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The development of aortic stenosis (AS) is still under considerable discussion. Most likely, some of the same factors that develop and progress atherosclerosis are also in play for the development and progression of aortic valve disease. Especially high blood pressure, inflammation and high levels of low-density lipoprotein (LDL)-cholesterol seem to coincide with the development and progression of AS.1–3 However, what is increasingly clear is that the phenotypic presentation of AS has many causes and drivers for disease progression. In addition, different causes may lead to the same phenotype presentation in different patients, for example, in some patients, the driver is hypertension; in some, it is chronic inflammation and in some patients, it is high LDL-cholesterol that is the leading cause of development of AS. Furthermore, what also clouds our understanding of the pathogenesis of AS is that different causes might need to be at a certain level before the cause drives the development and progression of AS. A specific blood pressure load, a certain level of high-sensitivity C reactive protein and a certain level of LDL-cholesterol, all for a specific time duration, should be present before the factor drives the development of AS. Finally, different causes may affect the disease progression at different time points during the lifetime of AS development (eg, first inflammation, then ossification).
Diabetes has for more than 30 years been associated with the development of AS, as patients with AS have higher prevalence of diabetes than in the general population. Furthermore, several studies suggest that diabetes predisposes to AS and interacts with the severity of AS. Several studies show how hyperglycaemic and insulin resistance result in endothelial dysfunction, oxidation …
Contributors KW is the sole contributor to this editorial.
Funding The authors have 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.
Provenance and peer review Not commissioned; externally peer reviewed.
- Valvular heart disease