Computational modeling of acute myocardial infarction. Issue 10 (26th July 2016)

• Record Type: Journal Article
• Authors: Sáez, P.; Kuhl, E.
• Is Part Of: Computer methods in biomechanics and biomedical engineering. Volume 19:Issue 10(2016)
• Page Start: 1107
• Page End: 1115
• Publication Date: 2016-07-26
• Subjects: Biomechanics -- growth -- smooth muscle cells -- hypertension -- finite element method; Biomechanics -- Data processing -- Periodicals; Biomedical engineering -- Periodicals; Biomechanics -- Periodicals; Biomedical Engineering -- methods -- Periodicals; Computing Methodologies -- Periodicals; 612.7
• DOI: 10.1080/10255842.2015.1105965
• Languages: English
• ISSNs: 1025-5842

Abstract

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.