and remodelling processes induced by myocardial infarction (MI) of the heart is important, and the mechanical properties of the myocardium post‐MI can be indicative for effective treatments aimed at avoiding eventual heart failure. MI remodelling is a multiscale feedback process between the mechanical loading and cellular adaptation. In this paper, we use an agent‐based model to describe collagen remodelling by fibroblasts regulated by chemical and mechanical cues after acute MI, and upscale into a finite element 3D left ventricular model. We model the dispersed collagen fibre structure using the angular integration method and have incorporated a collagen fibre tension‐compression switch in the left ventricle (LV) model. This enables us to study the scar healing (collagen deposition, degradation, and reorientation) of a rat heart post‐MI. Our results, in terms of collagen accumulation and alignment, compare well with published experimental data. In addition, we show that different shapes of the MI region can affect the collagen remodelling, and in particular, the mechanical cue plays an important role in the healing process.
Highlights
Myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow decreases or stops to a part of the heart, causing damage to the heart muscle
We extend the 2D agent-based model developed in Fomovsky and Holmes[16] to 3D, to describe the collagen remodelling post-MI
We follow the experimental study of the infarcted left ventricle (LV) of rats by Fomovsky et al,[31] in which cryoinfarctions were created by sewing steel cylinders filled with liquid nitrogen into tissues under the epicardial surfaces of rat ventricles
Summary
Myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow decreases or stops to a part of the heart, causing damage to the heart muscle. The healing process in the heart poses a complex multiscale soft tissue problem, involving cardiac growth and remodelling (G&R). Cellular growth is often considered to be the cause for residual stress.[1] The myocardial stress and constitutive properties are considered to be the two key factors in myocardial G&R.2. There are typically two types of G&R modelling approaches at the continuum level. One is the volumetric growth (the density remains unchanged) following the G&R, and the other is the density growth (volume remains unchanged). G&R can be modelled using the growth tensor first introduced by Rödriguez et al.[3] For
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