Prof. Stroes gives an introduction to the symposium about different aspects of lipoprotein(a) (Lp(a)), that was held during the virtual ESC 2020 congress.
Prof. Bittner summarizes findings from post-hoc analyses of FOURIER and ODYSSEY OUTCOMES on the relationship between Lp(a) lowering by PCSK9 inhibition and CV risk.
RNA therapeutics can reduce production of apo(a) in hepatocytes and thereby prevent assembly of Lp(a). This presentation provides an overview of phase 2 studies with antisense mediated Lp(a) lowering.
Prof. Laufs discusses the role of triglycerides and Lp(a) in the context of residual risk.
High Lp(a) levels are associated with increased risk of CV events. Pia Kamstrup presents the evidence from studies and in addition talks about challenges when determining Lp(a) levels.
Nick Nurmohamed explains what Lp(a) is and how correction of LDL-c for Lp(a) reduces genetic testing for FH.
Prof. Jukema explains the main principles for LDL-c-lowering therapy as described in the 2019 ESC/EAS guidelines and discusses results from several trials that investigated the effect of Lp(a) on CV outcomes.
Which lipids/lipoproteins, besides LDL-c, play a role in determining CV risk and can help targeting therapy in those with residual lipid risk?
Prof. Landmesser shows data that form the rationale behind new guideline recommendations, among which the lower LDL-c target for patients at very high risk.
Erin Bohula explains which determinants of residual CV risk we nowadays know and presents study results on how to target these.
Prof. Steg presents data of the ODYSSEY Outcomes trial in specific subgroups of ACS patients that benefit most from alirocumab therapy, and discusses the effect of this PCSK9 inhibitor by baseline Lp(a) levels.
Lp(a) meeting Prof. Marcovina emphasizes the importance of considering apo(a) size polymorphism when measuring Lp(a) levels in patients and discusses the Lp(a) Standardization Program.
Lp(a) meeting Existing clinical LDL-c assays cannot distinguish LDL-c from Lp(a)-c. Dr. Yeang discusses how Lp(a)-c is included in LDL-c measurements and what the clinical impact of measuring Lp(a)-c can be.
Lp(a) meeting Pia Kamstrup shares data of two general population studies that reveal the effects of elevated Lp(a) levels on CV events, and effects of Lp(a) risk genotypes, which are consistent with Lp(a) being a causal risk factor for CVD.
Lp(a) meeting Prof. Tsimikas discusses the phase 2 apo(a)-LRx trial that evaluated Lp(a) lowering with an antisense oligonucleotide and presents NHLBI recommendations on Lp(a) lowering.
Lp(a) meeting Small isoforms of Lp(a) are associated with high Lp(a) concentrations and increased CVD risk. The team of Kronenberg discovered a mutation in the Kringle-IV type 2 region of Lp(a), which has a modifying effect on Lp(a) levels and CVD risk.
Lp(a) meeting Elisa Waldmann shows prospective data on reduced CV event rates after regular Lp(a) apheresis in patients with high baseline Lp(a) levels and emphasizes the need of randomized controlled data.
Lp(a) meeting The prevalence of clinical FH was investigated in the Copenhagen General Population Study with adjustment for the cholesterol content in Lp(a). Prof. Nordestgaard shares possible ways to interpret these results.
Lp(a) meeting Zheng shows study results on the pathophysiological role of elevated Lp(a) and oxidized phospholipids levels in progression of aortic stenosis.
EAS 2019 Prof. Chapman lists the newest findings on the associations of Lp(a) levels, PCSK9 inhibitors and CV risk, based on new analyses of the FOURIER and ODYSSEY OUTCOMES trials.
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.
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.
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.
VBWG at ACC 2018 Several novel targets have been discovered and new lipid-modifying therapies are being developed to prevent CVD, beyond LDL-c. Elliot Brinton discusses several of these, including omega-3 prescriptions, pemafibrate, apoC3, Lp(a), and shares the first trial results.
Prof. John Kastelein describes 3 major disturbances in lipoprotein metabolism contributing to CV risk. Novel therapies are being developed to address residual risk after LDL-c eradication.
VBWG ACC 2017 Sotirios Tsimikas summarises the rationale of innovative therapeutic approaches targeting Lp(a), ApoC3 or ATP citric lyase and in what stage of clinical testing they currently are.
PCSK9 Expert Opinions Prof. Gilles Lambert describes the development of PCSK9 inhibitors since the discovery in 2002 of PCSK9 as a circulating protein targeting the LDL receptor for degradation. Now in 2017, results of outcome trials with a PCSK9 inhibitor are available.
Gilles Lambert, MD describes the discovery and biology of PCSK9 and the effect of PCSK9-inhibitors on LDL-C and Lp(a).
Sandra Revill Tremulis, founder of the Lipoprotein(a) Foundation, shares her experiences as a patient with elevated Lp(a), and consequently a high CV risk, despite a healthy lifestyle.
Prof. Klaus G. Parhofer (Munich, Germany) discusses the effects of currently available therapies to treat individuals with elevated Lp(a) levels, and shares a treatment algorithm to lower CV risk in these patients.
Individuals with elevated Lp(a) levels are at increased CV risk. Lp(a) levels are hardly responsive to currently available medication, so new therapeutic strategies are needed. Prof. Stroes summarises our understanding of Lp(a)-induced atherogenesis and how this may be targeted with novel therapies.