Dutch research
Work from Amsterdam UMC (Stroes, Nurmohamed, Kaiser, Stiekema, Wiegman, de Boer), Erasmus MC (Roeters van Lennep, Kaiser) and Leiden, and the Dutch role in the EAS consensus and the ESC 2025 update.
Topics
Every study, trial, video and milestone carries topic tags; these pages collect them.
Thrombosis and aspirin
The antifibrinolytic side of apo(a): venous thromboembolism data and the aspirin signals in ASPREE and MESA, coronary and valvular.
Lipoprotein apheresis
The German experience from 2008 onward, five- and twelve-year follow-up, and pelacarsen as its replacement.
Cascade screening
Testing relatives of index patients with high Lp(a): the Swedish programmes (LipoaScreen, STRIREG) and the guideline recommendations.
Familial hypercholesterolaemia and children
Lp(a) in FH cohorts and clinics, Lp(a) cholesterol inflating LDL-C, mutation-negative 'FH' explained by Lp(a), and paediatric measurement.
Ancestry and global distribution
Why medians differ by ancestry, why risk per nmol/L largely does not, and what that means for thresholds and for who qualifies for the outcomes trials.
Women
Sex differences in Lp(a) levels across the lifespan, menopause and hormone therapy, the 30-year Women's Health Study data and the venous thromboembolism signal.
Inflammation
Whether Lp(a) risk depends on inflammation (CRP, IL-6): the Copenhagen and biobank analyses, OxPL biology and what olpasiran does and does not change.
Guidelines and consensus
The EAS 2010 and 2022 statements, ESC/EAS 2019 and the 2025 focused update, the 2018 and 2026 US guidelines, NLA 2019 and 2024, CCS 2021, HEART UK 2019 and the Brussels declaration.
Therapy today
What can be done for a patient with high Lp(a) before the RNA drugs arrive: aggressive LDL-C lowering, PCSK9 inhibitors and their Lp(a) effect, CETP inhibition, aspirin signals, apheresis for the extreme case, and what statins, ezetimibe and lifestyle do not do.
RNA therapeutics
Antisense (pelacarsen) and siRNA (olpasiran, lepodisiran, zerlasiran) against LPA mRNA: the phase 1 and 2 trials, the durability data and the outcomes trials that will decide the field.
Mechanisms
Apo(a) and plasminogen homology, oxidised phospholipids, arterial wall inflammation and primed monocytes, plaque vulnerability, thrombosis: how the particle does its damage, largely from Dutch and Californian laboratories.
Aortic stenosis
Lp(a) as a causal factor in calcific aortic valve disease: the LPA GWAS signal, the Copenhagen cohorts, PET and CT progression studies, and the prospect of Lp(a) lowering as the first medical therapy for the valve.
Testing and measurement
Whom to test and when, mg/dL versus nmol/L, isoform-insensitive assays and the LC-MS/MS reference method, thresholds (30, 50, 70, 90 mg/dL; 75, 125, 150, 175, 200 nmol/L), the low testing rates and the once-in-a-lifetime recommendation.
Epidemiology and risk
Population cohorts, trial biobanks and registries: how much risk elevated Lp(a) carries for coronary disease, stroke, aortic stenosis, heart failure and mortality, in primary and secondary prevention, and how that risk sits alongside LDL-C and inflammation.
Genetics and causality
The LPA gene, the kringle IV type 2 copy-number variation, the SNPs that modify it, and the Mendelian randomisation studies (Clarke, Kamstrup, Burgess, Emdin, Björnson) that made Lp(a) a causal risk factor rather than a marker.
All tags
risk prediction 272PCSK9 inhibition 130diabetes 116stroke 104risk 76Statins 74plaque imaging 61pelacarsen 53trials 50olpasiran 42phase 3 36phase 2 28CETP inhibition 25heart failure 25Oral inhibition 23lepodisiran 13screening 12zerlasiran 12phase 1 11history 9education 9oral 8readout 6dementia 5europe 5outcomes trial 4congress 3United States 3ESC 2025 3siRNA 3secondary prevention 3primary prevention 2regulatory 2ESC/EAS 2025 2AHA 2024 2aha 2026 1ESC 2026 1ACC/AHA 2026 1New Horizons 2026 1AHA 2025 1small molecule 1ACC.25 1ALPACA 1policy 1KRAKEN 1ALPACAR 1parallax 1AHA 2023 1AHA 2022 1OCEAN(a)-DOSE 1ACC.22 1APOLLO 1canada 1antisense 1United Kingdom 1