Thomas G. Gleason, MD, MS
Year elected: 2017
Current membership category: Active
University of Pittsburgh School of Medicine
5200 Centre Ave., Suite 715
Pittsburgh, PA 15232
United States of America
I am currently the Ronald V. Pellegrini Professor and Chief of the Division of Cardiac at the University of Pittsburgh and Co-Director of the Heart and Vascular Institute at UPMC with primary academic and clinical interests focused on valvular heart disease, thoracic aortic disease and vascular biology. My clinical research interests include the innovation of techniques for aortic valve repair and preservation, a distinct area within cardiac surgery that has been poorly developed. My most significant clinical contribution to the field in this regard has been the designing of a novel technique to repair severely regurgitant bicuspid aortic valves (BAV). I also developed a comprehensive, pathoanatomically-based arch reconstruction strategy for type A aortic dissection repair focused on reduction of neurologic complications.
I also established and direct the Thoracic Aortic Disease Research Laboratory within the McGowan Institute for Regenerative Medicine at the University of Pittsburgh to facilitate translational basic science research on the vascular biology and biomechanics of thoracic aortic diseases. In 2003, I began and have since maintained a thoracic aortic tissue bank to facilitate this research that now houses over 700 thoracic aortic tissue samples, over 550 aortic smooth muscle cell lines (of which many have now been immortalized for more controlled experimental use) and over 75 endothelial cell lines. These assets in total allow me to optimally design and direct studies aimed at identifying the cause of thoracic aortic aneurysm formation most specifically in the context of BAV-associated aortopathy. I currently hypothesize that reactive oxygen species play a pivotal role in the TAA formation and we introduced the novel theory that the BAV-associated aortopathy is mediated by cellular oxidative stress, altered biomechanics in the wall, and a unique matrix remodeling process--all of which are mechanisms distinct from those occurring in degenerative aneurysms.