{"id":"c7326d955da9","type":"article","url":"https://hartvaat.nl/2022/03/22/pelacarsen-op-lp-a-cholesterol-en-gecorrigeerd-ldl-cholesterol/","title":"Pelacarsen op Lp(a)-cholesterol en gecorrigeerd LDL-cholesterol","title_en":"Effect of Pelacarsen on Lipoprotein(a) Cholesterol and Corrected Low-Density Lipoprotein Cholesterol.","category":"cholesterol","category_label":"Cholesterol","professions":["apotheker","cardioloog","internist"],"tags":["ezetimibe","ldl-cholesterol","lipide-aferese","lipoproteïne-a","lipoproteïne-a-therapeutisch-doel","pelacarsen"],"journal":"Journal of the American College of Cardiology","doi":"10.1016/j.jacc.2021.12.032","source_url":"https://doi.org/10.1016/j.jacc.2021.12.032","authors":["Calvin Yeang","Ewa Karwatowska-Prokopczuk","Fei Su","Brian Dinh","Shuting Xia","Joseph L Witztum","Sotirios Tsimikas"],"significance":7,"published":"2022-03-22","source_date":"2022-03-22","image":"","kennis":["https://hartvaat.nl/kennis/lipiden/ldl-cholesterol-mechanisme/"],"congress":"","summary_en":"This analysis quantified the effect of pelacarsen on Lp(a)-associated cholesterol and its impact on corrected LDL cholesterol measurements, demonstrating that apparent LDL cholesterol includes a substantial Lp(a)-derived component that should be accounted for in treatment decisions.","created":"2026-07-03T10:29:40Z","updated":"2026-07-03T13:28:47Z","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":"Analyse van het effect van pelacarsen (Lp(a)-verlagend antisense) op Lp(a)-cholesterol en gecorrigeerd LDL. Kwantificeert de Lp(a)-bijdrage aan LDL.","abstract_original":"BACKGROUND: Laboratory methods that report low-density lipoprotein cholesterol (LDL-C) include both LDL-C and lipoprotein(a) cholesterol [Lp(a)-C] content. OBJECTIVES: The purpose of this study was to assess the effect of pelacarsen on directly measured Lp(a)-C and LDL-C corrected for its Lp(a)-C content. METHODS: The authors evaluated subjects with a history of cardiovascular disease and elevated Lp(a) randomized to 5 groups of cumulative monthly doses of 20-80 mg pelacarsen vs placebo. Direct Lp(a)-C was measured on isolated Lp(a) using LPA4-magnetic beads directed to apolipoprotein(a). LDL-C was reported as: 1) LDL-C as reported by the clinical laboratory; 2) LDL-Ccorr = laboratory-reported LDL-C - direct Lp(a)-C; and 3) LDL-CcorrDahlén = laboratory LDL-C - [Lp(a) mass × 0.30] estimated by the Dahlén formula. RESULTS: The baseline median Lp(a)-C values in the groups ranged from 11.9 to 15.6 mg/dL. Compared with placebo, pelacarsen resulted in dose-dependent decreases in Lp(a)-C (2% vs -29% to -67%; P = 0.001-<0.0001). Baseline laboratory-reported mean LDL-C ranged from 68.5 to 89.5 mg/dL, whereas LDL-Ccorr ranged from 55 to 74 mg/dL. Pelacarsen resulted in mean percent/absolute changes of -2% to -19%/-0.7 to -8.0 mg/dL (P = 0.95-0.05) in LDL-Ccorr, -7% to -26%/-5.4 to -9.4 mg/dL (P = 0.44-<0.0001) in laboratory-reported LDL-C, and 3.1% to 28.3%/0.1 to 9.5 mg/dL (P = 0.006-0.50) increases in LDL-CcorrDahlén. Total apoB declined by 3%-16% (P = 0.40-<0.0001), but non-Lp(a) apoB was not significantly changed. CONCLUSIONS: Pelacarsen significantly lowers direct Lp(a)-C and has neutral to mild lowering of LDL-Ccorr. In patients with elevated Lp(a), LDL-Ccorr provides a more accurate reflection of changes in LDL-C than either laboratory-reported LDL-C or the Dahlén formula."}