Currently only small numbers of ASCVD patients achieve target LDL-c levels due to certain issues surrounding lipid lowering therapy. Prof. John Kastelein discusses the role of PCSK9 inhibition and future perspectives on lipid lowering.

A post-hoc analysis showed reduced LDL-c levels and improved lipid profiles up to 180 days with one or two doses of inclisiran on top of standard care in the presence and absence of diabetes, compared to placebo.

AHA 2018 In the ANITSCHKOW study, patients with very high Lp(a) were treated with evolocumab 420 mg once monthly. The 14% lowering in Lp(a) was not sufficient to eliminate the inflammatory stimulans induced by Lp(a).

AHA 2018 Lp(a) is a highly prevalent risk factor, with to date no therapy to lower its levels. A phase 2b study now shows that an antisense oligonucleotide potently lowers production of Lp(a), to optimal levels.

AHA 2018 A randomized phase 2b trial showed safety and efficacy of the antisense nucleotide AKCEA-APO(a)-Lrx at reducing Lp(a) levels in patients with CVD.

AHA 2018 The updated cholesterol guidelines help physicians to personalize treatment based on risk assessment, and now include CAC measurement to guide treatment decisions in certain patients.

Meta-analysis of individual-patient data shows that elevated Lp(a) levels of 50 mg/dL or higher were associated with an increased hazard ratio of CV events, independent of other risk factors and statin or placebo treatment.

This is a summary of the presentation by John Kastelein, in which he discusses targeting PCSK9 in clinical practice, focusing on issues surrounding prescription of PCSK9 monoclonal antibodies.

In high Lp(a)-associated CV risk patients, reduction of Lp(a) with PCSK9 inhibition lowered this risk, even at very low LDL-c levels.

Trials on lowering Lp(a) have thusfar failed to show a CV outcome benefit. Brian Ference describes a more informative approach to look at Lp(a) data to identify who may benefit from Lp(a)-lowering therapy.

Elevated Lp(a) is now officially considered a genetically determined risk factor for CVD in the USA. Chapman summarizes how Lp(a) is atherogenic and how novel therapies may target this process.

In two prospective population cohorts, the increased CVD risk in individuals with high Lp(a) levels was reduced when LDL-c levels were <2.5 mmol/L.