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Congestive Heart Failure (CHF) is among the heart diseases which accounted for > 54% of deaths world-wide in 2013 in a World Health Organizations report. CHF patients most often have a more sensitized carotid body (CB) chemoreceptor than normal. CB neural output stimulates output from the sympathetic nervous system. Increased CB output in CHF has in animal models been attributed to a loss of shear stress on the luminal surfaces of the CBs’ vascular endothelial cells. This down regulates KLF2. Methods to remove or attenuate the CB’s activity have been devised. These and variations of them could be therapeutic for CHF patients.

The Damaging Impact of Chronic Heart Failure on A Critical Interoreceptor and the Therapy for it