Key result
Elevated Lipoprotein(a) levels act as an independent, causative risk factor for the development and progression of calcific aortic valve stenosis.
Why the study?
Calcific aortic valve stenosis causes significant morbidity and mortality in the elderly, and studies have implicated Lp(a) as a strong genetic causative risk factor.
This review highlights the causative role of elevated Lipoprotein(a) in the pathogenesis and progression of calcific aortic valve stenosis, suggesting that lowering Lp(a) could be a potential therapeutic strategy.
Supports Lp(a) as a potential target in calcific aortic stenosis; leaves open whether lowering it alters progression or outcomes.
Calcific aortic valve stenosis is the most common valve disease in the elderly population and is associated with significant morbidity and mortality. This condition is characterised by gradual fibrosis, thickening, and calcification of the affected leaflets, leading to decreased leaflet mobility and increased obstruction of the blood flow from the left ventricle. Lipoprotein(a) [Lp(a)] is a complex polymorphic lipoprotein with proatherogenic, proinflammatory, and prothrombotic properties. Several epidemiologic and clinical studies have described elevated Lp(a) levels as an independent causative risk factor for cardiovascular disease, including coronary artery disease, stroke, peripheral artery disease, heart failure, and venous thromboembolism. On the other hand, several studies have also described Lp(a) as a strong genetic causative risk factor for aortic valve calcification and aortic valve stenosis. In this review, the authors present and discuss the scientific and clinical evidence pertaining to the role of Lp(a) in calcific aortic valve stenosis. INTRODUCTIO
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Kosmas et al. (2019) conducted a review in Calcific Aortic Valve Stenosis. Lipoprotein(a) was evaluated. Elevated Lipoprotein(a) levels act as an independent, causative risk factor for the development and progression of calcific aortic valve stenosis.
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