{"id":"434f28964449","type":"article","url":"https://hartvaat.nl/2025/01/28/lp-a-en-ldl-cholesterol-onafhankelijke-cv-risicopaden/","title":"Lp(a) en LDL-cholesterol: onafhankelijke CV-risicopaden","title_en":"Independence of Lipoprotein(a) and Low-Density Lipoprotein Cholesterol-Mediated Cardiovascular Risk: A Participant-Level Meta-Analysis.","category":"cholesterol","category_label":"Cholesterol","professions":["cardioloog","internist"],"tags":["dyslipidemie","ezetimibe","hdl-cholesterol","ldl-cholesterol","lipide-aferese","lipidenverlaging","lipoproteïne-a","lipoproteïne-a-therapeutisch-doel","pelacarsen","statines"],"journal":"Circulation","doi":"10.1161/CIRCULATIONAHA.124.069556","source_url":"https://doi.org/10.1161/CIRCULATIONAHA.124.069556","authors":["Harpreet S Bhatia","Simon Wandel","Peter Willeit","Anastasia Lesogor","Keith Bailey","Paul M Ridker","Paul Nestel","John Simes","Andrew Tonkin","Gregory G Schwartz","Helen Colhoun","Christoph Wanner","Sotirios Tsimikas"],"significance":7,"published":"2025-01-28","source_date":"2025-01-28","image":"","kennis":["https://hartvaat.nl/kennis/lipiden/lp-a-verhoogd/","https://hartvaat.nl/kennis/lipiden/ldl-cholesterol-mechanisme/"],"congress":"","summary_en":"This participant-level analysis confirmed that Lp(a) and LDL cholesterol represent independent cardiovascular risk pathways, supporting the concept that both must be addressed for comprehensive atherosclerotic risk reduction.","created":"2026-07-03T10:31:27Z","updated":"2026-07-03T13:30:28Z","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 bevestigde dat Lp(a) en LDL-cholesterol onafhankelijke cardiovasculaire risicopaden vertegenwoordigen. Verlaging van beide is nodig voor optimale risicoreductie, wat dubbele therapie ondersteunt.","abstract_original":"BACKGROUND: Low-density lipoprotein cholesterol (LDL-C) and lipoprotein(a) (Lp[a]) levels are independently associated with atherosclerotic cardiovascular disease (ASCVD). However, the relationship between Lp(a) level, LDL-C level, and ASCVD risk at different thresholds is not well defined. METHODS: A participant-level meta-analysis of 27 658 participants enrolled in 6 placebo-controlled statin trials was performed to assess the association of LDL-C and Lp(a) levels with risk of fatal or nonfatal coronary heart disease events, stroke, or any coronary or carotid revascularization (ASCVD). The multivariable-adjusted association between baseline Lp(a) level and ASCVD risk was modeled continuously using generalized additive models, and the association between baseline LDL-C level and ASCVD risk by baseline Lp(a) level by Cox proportional hazards models with random effects. The joint association between Lp(a) level and statin-achieved LDL-C level with ASCVD risk was evaluated using Cox proportional hazards models. RESULTS: Compared with an Lp(a) level of 5 mg/dL, increasing levels of Lp(a) were log-linearly associated with ASCVD risk in statin- and placebo-treated patients. Among statin-treated individuals, those with Lp(a) level >50 mg/dL (≈125 nmol/L) had increased risk across all quartiles of achieved LDL-C level and absolute change in LDL-C level. Even among those with the lowest quartile of achieved LDL-C level (3.1-77.0 mg/dL), those with Lp(a) level >50 mg/dL had greater ASCVD risk (hazard ratio, 1.38 [95% CI, 1.06-1.79]) than those with Lp(a) level ≤50 mg/dL. The greatest risk was observed with both Lp(a) level >50 mg/dL and LDL-C level in the fourth quartile (hazard ratio, 1.90 [95% CI, 1.46-2.48]). CONCLUSIONS: These findings demonstrate the independent and additive nature of Lp(a) and LDL-C levels for ASCVD risk, and that LDL-C lowering does not fully offset Lp(a)-mediated risk."}