Statin use for nonrheumatic calcific aortic valve stenosis

Abstract

Significant benefit of statin therapy in retarding hemodynamic deterioration was identified by favorable effects concerning annualized changes in peak aortic valve jet velocity and peak aortic valve pressure gradient; on the contrary, in statin-treated patients with aortic stenosis, no significant improvement was found for annualized changes in mean aortic valve pressure gradient and AVA and clinical outcomes.

High-mobility group box-1 protein induces osteogenic phenotype changes in aortic valve interstitial cells

“…Despite promising animal experiments, 32 several clinical trials showed that statins failed to alter the progression of aortic stenosis. 33,34 We demonstrated the role of HMGB1 in vitro, with emphasis on its pro-inflammation effect, but it may have other effects. This protein could be a new target for therapeutic intervention.…”

Insights Into Aortic Sclerosis and Its Relationship With Coronary Artery Disease

“…[66][67][68][69] Additionally, several meta-analyses found no significant differences between subjects treated with and without statins in terms of major echocardiographic findings (mean AV pressure gradient and AV area) or overall clinical outcomes. [70][71][72] These collective findings suggest that (1) statins are unlikely to significantly affect the course of AS, (2) AVS may be a more appropriate target for statins but further research is needed given the scarcity of data, and (3) statins have multifactorial effects that may not be fully characterized yet.…”

Is there evidence for statins in the treatment of aortic valve stenosis?

“…Finally, neo-angiogenesis contributes to AS development[ 30 , 31 ] and is responsible for reduced concentrations of the anti-angiogenesis protein chondromodulin-1 in damaged aortic valve tissue[ 32 ]. The resulting cell apoptosis, extracellular matrix formation and consequent thickening and calcification of the cusps, decreases aortic valve mobility and orifice areas, ultimately leading to an increased pressure gradient[ 33 ]. Nevertheless, there are some fundamental differences in the underlying molecular mechanisms with an early inflammation affecting fibroblasts in AS as opposed to late onset of inflammation in smooth muscle cells in CAD.…”