AI Networking Cookbook: Practical recipes for AI-assisted network automation and development
TL;DR
Evidence suggests that lower Lp(a) levels are a consequence of hepatic dysfunction rather than protective against cardiovascular disease, and recognition of this paradox may improve risk stratification and interpretation of Lp(a) in patients with MASLD.
Accumulating evidence indicates that considering the prothrombotic activities of Lp(a) will impact clinical management of Lp(a) and the deployment of Lp(a)-lowering therapies.
This narrative review summarizes the molecular biology, genetics, epidemiology, pathophysiological mechanisms, and clinical relevance of Lp(a), and critically examines current and emerging therapeutic strategies aimed at reducing Lp(a)-mediated cardiovascular risk.
Emerging evidence links Lp(a) to atrial fi brillation, broadening its clinical relevance and integrating Lp(a) testing into risk assessment and preparing for targeted therapies are critical steps in modern cardiovas-cular prevention.
Current evidence supports strong biological efficacy, but definitive proof of clinical benefit awaits ongoing randomized cardiovascular outcomes trials, including Lp(a)HORIZON (pelacarsen), OCEAN(a)-Outcomes (olpasiran) and ACCLAIM-Lp(a) (lepodisiran).
Novel unapproved therapies, including an antisense oligonucleotide, small interfering RNAs, and an oral small molecule have demonstrated Lp(a) reductions of up to 99% and are being tested in ongoing cardiovascular outcomes trials to determine whether pharmacologic Lp(a) lowering translates into reduced cardiovascular e...
The Lp(a) treatment landscape has moved from basic science to an active late-stage clinical pipeline and positive outcomes from these CVOTs could lead to regulatory approvals and guideline updates affecting hundreds of millions of high-risk patients globally.
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