Electromechanical computational modeling of heart failure provides extensive analysis of cardiac pathophysiological features

Scritto il 13/01/2026
da Eva Casoni

Biomech Model Mechanobiol. 2026 Jan 13;25(1):15. doi: 10.1007/s10237-025-02038-2.

ABSTRACT

This study applies a high-performance, fully coupled 3D-0D electromechanical model to simulate cardiac function across multiple scenarios of heart failure with reduced ejection fraction (HFrEF), including ventricular tachycardia post-myocardial infarction and acute hypertension. By integrating biomechanical deformation, electromechanical coupling, and hemodynamic feedback, the model provides a comprehensive analysis of different stages of heart failure. A physiologically detailed 3D-0D electromechanical model was used to simulate pressure-volume loops under different pathological conditions. The model incorporates hemodynamic coupling within an electromechanical framework to quantify left ventricular performance markers in virtual scenarios. Additionally, myocardial strains along the principal fiber direction were computed to assess systolic dysfunction and deformation. The simulations accurately predicted the hemodynamic impact of HFrEF according to their electrophysiological and mechanical properties. The computationally derived pressure-volume loops demonstrated a strong agreement with clinical findings, highlighting key features of HFrEF such as reduced stroke volume, impaired contractility, and decreased ejection fraction. Furthermore, scar-related conduction abnormalities were associated with an increased risk of ventricular tachycardia, with failing hearts exhibiting greater hemodynamic instability during arrhythmic episodes. The proposed computational framework provides a powerful tool for investigating HFrEF progression and electromechanical dysfunction. By accurately replicating pressure-volume loop characteristics and hemodynamic alterations commonly seen in clinical settings, this model enhances the understanding of HFrEF and may support the development of targeted therapeutic strategies.

PMID:41530433 | DOI:10.1007/s10237-025-02038-2