Abstract
Myocardial infarction (MI) rapidly impairs cardiac contractile function and instigates maladaptive remodeling leading to heart failure. Patient-specific models are a maturing technology for developing and determining therapeutic modalities for MI that require accurate descriptions of myocardial mechanics. While substantial tissue volume reductions of 15–20% during systole have been reported, myocardium is commonly modeled as incompressible. We developed a myocardial model to simulate experimentally-observed systolic volume reductions in an ovine model of MI. Sheep-specific simulations of the cardiac cycle were performed using both incompressible and compressible tissue material models, and with synchronous or measurement-guided contraction. The compressible tissue model with measurement-guided contraction gave best agreement with experimentally measured reductions in tissue volume at peak systole, ventricular kinematics, and wall thickness changes. The incompressible model predicted myofiber peak contractile stresses approximately double the compressible model (182.8 kPa, 107.4 kPa respectively). Compensatory changes in remaining normal myocardium with MI present required less increase of contractile stress in the compressible model than the incompressible model (32.1%, 53.5%, respectively). The compressible model therefore provided more accurate representation of ventricular kinematics and potentially more realistic computed active contraction levels in the simulated infarcted heart. Our findings suggest that myocardial compressibility should be incorporated into future cardiac models for improved accuracy.
Highlights
Myocardial infarction (MI) rapidly impairs cardiac contractile function and instigates maladaptive remodeling leading to heart failure
We developed an in silico model of cardiac function with and without MI based on extensive datasets from a single ovine heart collected in vivo, ex situ, and ex vivo (Figs. 2 and 3), including image and data registration, regional heterogeneity, electrophysiology, and organ-level function integration
We modeled the distinctive compressible material behavior observed in the myocardium by assuming it to be nearly incompressible in diastole, but compressible in systole to allow for volume reductions while actively contracting[22]
Summary
Myocardial infarction (MI) rapidly impairs cardiac contractile function and instigates maladaptive remodeling leading to heart failure. MI induces myocardial fibrosis, which includes significant compositional, structural, and functional changes during the transition from infarcted myocardium to scar t issue[2]. This maladaptive remodeling process is typically severe and irreversible, leading to dilatation of the left ventricle (LV), wall thinning, papillary muscle displacement, mitral valve leaflet tethering and regurgitation, and mitral annular dilatation[3]. These profound pathophysiological changes collectively induce progressive heart failure (HF)[4]. The development of computational models of myocardial behaviour remains a challenging area, as several fundamental phenomena remain incompletely understood
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