Key result
Lipoprotein(a) is implicated in the pathophysiology of aortic stenosis, though this abstract provides no quantitative results.
Why the study?
No medical therapy has demonstrated an ability to slow or halt progression of calcific aortic stenosis despite its increasing healthcare burden.
Calcific aortic stenosis (AS) is the most common form of valvular heart disease in the Western world, and its healthcare burden is expected to double over the next 50 years.1 Currently, no medical therapy has demonstrated an ability to slow or halt progression of this common condition. While surgical or percutaneous aortic valve replacement is the only available treatment, important questions still remain with respect to the optimal timing of intervention, associated procedural risks and long-term durability. The quest to develop novel treatments to prevent or slow down AS, potentially removing the need for surgical intervention altogether, has not been successful up to now. Atherogenic apolipoprotein B-containing lipoproteins, like low-density lipoprotein (LDL) and lipoprotein(a) (Lp(a)), have been clearly implicated in the pathophysiology of AS, in particular in the initiation phase of the disease and with incident AS. However, multiple randomised clinical trials Simvastatin and Ezetimibe in Aortic Stenosis (SEAS), Scottish Aortic Stenosis and Lipid Lowering Trial, Impact in Regression (SALTIRE)
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Tzolos et al. (2021) conducted an editorial in Calcific aortic stenosis. Lipoprotein(a) was evaluated. Lipoprotein(a) is implicated in the pathophysiology of aortic stenosis, though this abstract provides no quantitative results.
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