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Abstract

Atorvastatin Therapy Is Not Associated with Slowing the Progression of Aortic Stenosis: Findings of a Randomized Controlled Trial by Yunes Panahi, Amirhossein Sahebkar, Hamid Reza Taghipour, Yahya Dadjou, Bahram Pishgoo, Amir Sobh Rakhshankhah

Background: Aortic stenosis (AS) is the most common type of valvular cardiac disorders. AS has many risk factors in common with atherosclerosis. Hypercholesterolemia is an important pathomechanism for AS. However, the im-pact of statin drugs on slowing AS progression has not yet been well established.
Objective: To investigate the impact of statin therapy on slowing AS progression.
Methods: This was a randomized double-blind placebo-controlled trial in which 75 patients with mild to moderate AS were randomized to receive either simvastatin (20 mg/day) or placebo for a period of one year. Serum lipid profile, C-reactive protein (CRP), and echocardiographic parameters were evaluated at baseline as well as at the end of trial.
Results: Treatment with atorvastatin was associated with significant decreases in total cholesterol, triglycerides, and LDL-C and an elevation of HDL-C. None of the lipid profile parameters changed in the placebo group. Serum CRP was not significantly altered in any of the groups. Left ventricular end-systolic volume was significantly in-creased by the end of trial in the statin group (p = 0.012). In the placebo group, significant increases were ob-served for aortic valve mean (p = 0.017) and peak (p < 0.001) gradient. Other echocardiographic measures re-mained statistically unchanged in the statin and placebo groups. The number of patients whose disease progressed into severe stage was comparable between the groups and post-trial echocardiographic assessment did not reveal any significant change in the severity of AS between atorvastatin and placebo (p > 0.05).
Conclusions: The findings of the present randomized trial did not support a beneficial effect of statin therapy (20 mg/day) against AS progression in Iranian patients with mild to moderate disease.

DOI: 10.7754/Clin.Lab.2012.120319