Key result
Simulated LCx infarction yields the most severe impairment in computational models, dropping LVEF to ~32%.
Why the study?
Understanding how infarct location in LAD, RCA, or LCx territories influences electromechanical behavior is essential for linking scar topology to functional impairment and arrhythmogenic risk.
Does infarct location (LAD, RCA, LCx) affect electromechanical and hemodynamic behavior in a computational biventricular model?
Does infarct location (LAD, RCA, LCx) affect electromechanical and hemodynamic behavior in a computational biventricular model?
In a computational biventricular model, infarct location significantly modulates cardiac electromechanical and hemodynamic behavior, with LCx scars causing the most severe impairment and arrhythmogenic events.
Answers are grounded in this paper and cite their sources.
May differentially impair LVEF and trigger ectopy by location in models; leaves open translation to clinical post-MI care.
Myocardial infarction alters both electrical activation and mechanical performance of the ventricles, with the specific location of the scar strongly influencing the resulting electromechanical behavior. Depending on whether the infarct affects the left anterior descending (LAD), right coronary artery (RCA), or left circumflex (LCx) territories, the patterns of depolarization, wall motion, and hemodynamic output differ markedly. Understanding these location-dependent effects is essential for linking scar topology to functional impairment and arrhythmogenic risk. We developed a realistic biventricular heart model and generated scarred variants by introducing infarcts occupying 13.2% of the left ventricle (LV) in each of the three coronary territories. Simulations were performed using the CARPentry framework, which couples ionic models for both the myocardium and Purkinje conduction system with mechanical models incorporating stretch-activated channels (SACs), active tension generation, and nonlinear tissue mechanics, integrated with the CircAdapt lumped-parameter circulation model. For the same infarction volume, the RCA scar produced a greater reduction in LV ejection fraction (LVEF) compared to the LAD scar (14.6% vs 9.9% decrease relative to the healthy case). The area exhibiting SAC-induced depolarization was also larger in the RCA case. The LCx infarction caused the most severe impairment. No stable EF was observed, and among the last six sinus beats of the 12-beat simulation, the highest LVEF reached only 32.4% (vs. 50.7% in the healthy heart). The pressure–volume loops during these beats showed clear beat to beat changes and ectopic activity. The findings demonstrate that infarct location substantially modulates cardiac electromechanical and hemodynamic behavior. Among the investigated cases, the LAD scar had the least impact, while the LCx scar caused the strongest impairment and triggered arrhythmogenic events, highlighting the importance of regional vulnerability in post-infarction remodeling.
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Moradicheghamahi et al. (2026) studied Myocardial infarction. Simulated myocardial infarction in LAD, RCA, or LCx territories vs. Healthy heart model was evaluated on Left ventricular ejection fraction (LVEF). In a computational model, simulated LCx infarction caused the most severe impairment (max LVEF 32.4% vs 50.7% healthy), while RCA and LAD scars reduced LVEF by 14.6% and 9.9% respectively.
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