Key result
Lipoprotein(a) represents an independent risk factor for calcific aortic valve disease and mediates its development through endothelial dysfunction, oxidized phospholipids, and valve calcification.
Why the study?
Calcified aortic valve disease lacks effective drug treatments, and clinical trials targeting lipoprotein(a) reduction as a primary endpoint are lacking despite its crucial pathophysiological role.
Lp(a) is a causal risk factor and active pathophysiological driver in calcific aortic valve disease, highlighting the need for targeted Lp(a)-lowering clinical trials.
Lp(a) may warrant investigation as a therapeutic target in calcific aortic valve disease; leaves open whether lowering it improves outcomes in trials.
Calcified aortic valve disease (CAVD) is the most common valvular cardiovascular disease with increasing incidence and mortality. The primary treatment for CAVD is surgical or transcatheter aortic valve replacement and there remains a lack of effective drug treatment. Recently, lipoprotein (a) (Lp(a)) has been considered to play a crucial role in CAVD pathophysiology. Multiple studies have shown that Lp(a) represents an independent risk factor for CAVD. Moreover, Lp(a) mediates the occurrence and development of CAVD by affecting aortic valve endothelial dysfunction, indirectly promoting foam cell formation through oxidized phospholipids (OxPL), inflammation, oxidative stress, and directly promotes valve calcification. However, there is a lack of clinical trials with Lp(a) reduction as a primary endpoint. This review aims to explore the relationship and mechanism between Lp(a) and CAVD, and focuses on the current drugs that can be used as potential therapeutic targets for CAVD.
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Hu et al. (2022) conducted a review in Calcific Aortic Valve Disease (CAVD). Lipoprotein(a) represents an independent risk factor for calcific aortic valve disease and mediates its development through endothelial dysfunction, oxidized phospholipids, and valve calcification.
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