Key result
In a 3D model, LV infarct fractions above ~10-15% progressively impair EF and trigger premature activations.
Why the study?
Sudden cardiac death after MI remains a major problem, partly driven by incompletely understood electromechanical feedback mechanisms involving scar stiffness, border zone remodeling, and stretch-activated channels.
Computational modeling demonstrates that infarct volume fractions above 10-15% trigger premature activations via stretch-activated channels, providing mechanistic insight into post-infarction arrhythmic risk and heart failure progression.
Answers are grounded in this paper and cite their sources.
Model elucidates MEF in post-MI arrhythmogenesis; extends computational insights but leaves clinical translation open.
Sudden cardiac death after myocardial infarction (MI) remains a major clinical problem, partly driven by complex electromechanical feedback mechanisms that are not fully understood. In particular, the interplay between scar stiffness, border zone (BZ) remodeling, mechano-electric feedback (MEF) through stretch-activated channels (SACs), and cross-bridge formation, can strongly influence ventricular function and arrhythmogenic risk. In this study, we developed a 3D finite element model of human ventricular electromechanics coupled with a closed-loop circulation model to investigate the impact of scar size on cardiac function. Before addressing scar effects, we first analyzed the spatial resolution of the mesh to ensure reliable electromechanical predictions. Within the present electromechanical framework and mechanical discretization, spatial resolutions of approximately 1.0-1.3 mm were required to capture SAC-driven depolarizations in the BZ. Using this confirmed to be suitable resolution, we examined infarct volume fractions (IVFs) from 5-20% of the left ventricle (LV). Increasing IVF progressively impaired contractility and ejection fraction, with a nonlinear threshold emerging between 10% and 15% IVF in the primary models studied here, above which SACs elicited premature activations which disrupted sinus-driven dynamics, and produced irregular multi-beat PV-loop patterns. These findings highlight two key insights: spatial resolution is critical for capturing SAC-mediated feedback accurately, and scar extent strongly influences the severity of this feedback, with larger scars significantly altering ventricular dynamics. Together, this work provides mechanistic understanding of how scar enlargement can accelerate heart failure progression and arrhythmic risk through nonlinear MEF.
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Moradicheghamahi et al. (2026) studied Myocardial infarction. Infarct volume fraction (IVF) 5-20% was evaluated on Contractility, ejection fraction, and stretch-activated channel (SAC)-driven depolarizations. In a 3D computational model, increasing infarct volume fraction above a 10-15% threshold progressively impaired contractility and ejection fraction, triggering premature activations.
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