Naomi Chesler, Ph.D.
Naomi C. Chesler obtained her BS in Engineering (General) from Swarthmore College, MS in Mechanical Engineering from MIT and PhD in Medical Engineering from the Harvard-MIT Division of Health Sciences and Technology. She is Director of the Edwards Lifesciences Center for Advanced Cardiovascular Technology at the University of California, Irvine and Professor of Biomedical Engineering. Her contributions to research are in two main areas: cardiovascular biomechanics and engineering education. With regard to the first, she is internationally recognized for her work in cardiovascular biomechanics and mechanobiology. She has been continuously funded by the NIH for over 10 years. Her contributions to engineering education center around the impact of novel approaches to physiology instruction on student learning and how students learn engineering using a learning sciences approach. This work has been supported by several concurrent grants from the NSF. She has been the recipient of numerous awards, including the NSF Career award, Denice D. Denton Emerging Leader Award, Polygon Teaching Award for Biomedical Engineering, two Fulbright Scholar Awards, Fellow of the American Society of Mechanical Engineers, Fellow of the American Institute of Medical and Biological Engineering, Fellow of the International Academy of Medical and Biological Engineering and was named recipient of the 2014 Diversity Award from the Biomedical Engineering Society and the 2017 Diversity Award from the UW-Madison College of Engineering. In 2019, she was awarded the ASME MacDonald Award for excellence in mentoring and advising other professionals in the field and founded Building STEM Equity, LLC (buildingSTEMequity.com) to promote diversity, equity and inclusion in science, technology, engineering, and mathematics (STEM) disciplines.
Title: The Biomechanics of Pulmonary Hypertension Secondary to Left Heart Failure
Abstract: Pulmonary hypertension (PH) due to left heart failure (PH-LHF) is the most common cause of PH. This disease begins as pulmonary venous hypertension and then progresses to combined arterial and venous hypertension, which increases morbidity and mortality. The biomechanical and mechanobiological mechanisms that drive the transition from the first to the second, identified hemodynamically by increased pulmonary vascular resistance, are not well understood. We take an integrated experimental-modeling approach to advance knowledge in this area. We take a similar approach to understanding the impact of impaired left heart function on right heart function. Robust assessment of right heart mechanical function requires invasive catheterization with pressure-volume loop analysis at varying preloads. Discovering the mechanical mechanisms of pulmonary vascular and right ventricular dysfunction in PH-LHF is critical to understanding disease progression and developing novel therapies to prevent right ventricular and pulmonary vascular deterioration in response to LHF progression.
Dr. Christine Schmidt