Abstract
Calcific aortic stenosis is a progressive disease that has become more prevalent in recent decades. Despite advances in research to uncover underlying biomechanisms, and development of new generations of prosthetic valves and replacement techniques, management of calcific aortic stenosis still comes with unresolved complications. In this review, we highlight underlying molecular mechanisms of acquired aortic stenosis calcification in relation to hemodynamics, complications related to the disease, diagnostic methods, and evolving treatment practices for calcific aortic stenosis.
Highlights
Calcific aortic stenosis (AS) is the most common valve disease in developed countries [1, 2], in which valves thicken and stiffen, and in some cases nodular deposits form, limiting valve function
Aortic valve (AV) leaflets consist of three layers: the ventricularis layer is elastin-rich and located on the ventricular side; the spongiosa is made of proteoglycans that provide lubrication for the other layers; and a fibrosa layer made of a dense collagen network is on the aortic side of the valve [7, 8], which provides much of the structural support in response to mechanical forces [9]
A study of 699 high-risk patients with severe aortic stenosis who were randomly treated with Surgical aortic valve replacement (SAVR) and transcatheter aortic valve replacement (TAVR) in PARTNER 1 trial showed that 1year mortality rates were similar between the transcatheter and surgically treated groups (24.2% TAVR vs. 26.8% SAVR), but hemodynamics and post-operative outcomes were significantly different
Summary
Calcific aortic stenosis (AS) is the most common valve disease in developed countries [1, 2], in which valves thicken and stiffen, and in some cases nodular deposits form, limiting valve function. This may result in valve regurgitation with concomitant stenosis. Calcific AS is a progressive disease that advances with age [3, 4], affecting ∼0.2% of people 50–59 years of age and increasing to 9.8% for 80–89 years [5, 6]. In this review we highlight engineering perspectives toward recent advancements in the treatment of AS, underlying molecular pathways and mechanisms of the calcification process, clinical characteristics, hemodynamics, complications of calcific AS, diagnoses, and common treatment practices for calcific AS
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