title: 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.
authors.affiliation: a Mathematical Institute, University of Oxford , Oxford , UK .
authors.forename: P
authors.initials: P
authors.lastname: Sáez
authors.affiliation: b Department of Mechanical Engineering , Stanford University , Stanford , CA , USA .
authors.forename: E
authors.initials: E
authors.lastname: Kuhl
mesh_terms: D016923:Cell Death; D003094:Collagen / Q000378:metabolism; D003198:Computer Simulation; D006352:Heart Ventricles / Q000473:pathology; D006801:Humans; D008955:Models, Cardiovascular; D009203:Myocardial Infarction / Q000473:pathology*; D009206:Myocardium / Q000473:pathology; D032383:Myocytes, Cardiac / Q000473:pathology
chemical_list: D003094:Collagen
keywords: Biomechanics; finite element method; growth; hypertension; smooth muscle cells