High cholesterol and calcification are to blame for aortic valve disease

(CHICAGO) High cholesterol levels can lead to fatty deposits in the aortic valve. These deposits may induce undifferentiated cells to transform to bone-forming cells that calcify and narrow the aortic valve, according to researchers. Narrowing of the aortic valve is a common condition that causes the heart to have to squeeze harder to support normal blood flow, causing the heart muscle to enlarge and eventually fail. A study published today in Circulation authored by researchers at Northwestern and the Mayo Clinic is the first to explain the mechanism responsible for this process.

Aortic valvular disease is the most common reason for surgical valve replacement. No medical therapy has been proven to alter the progression of aortic valve disease. We conducted a test on laboratory model of aortic stenosis to determine whether high cholesterol led to the fatty deposits and resulting bone formation in the aortic valve and whether this progression could be controlled with the use of statins, explains lead author Nalini Rajamannan, MD, cardiologist, Northwestern Memorial Hospital and assistant professor of cardiology, The Feinberg School of Medicine at Northwestern University.

Our lab studies showed that statins greatly reduced the prevalence of the bone-forming cells and reduced the extent of changes in the aortic valve, said Dr. Rajamannan. Our findings, combined with recent retrospective clinical studies that showed that statins in patients slowed the rate of progression for aortic valve disease, point to possible benefits of using statins to treat patients with early stages of the aortic valve disease process. Earlier statin use may prolong the time to severe disease and the need for surgical valve replacement. Statins are drugs that block the formation of cholesterol in the liver and increase the production of the receptors on liver cells that clean the bad cholesterol from the blood.

We need to do large randomized trials using stat

Contact: Amanda Widtfeldt
Northwestern Memorial Hospital

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