Computational modeling of acute myocardial infarction

Abstract

Myocardial infarction, commonly known as heart attack, is caused by reduced blood supply and damages the heart muscle because of a lack of oxygen. Myocardial infarction initiates a cascade of biochemical and mechanical events. In the early stages, cardiomyocytes death, wall thinning, collagen degradation, and ventricular dilation are the immediate consequences of myocardial infarction. In the later stages, collagenous scar formation in the infarcted zone and hypertrophy of the non-infarcted zone are auto-regulatory mechanisms to partly correct for these events. Here we propose a computational model for the short-term adaptation after myocardial infarction using the continuum theory of multiplicative growth. Our model captures the effects of cell death initiating wall thinning, and collagen degradation initiating ventricular dilation. Our simulations agree well with clinical observations in early myocardial infarction. They represent a first step toward simulating the progression of myocardial infarction with the ultimate goal to predict the propensity toward heart failure as a function of infarct intensity, location, and size.

Keywords:

• Biomechanics
• growth
• smooth muscle cells
• hypertension
• finite element method

Notes

No potential conflict of interest was reported by the authors.

Applied Mechanics and Bioengineering, Aragon Institute of Engineering Research, University of Zaragoza, Zaragoza, Spain.

Additional information

Funding

This study was supported by the National Institutes of Health [grant number U01 HL119578] to Ellen Kuhl.