{"id":"53e412f7e2a6","type":"article","url":"https://hartvaat.nl/2026/10/01/lipoproteine-a-bevordert-atherosclerose-en-trombose-mechanismen-en-klinische-imp/","title":"Lipoproteïne(a) bevordert atherosclerose en trombose — mechanismen en klinische implicaties","title_en":"Lipoprotein(a): a unique lipoprotein at the crossroads of atherosclerosis and thrombosis.","category":"cholesterol","category_label":"Cholesterol","professions":["cardioloog","internist"],"tags":[],"journal":"Current opinion in lipidology","doi":"10.1097/MOL.0000000000001049","source_url":"https://doi.org/10.1097/MOL.0000000000001049","authors":["Michael B Boffa","Marlys L Koschinsky"],"significance":5,"published":"2026-09-12","source_date":"2026-10-01","image":"https://hartvaat.nl/global/img/6e2cc0469790.webp","kennis":["https://hartvaat.nl/kennis/lipiden/lpa-meten-wanneer-waarom/","https://hartvaat.nl/kennis/preventie/aspirine-primaire-preventie/"],"congress":"","summary_en":"This narrative review examines the dual pathophysiological role of elevated lipoprotein(a) [Lp(a)] in atherosclerosis and thrombosis. Evidence indicates that Lp(a) promotes vulnerable plaque formation through oxidized phospholipids and fosters a lysis-resistant clot architecture, with clinical data suggesting a specific primary prevention benefit from aspirin in high-Lp(a) patients. These insights highlight that accounting for Lp(a)’s prothrombotic properties should directly inform clinical management and the strategic use of emerging Lp(a)-lowering therapies.","created":"2026-09-06T00:47:29Z","updated":"2026-09-06T00:47:34Z","licence":"Citeer vrij, met bronvermelding en een link naar hartvaat.nl (de url van het record). Samenvattingen zijn redactioneel werk van HartVaat; de oorspronkelijke publicaties blijven van hun uitgevers (doi). Geen medisch advies.","body_markdown":"Deze overzichtsstudie beschrijft de pathofysiologische rol van verhoogd lipoproteïne(a) [Lp(a)] bij atherosclerotische cardiovasculaire ziekte en trombose. Preclinisch en klinisch bewijs toont aan dat Lp(a) via geoxideerde fosfolipiden kwetsbare plaques bevordert en een lyse-resistente clot-architectuur induceert, waarbij patiënten met verhoogde waarden mogelijk baat hebben bij aspirine in de primaire preventie. Deze inzichten onderstrepen dat het rekening houden met de prothrombotische eigenschappen van Lp(a) direct van invloed is op het klinisch management en de inzet van Lp(a)-verlagende therapieën.","abstract_original":"PURPOSE OF REVIEW: Elevated plasma concentrations of lipoprotein(a) [Lp(a)] are a causal and independent risk factor for atherosclerotic cardiovascular disease and an emerging therapeutic target. However, despite Lp(a) being on the cusp of widespread clinical consideration, fundamental questions regarding the pathophysiology of Lp(a) remain, most notably its contribution to atherothrombosis. This review will summarize recent evidence for both indirect and direct prothrombotic roles of Lp(a). RECENT FINDINGS: Preclinical studies show that the proinflammatory properties of Lp(a) - largely attributable to its cargo of oxidized phospholipids - promote vulnerable plaques through effects on vascular and immune/inflammatory cells. Advanced imaging techniques show that elevated Lp(a) is associated with vulnerable plaque phenotypes in patients. Regarding thrombosis, previous assumptions that Lp(a) is antifibrinolytic have given way to an emerging picture that Lp(a) promotes a lysis-resistant clot architecture while stimulating the coagulation cascade and potentiating platelet responses. Indeed, clinical studies have demonstrated that patients with elevated Lp(a) specifically accrue clinical benefit from aspirin in the primary prevention setting. SUMMARY: That elevated Lp(a) is both directly and indirectly prothrombotic remains to be proven by additional clinical and animal model studies Nonetheless, the 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."}