Ohio State Researchers Examine How Fibrosis Affects Heart’s Natural Pacemaker
Future studies are needed to determine whether inhibiting or increasing one of the identified proteins during heart failure progression can prevent some of the SAN dysfunction and reduce the need for pacemakers.
“We know these fibroblasts are important for normal SAN activity,” Fedorov said. “The SAN is like a car battery. In order for the car to run, it needs a battery and insulated wires for good conductivity. The SAN generates an electrical signal and conducts it to the atria through a pathway of cells. But if you have too much fibrosis around those cells, it can disrupt that signal, leading to a heartbeat that’s too slow or irregular.”
“Efficient treatment for patients with SAN arrhythmias can be possible only with a fundamental understanding of how things work at the cellular level. We believe that our mapping of the human SAN fibroblast – the first of its kind – will open up exciting new therapeutic avenues to treat patients with SAN arrhythmias,” said Anuradha Kalyanasundaram, first author and a research scientist in the Ohio State Department of Physiology and Cell Biology.
Researchers used human hearts donated for research by organ donor families through Lifeline of Ohio and by heart failure patients of the Ohio State Wexner Medical Center Division of Cardiac Surgery.
This research was funded by the National Institutes of Health, Leducq Foundation and the Bob and Corinne Frick Center for Heart Failure and Arrhythmia, the nation’s first center dedicated to treating those with heart failure and arrhythmia.
Other Ohio State researchers include Ning Li, Miranda Gardner, Esthela Artiga, Brian Hansen, Amy Webb, Michael Freitas, Maciej Pietrzak, Dr. Bryan Whitson, Dr. Nahush Mokadam and Paul Janssen.
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Media Contact: Amy Colgan, Wexner Medical Center Media Relations, 614-293-3737, [email protected]
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