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Aortic valve stenosis (AS) is the most common valvular heart disease in the Western world, affecting about 3% of the population over 75 years of age and after onset of symptoms is associated with adverse events including death.1 With the ageing of the population, AS likely will become an increasingly important health issue. Despite this grim prospect, a therapeutic strategy to slow the progression of AS has not been developed and the only effective treatment is aortic valve replacement. Furthermore, AS is a progressive condition, but the rate of progression is quite variable from individual to individual. The predilection of AS in the older individuals has led to the belief that AS was an inevitable result of a degenerative process, but research has shown that it is an active process involving multiple metabolic pathways, raising the possibility that the process can potentially be modified or interrupted.2
Epidemiological studies have shown that AS is associated with traditional atherosclerotic risk factors such as hypertension, smoking, diabetes and increased cholesterol. At the molecular level, AS also shares common features with atherosclerosis including lipid infiltration, inflammation, fibrosis and calcification in the subendothelial space and lamina fibrosa. Since lipoproteins are involved in several putative pathways in the development of AS, lipid-lowering agents such as statins would be expected to …
Funding The author has not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting or dissemination plans of this research.
Provenance and peer review Commissioned; externally peer reviewed.
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