Post-infarct evolution of ventricular and myocardial function

Area of Science:

• Cardiovascular Mechanics
• Computational Biology
• Biomedical Engineering

Background:

• Adverse ventricular remodeling post-myocardial infarction (MI) can lead to heart failure (HF).
• Understanding the relationship between myocardial material property changes and cardiac function is crucial for developing new therapies.
• Finite element modeling offers a powerful tool to investigate these complex mechanical interactions.

Purpose of the Study:

• To model the mechanical consequences of acute and chronic myocardial infarction (MI) using a finite element model.
• To investigate the impact of infarct characteristics (stiffening, thinning, fiber reorientation) on cardiac mechanics and function.
• To elucidate the mechanisms underlying the loss of contractile function and the development of heart failure (HF) post-MI.

Main Methods:

• A finite element model of cardiac mechanics was developed using a thick-walled truncated ellipsoidal geometry.
• Acute MI was simulated by inhibiting active stress generation.
• Chronic MI was modeled by incorporating infarct material stiffening, wall thinning, and fiber reorientation.

Main Results:

• Acute MI resulted in a 25% decrease in stroke work.
• Infarct stiffening, wall thinning, and fiber reorientation did not significantly alter overall pump function.
• However, these chronic changes redistributed mechanical work density in healthy adjacent tissues, indicating impaired function in these areas.

Conclusions:

• The relative loss in pump function following MI exceeds the loss in healthy myocardial tissue due to impaired mechanics in adjacent regions.
• Chronic changes in infarct properties significantly affect the mechanical environment of surrounding healthy myocardium.
• These findings highlight the complex interplay between infarct characteristics and cardiac function, offering insights for potential therapeutic strategies.