The diminutive size of our aortic valve -- just shy of a -- belies its essential role in pushing oxygen-rich blood from the heart into the aorta, our body's largest vessel, and from there to all other organs. Yet for decades, researchers have focused less on damaged valves than on atherosclerosis, the gradual hardening of the blood vessels themselves. Thanks, in part, to pigs at the University of Wisconsin (UW)-Madison's Arlington Agricultural Research Station, scientists are now catching up on understanding the roots of calcific aortic valve disease (CAVD). "For a long time, people thought CAVD was just the valvular equivalent of atherosclerosis," says Kristyn Masters (see photo at end), PhD, a Professor of Biomedical Engineering at UW-Madison and Vice Chair of the department. "Today, we know that valve cells are quite unique and distinct from the smooth muscle cells in our blood vessels, which explains why some treatments for atherosclerosis, such as statins, don't work for CAVD, and why the search for drugs has to start from scratch." A team led by Dr. Masters has cleared a longstanding hurdle in that search with a study published online on December 27, 2017 in PNAS. The researchers teased apart, for the first time, the early cascade of events that may eventually cause stenosis, a severe narrowing of the aortic valve that reduces blood flow to body tissues and weakens the heart. The only current treatment for stenosis is valve replacement, which typically requires risky and expensive open-heart surgery. "Our study sheds new light on the differences between atherosclerosis and CAVD, especially in terms of bottleneck events that we can target with drugs," says Dr. Masters, whose work is supported by the National Institutes of Health and the American Heart Association.
Login Or Register To Read Full Story