Electromechanical modeling of human ventricles with ischemic cardiomyopathy: numerical simulations in sinus rhythm and under arrhythmia

TL;DR

This paper presents a novel patient-specific 3D electromechanical model of the human ventricles with ischemic cardiomyopathy, capable of simulating sinus rhythm and ventricular tachycardia, integrating electrophysiology, mechanics, and hemodynamics for clinical insights.

Contribution

The study introduces a new coupled electromechanical and circulatory modeling framework for ischemic cardiomyopathy, enabling detailed simulations of arrhythmias and hemodynamics in a patient-specific context.

Findings

The model accurately reproduces ventricular activity in sinus rhythm and VT.

Different circulatory parameters yield similar hemodynamic outcomes.

The VT was classified as unstable based on simulation results.

Abstract

We developed a novel patient-specific computational model for the numerical simulation of ventricular electromechanics in patients with ischemic cardiomyopathy (ICM). This model reproduces the activity both in sinus rhythm (SR) and in ventricular tachycardia (VT). The presence of scars, grey zones and non-remodeled regions of the myocardium is accounted for by the introduction of a spatially heterogeneous coefficient in the 3D electromechanics model. This 3D electromechanics model is firstly coupled with a 2-element Windkessel afterload model to fit the pressure-volume (PV) loop of a patient-specific left ventricle (LV) with ICM in SR. Then, we employ the coupling with a 0D closed-loop circulation model to analyze a VT circuit over multiple heartbeats on the same LV. We highlight similarities and differences on the solutions obtained by the electrophysiology model and those of the electromechanics model, while considering different scenarios for the circulatory system. We observe that very different parametrizations of the circulation model induce the same hemodynamical considerations for the patient at hand. Specifically, we classify this VT as unstable. We conclude by stressing the importance of combining electrophysiological, mechanical and hemodynamical models to provide relevant clinical indicators in how arrhythmias evolve and can potentially lead to sudden cardiac death.