University Honors

Mitral valve degeneration is a common age-related condition that progressively impairs cardiac function by reducing the flexibility and structural integrity of the valve leaflets. The mitral valve regulates blood flow from the left atrium to the left ventricle, and its dysfunction can lead to regurgitation, a condition in which the valve fails to close fully and allows backward flow into the atrium. A key contributor to this degeneration is the gradual breakdown of elastin, an extracellular matrix (ECM) protein that enables the valve leaflets to stretch and recoil during each heartbeat. As elastin deteriorates, mechanical loading shifts to stiffer collagen fibers, which can alter leaflet motion and contribute to disorders such as mitral valve prolapse. Previous research has characterized tissue behavior after complete or nearly complete removal of elastin, but aging occurs as a gradual process rather than an abrupt loss of the ECM components. As a result, little is known about how progressive elastin degradation affects the mechanical properties of mitral valve tissue over time. This project addresses this gap by quantifying tissue-level mechanical changes in porcine mitral valve anterior leaflets following controlled, stepwise degradation of elastin. The study employs three methods: (i) biaxial tension and stress-relaxation testing of untreated leaflet samples to establish baseline properties, (ii) enzymatic treatment at defined time intervals to selectively degrade elastin, and (iii) repeated biaxial mechanical testing after each degradation stage. By correlating changes in mechanical response with the time course of elastin loss, this work aims to clarify how aging-like ECM remodeling alters valve function. These findings are expected to improve understanding of how degenerative processes develop and may ultimately inform more effective surgical repair strategies and computational models of valve mechanics.