Contractile Adaptation of the Left Ventricle Post-myocardial Infarction: Predictions by Rodent-Specific Computational
Emilio A Mendiola1, Sunder Neelakantan1, Qian Xiang2
1Computational Cardiovascular Bioengineering Laboratory, Department of Biomedical Engineering, Texas A&M University, College Station, TX, USA.
Annals of Biomedical Engineering
|November 17, 2022
Summary
Myocardial infarction (MI) triggers cardiac remodeling. Computational models reveal altered active tension and myofiber mechanics in rat hearts post-MI, offering insights into heart function and failure progression.
Area of Science:
- Cardiovascular Research
- Computational Biology
- Biomedical Engineering
Background:
- Myocardial infarction (MI) causes cardiac myocyte death and fibrotic scarring, leading to left ventricular free wall (LVFW) remodeling.
- This remodeling alters cellular and extracellular components heterogeneously, impacting diastolic and systolic functions and potentially causing heart failure.
- While passive remodeling is understood, active LVFW properties and their organ-level effects post-MI remain understudied.
Purpose of the Study:
- To develop high-fidelity rodent cardiac models (RCCMs) of MI to investigate heterogeneous active remodeling.
- To analyze changes in active tension, myofiber mechanics, and infarct region properties over time post-MI.
- To explore the relationship between regional remodeling and overall left ventricular (LV) function.
Main Methods:
- Created finite-element (FE) rat cardiac models (RCCMs) using extensive datasets from MI rat hearts (1-wk to 4-wk post-MI).
- Integrated detailed imaging data (geometry, fiber architecture, infarct zone via late gadolinium enhancement).
- Performed in-silico experiments to predict active tension, myofiber mechanics, and strain patterns.
Main Results:
- Models predicted higher active tension in remote myocardium early post-MI, returning to control levels later.
- Late-stage MI hearts showed smaller myofiber ranges and reduced fiber helicity, correlating with lower contractile forces needed for measured ejection fractions.
- Infarct region collagen orientation had minimal impact on organ function; reduced/positive end-systolic circumferential strains indicated infarct properties.
Conclusions:
- Computational cardiac models provide detailed insights into regional passive and active remodeling post-MI.
- These models complement traditional assessments, offering a more comprehensive understanding of cardiac performance.
- Patient-specific simulations hold promise for advancing individualized prognosis and intervention strategies for MI.
