Study of Myocardial Viscoelasticity in Myocardial Infarction and Aortic Stenosis Models by Brillouin Scattering (CAT#: STEM-ST-0150-YJL)

Introduction

Cardiac function relies not only on the ability of the sarcomere to contract and relax, but also on the preservation of the shape and structure of the organ. The mechanical properties of the myocardial tissue determine how sarcomeres shorten and develop force independently of the preexisting loading conditions. Heart diseases are often associated with dysregulation of these mechanical properties, which lead to remodeling of the ventricular wall, tissue stiffness and progressively to dysfunction. Specifically, changes in myocardial viscoelasticity are linked to dynamic stiffness and heart disease. However, assessing these properties directly and at a local scale is challenging.
Myocardial infarction is caused by the blockage of a coronary artery, which deprives cardiac cells from the necessary oxygen and nutrients. This results in massive cardiomyocyte death and a steep decline in cardiac contraction. Similarly, myocardial hypertrophy is initially developed as a compensatory response to aortic stenosis or to other pathological conditions demanding increased contractile capacity.