Steven Poelzing, Ph.D.
Solving the mystery of sudden cardiac death
What causes the heart's electrical system to malfunction?
Scientists are increasingly aware that sudden cardiac death — a significant cause of mortality in the United States and around the world — is linked to genetic mutations in cardiac proteins, or changes in those same proteins during diseases such as heart failure, ischemia, or diabetes.
One cardiac gap junction protein of interest, Connexin43, or Cx43, allows the spread of electrical activity between cardiac myocytes to coordinate uniform, synchronized contraction. Conventional theory suggests that reducing Cx43 expression slows the spread of electrical activity — conduction — in the heart and increases risk of arrhythmias leading to sudden death. The experimental relationships between conduction slowing, sudden cardiac death, and loss of Cx43 are not straightforward. Conflicting findings have led to a lack of experimental agreement on the degree of conduction slowing expected from a quantifiable reduction of Cx43.
Poelzing hypothesizes that the spread of electrical activity between cardiac myocytes is not only mediated through connexins, but also through electric fields between myocytes. His laboratory has demonstrated that the hydration state of the heart can mask or unmask conduction slowing in the presence of reduced Cx43 expression. Poelzing seeks to determine how pathological insults such as cardiac inflammation and edema modulate the risk of sudden death in the young and how age changes this relationship.
- Associate Professor, Fralin Biomedical Research Institute at VTC
- Associate Professor, Department of Biomedical Engineering and Mechanics, College of Engineering
- Associate Professor, Department of Internal Medicine, School of Medicine
- Co-Director, Translational Biology, Medicine, and Health Graduate Program
Veeraraghavan R, Lin J, Keener JP, Gourdie RG, Poelzing S. (2016). Potassium Channels in the Cx43 Gap Junction Perinexus Modulate Ephaptic Coupling: An Experimental and Modeling Study. Pflugers Archiv.
Veeraraghavan R, Lin J, Hoeker GS, Keener JP*, Gourdie RG*, Poelzing S*. (2015). Sodium channels in the Cx43 gap junction perinexus may constitute a cardiac ephapse: an experimental and modeling study. Pflugers Archive - European Journal of Physiology.
Greer-Short A, Poelzing S. (2015). Temporal response of ectopic activity in guinea pig ventricular myocardium in response to isoproterenol and acetylcholine. Frontiers in Physiology 6.
- University of Utah, Research Associate Professor, Bioengineering
- NASA Glenn Research Center, Consultant
- Case Western Reserve University, Research Assistant
- Wright State University, National Science Foundation Research Fellow
- MetroHealth Medical Center, Postdoctoral fellowship
- Case Western Reserve University, Ph.D., Biomedical Engineering
- Case Western Reserve University, MSE, Biomedical Engineering
- Wright State University, B.S., Biomedical Engineering
- Fellow, Heart Rhythm Society, 2015
- Fellow, American Heart Association, 2014
- Editorial Board, Frontiers in Cardiac Electrophysiology editorial board, 2010-Present
- Top Instructors in Engineering, University of Utah, 2008, 2009, 2010, 2011
- Michael Bilitch Fellowship in Cardiac Pacing and Electrophysiology, Heart Rhythm Society, 2004
Recent Media Coverage
Redirect ItemBig Lick of Science Podcast: Lub Dub: A Hearty Podcast , redirect Date: Aug 22, 2019