{"id":"08049ac99a1e","type":"article","url":"https://hartvaat.nl/2026/11/01/verhoogd-lipoproteine-a-niet-geassocieerd-met-veneuze-trombo-embolie-in-prospect/","title":"Verhoogd lipoproteïne(a) niet geassocieerd met veneuze trombo-embolie in prospectieve cohorten","title_en":"Association between elevated lipoprotein (a) and venous thromboembolism: A systematic review and meta-analysis.","category":"cholesterol","category_label":"Cholesterol","professions":["cardioloog","internist"],"tags":[],"journal":"Atherosclerosis","doi":"10.1016/j.atherosclerosis.2026.121922","source_url":"https://doi.org/10.1016/j.atherosclerosis.2026.121922","authors":["Mahmoud Abdelnabi","Chanokporn Puchongmart","Ramzi Ibrahim","Sofia Lakhdar","Sammudeen Ibrahim","Hoang Nhat Pham","Luke Dreher","Hussein Abdul Nabi","Juan Farina","Chadi Ayoub","Reza Arsanjani"],"significance":4,"published":"2026-11-06","source_date":"2026-11-01","image":"","kennis":["https://hartvaat.nl/kennis/farmacologie/antiaritmica-farmacologie/","https://hartvaat.nl/kennis/lipiden/dyslipidemie-overzicht/"],"congress":"","summary_en":"A systematic review and meta-analysis of 11 observational studies (63,325 participants) evaluated the association between elevated lipoprotein(a) [Lp(a)] and venous thromboembolism (VTE) risk. While the pooled estimate suggested a borderline increased risk (OR/HR 1.34; p=0.049), this was driven entirely by case-control studies. Prospective cohort data showed no association (HR 0.99; 95% CI 0.85-1.15), indicating that the observed link in retrospective designs likely reflects bias or residual confounding Clinicians should not currently use Lp(a) levels to stratify VTE risk or guide preventive strategies.","created":"2026-10-30T02:17:18Z","updated":"2026-10-30T02:17:18Z","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":"Een systematische review en meta-analyse van elf observationele studies (63.325 deelnemers) onderzocht de relatie tussen verhoogd lipoproteïne(a) en het risico op veneuze trombo-embolie (VTE). Hoewel de gecombineerde analyse een licht verhoogd risico suggereerde (OR/HR 1,34; p=0,049), bleek dit effect volledig gedreven door case-control studies. Prospectieve cohortonderzoeken toonden geen verband (HR 0,99; 95%-BI 0,85-1,15), wat wijst op mogelijke vertekening of residual confounding. Voor de klinische praktijk betekent dit dat er op dit moment geen aanleiding is om Lp(a)-spiegels te gebruiken voor het inschatten van VTE-risico of voor preventieve maatregelen.","abstract_original":"BACKGROUND: Elevated lipoprotein(a) [Lp(a)] is an established cardiovascular risk factor linked to atherogenesis, inflammation, and thrombosis; however, its association with venous thromboembolism (VTE) remains uncertain, with inconsistent findings across observational studies. AIMS: To systematically evaluate the association between elevated Lp(a) levels and VTE risk and to examine differences by study design. METHODS: PubMed/MEDLINE, Embase, Scopus, Web of Science, and Cochrane Library were searched from inception through January 2026 for observational studies assessing Lp(a) and VTE. Effect estimates (odds ratios [ORs] or hazard ratios [HRs]) were pooled using DerSimonian-Laird random-effects models with Hartung-Knapp adjustment. Heterogeneity was assessed using I2 and τ2. Risk of bias was evaluated with ROBINS-E, publication bias with funnel plots, Egger's and Begg's tests, and certainty of evidence using GRADE. The primary outcome was VTE; secondary outcomes included deep vein thrombosis (DVT), pulmonary embolism (PE), and recurrent VTE. RESULTS: Eleven studies (6 case-control, 5 cohort; 63,325 participants; 3581 VTE events) were included. Elevated Lp(a) was associated with a borderline increased VTE risk (pooled OR/HR 1.34 [95% CI 1.00-1.80]; P = 0.049), with high heterogeneity (I2 = 77.8%) and a wide prediction interval (0.56-3.21). In stratified analyses, case-control studies showed a significant association (OR 1.88 [1.25-2.81]; I2 = 57.2%), whereas cohort studies showed no association (HR 0.99 [0.85-1.15]; I2 = 0%), with significant between-group differences (p < 0.0001). CONCLUSIONS: The association between elevated Lp(a) and VTE appears limited to case-control studies and is not supported by prospective cohort data, suggesting potential bias or residual confounding. Further large-scale and genetic studies are warranted to clarify this relationship."}