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Aortic stenosis is common and potentially fatal. Recent key insights into the pathophysiology of this disease suggest it is likely to represent a self-perpetuating cycle of injury where tissue calcification is the major driver. Also, the mechanisms governing this appear closely related to calcium homeostasis and bone metabolism. Manipulation of these processes may offer a means by which aortic stenosis progression can be inhibited using drugs currently licensed to treat osteoporosis. Indeed, a prospective randomized controlled trial is currently underway for determining whether denosumab or bisphosphonates can slow aortic stenosis disease. If successful, this would meet a major unmet clinical need.

Original publication

DOI

10.1586/14779072.2015.1037284

Type

Journal article

Journal

Expert rev cardiovasc ther

Publication Date

05/2015

Volume

13

Pages

461 - 463

Keywords

18F-fluoride, aortic stenosis, bisphosphonates, calcification, denosumab, osteoporosis, Aortic Valve Stenosis, Bone and Bones, Calcium, Denosumab, Diphosphonates, Disease Progression, Humans, Osteoporosis, Randomized Controlled Trials as Topic