UROP Project

A Computational Model for the Study of Ventricular Remodeling and Ischemic Mitral Regurgitation



Jan Müller

Program Director UROP


+49 241 80-90299


Key Info

Basic Information

Project Offer-Number:
UROP Abroad
Mechanical Engineering
Organisation unit:
Language Skills:
English / German
Computer Skills:
Ellen Kuhl


Cardiovascular disease is the number one cause of death in the United States and most other developed countries in the world. In the majority of patients, cardiovascular disease is acquired rather than congenital. For example, coronary artery disease is caused by plaque occlusion of one or multiple coronary arteries. As a result, a region of the myocardium, normally perfused by the occluded arteries, may be lacking sufficient oxygen. In several steps this ischemic region becomes first akinetic and then is progressively replaced by inactive scar tissue rich in collagen. During disease progression this scar and the surrounding region first of all do not contribute to the active role of the heart muscle, thus reduce pumping efficiency of the affected ventricle. Secondly, scar formation may disrupt normal electrophysiology and in many cases causes arrhythmic electrical conduction patterns. Lastly, ventricular adaptation to the altered mechanics of the scar area, also called ventricular remodeling, may initiate a down-ward spiral during which increasing ventricular volume causes increased wall stress, which in turn increases intraventricular diameter and so forth. Aside from reduced ejection fraction and overall ventricular function, when the left ventricular is affected, ventricular remodeling disrupts the natural force balance of the mitral-ventricular-complex. The mitral valve, one of the four heart valves that ensure unidirectional blood flow throughout the heart, is located between the left atrium and the left ventricle. During ventricular remodeling, the papillary muscles, protrusions from the endocardial left ventricular wall that are attached to the mitral valve through so called chordae tendinae, and the posterior annulus, the transition region between ventricular myocardium and the mitral valve, are being displaced laterally. This lateral motion deforms the mitral valve and restricts leaflet motion. In consequence, the mitral valve fails to coapt properly. The resulting backflow of blood through the leaking mitral valve is termed regurgitant flow and the pathologic occurrence is known as ischemic mitral regurgitation.


The goal of the present work is to use the continuum mechanical theory of growth and remodeling to recreate the above pathological complex. The student is provided with a patient-specific heart geometry, the material subroutines for isotropic and anisotropic ventricular growth, and a work station with a license of Abaqus, a non-linear, implicit finite element solver. We believe this project will greatly benefit the student in that it will familiarize the student with one of the most commonly used non-linear finite element solvers, necessitate the student to study cardiac anatomy, physiology, and pathophysiology, and provide the student with insights in non-linear continuum theory. The preliminary workflow is as follows: 1) Import the patient specific heart geometry in Abaqus 2) Assign previously determined fiber directions to the finite element model 3) Determine physiological parameters for the material and growth model 4) From a literature review determine a common infarct location and infarct area 5) Identify this region in the finite element model and assign different material parameters to this region based on literature data on scar tissue 6) Model the above pathological complex and study the effect of scar tissue formation in the left ventricle on intraventricular volume, diameter, papillary muscle location and displacement of the posterior annulus.


Mandatory: basic mechanics, Desirable: continuum mechanics, biomechanics, finite elements

Full Address

Stanford University
496 Lomita Mall, Durand 217
CA 94305 Stanford