Rosuvastatin Slows the Progression of Aortic Stenosis Caused by Hypertension Regardless of Its Lipid-Lowering Effects

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Abstract

Background
There is epidemiological evidence associating cardiovascular risk factors with aortic valve stenosis. The development of aortic valve stenosis has been recently demonstrated in a hypertensive animal model. We hypothesize that treatment with rosuvastatin modifies this transformation.
Objective
To evaluate the effect of rosuvastatin on the development of aortic valve stenosis.
Material and Methods
Hypertension was induced in 43 male NZ rabbits by a one-kidney, one-clip Goldblatt procedure. The animals were randomly assigned to 3 groups: HT (n=17) without  treatment; HT+R (n=14) treated with rosuvastatin 2.5 mg/kg/day and HT+R+C (n=12) treated with rosuvastatin 2.5 mg/kg/day + cholesterol-enriched diet to keep baseline cholesterol levels. A control group (CG) underwent sham surgery (n=15). The characteristics of the aortic valve were measured by echocardiography at baseline, 3 and 6 months after inducing hypertension.
Results
After 6 months of follow-up, SBP and DBP presented greater increase in the group HT (49% and 40%, respectively; p <0.001) compared to groups treated with rosuvastatin (SBP = 23% and 25%; DBP = 28% and 26%; p <0.001 for HT+R and HT+R+C, respectively). Total cholesterol decreased by 45.7% (p <0.01) only in HT+R group. The aortic valve became thickened in the HT group (0.50 ± 0.01 vs. 0.62 ± 0.02 mm; p <0.01); there were no significant differences in HT+R and HT+R+C. Finally, the aortic valve area was reduced in HT (0.277 ± 0.024 vs. 0.208 ± 0.014 cm2; p <0.05), had no differences in HT+R and HT+R+C, and presented a non-significant increase in CG (0.264 ± 0.022 vs. 0.32 ± 0.016 cm2; p=0.07).
Conclusions
Rosuvastatin slows the progression of aortic valve stenosis caused by hypertension. This protection might be independent of the lipid-lowering effect of the drug.