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REFLECTIONS
Dyslipidaemia
Dyslipidaemia Global Newsletter #11 2026

by high costs, physician underprescribing, and strict insurance
barriers. As the therapeutic landscape evolves to include highly CLICK HERE Dyslipidaemia
accessible oral agents and potential permanent gene editing, FOR THE LINK TO FULL ARTICLE
PCSK9 inhibition is poised to overcome current treatment
barriers and radically reshape the global management of CVD.

Lipoprotein(a)-lowering therapies: A promising future.
Zhang J, et al. Eur Heart J. 2026 Feb 13:ehag092. Online ahead of print.

Lipoprotein(a) (Lp(a)) has recently emerged as a significant, genetically determined contributor to the residual CV risk. Unlike LDL-C,
Lp(a) levels are almost entirely determined by genetics, reaching adult levels early in life and acting as a highly atherogenic and
prothrombotic particle in the bloodstream. Despite its strong association with premature ASCVD and calcific aortic valve stenosis
(CAVS), elevated Lp(a) has historically been difficult to treat because traditional lipid-lowering therapies and lifestyle modifications
have minimal impact on its concentrations.

This state-of-the-art review aims to summarise the current landscape of Lp(a)-lowering therapies, detailing the limitations of existing
treatments while providing a comprehensive update on emerging, highly potent therapeutics. The authors synthesised existing
epidemiological data and clinical trial results to evaluate the safety, efficacy, and administrative mechanisms of both currently
available lipid-lowering drugs and novel agents currently in Phase II and Phase III development.

Comparison of the mechanism, administration, and Lp(a)-lowering effects
of currently available lipid-lowering therapies

apoB, apolipoprotein B; ATP, adenosine triphosphate; HMG-CoA, 3-hydroxy-3-methylglutaryl coenzyme A; PCSK9, proprotein convertase subtilisin/kexin type 9;
siRNA, small interfering ribonucleic acid.

Conventional CV therapies are largely ineffective for targeted Lp(a) reduction. Statins, ezetimibe, and bempedoic acid show
virtually no clinically significant effect on Lp(a) levels. While niacin and currently appr oved PCSK9 inhibitors (like evolocumab and
alirocumab) offer modest reductions (around 20% to 30%), they have not proven sufficient to eliminate the specific residual risk
conferred by severely elevated Lp(a). Until recently, lipoprotein apheresis remained the only highly effective method, yielding up
to a 68% reduction after a single session, but its high cost, invasive nature, and need for frequent clinical visits severely limit its
widespread use.

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