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ACE linked to calcium growth on aortic valve

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www.ProHealth.com • October 22, 2002


Future studies may find that ACE inhibitors, a class of drugs now taken by people with high blood pressure, could slow down or prevent the development of aortic valve calcium, say University of Washington researchers. Currently, the only treatment for severe calcium in the aortic valve is surgical replacement.

"Since we already know that ACE inhibition has benefit in a similar disease, atherosclerosis, further study of this therapy in calcific aortic valvular disease makes a lot of sense," says the lead author, Dr. Kevin O’Brien, an associate professor of medicine in the UW School of Medicine’s Division of Cardiology.

In the study, published in the Oct. 22 issue of Circulation, O’Brien and colleagues analyzed 21 human aortic valves, either from autopsy or from people who were having their valves replaced. Angiotensin-converting enzyme, or ACE, was not detected in normal aortic valves, but was present in all valves with lesions.

ACE was found in association with LDL cholesterol, both in lesions and in the bloodstream, raising the possibility that LDL carries the ACE into lesions, where the ACE then contributes to aortic valve disease development. The findings also raise the possibility that the association of ACE with LDL particles may be relevant to a number of diseases in which LDL accumulates, such as atherosclerosis and some renal diseases.

In March, O’Brien and colleagues published an article demonstrating that use of statins, which lower LDL levels, is associated with a lower rate of aortic valve calcification. According to O’Brien, "The new findings raise the possibility that ACE inhibitors also might be of benefit in patients with this disease."

However, O’Brien cautions that much more study is needed before ACE inhibitors are used routinely in patients with aortic valve disease.

The study was funded, in part, by King Pharmaceuticals, which manufactures an ACE inhibitor.

Other authors of the paper include Drs. Jeffrey L. Probstfield, David M. Shavelle, Michael T. Caulfield, Catherine M. Otto, and Thomas O. McDonald, M.S., all of the Division of Cardiology at UW, and Dr. Katherine Olin-Lewis of the Division of Metabolism, Endocrinology and Nutrition. Shavelle is currently at Harbor-UCLA Medical Center in Torrance, Calif, and Caulfield is currently at Massachusetts General Hospital Boston.



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