{"id":"9902dcf950d8","type":"article","url":"https://hartvaat.nl/2019/09/01/persisterende-arteriele-wandinflammatie-bij-verhoogd-lp-a-ondanks-lage-ldl/","title":"Persisterende arteriële wandinflammatie bij verhoogd Lp(a) ondanks lage LDL","title_en":"Persistent arterial wall inflammation in patients with elevated lipoprotein(a) despite strong low-density lipoprotein cholesterol reduction by proprotein convertase subtilisin/kexin type 9 antibody treatment.","category":"cholesterol","category_label":"Cholesterol","professions":["cardioloog","internist"],"tags":["anemie-ckd","aortainsufficiëntie","aspirine","cetp-remmers","diabetes-en-hart","dyslipidemie","ezetimibe","inflammatie","ldl-cholesterol","lipide-aferese","lipidenverlaging","lipoproteïne-a","lipoproteïne-a-therapeutisch-doel","niet-statine-therapie","ouderen","pcsk9-remmers","pelacarsen","perifeer-vaatlijden","soul-trial","statines"],"journal":"European heart journal","doi":"10.1093/eurheartj/ehy862","source_url":"https://doi.org/10.1093/eurheartj/ehy862","authors":["Lotte C A Stiekema","Erik S G Stroes","Simone L Verweij","Helina Kassahun","Lisa Chen","Scott M Wasserman","Marc S Sabatine","Venkatesh Mani","Zahi A Fayad"],"significance":7,"published":"2019-09-01","source_date":"2019-09-01","image":"","kennis":["https://hartvaat.nl/kennis/lipiden/lpa-meten-wanneer-waarom/","https://hartvaat.nl/kennis/lipiden/lp-a-verhoogd/"],"congress":"","summary_en":"This imaging study showed that arterial wall inflammation persists in patients with elevated Lp(a) despite strong LDL cholesterol lowering with statins and PCSK9 inhibitors, suggesting that Lp(a)-driven inflammation requires specific Lp(a)-lowering therapy.","created":"2026-07-03T10:28:07Z","updated":"2026-07-03T13:27:18Z","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":"Studie die aantoont dat arteriële wandinflammatie persisteert bij patiënten met verhoogd Lp(a) ondanks sterke LDL-verlaging. Lp(a) als onafhankelijke inflammatoire risicofactor.","abstract_original":"AIMS: Subjects with lipoprotein(a) [Lp(a)] elevation have increased arterial wall inflammation and cardiovascular risk. In patients at increased cardiovascular risk, arterial wall inflammation is reduced following lipid-lowering therapy by statin treatment or lipoprotein apheresis. However, it is unknown whether lipid-lowering treatment in elevated Lp(a) subjects alters arterial wall inflammation. We evaluated whether evolocumab, which lowers both low-density lipoprotein cholesterol (LDL-C) and Lp(a), attenuates arterial wall inflammation in patients with elevated Lp(a). METHODS AND RESULTS: In this multicentre, randomized, double-blind, placebo-controlled study, 129 patients {median [interquartile range (IQR)]: age 60.0 [54.0-67.0] years, Lp(a) 200.0 [155.5-301.5] nmol/L [80.0 (62.5-121.0) mg/dL]; mean [standard deviation (SD)] LDL-C 3.7 [1.0] mmol/L [144.0 (39.7) mg/dL]; National Cholesterol Education Program high risk, 25.6%} were randomized to monthly subcutaneous evolocumab 420 mg or placebo. Compared with placebo, evolocumab reduced LDL-C by 60.7% [95% confidence interval (CI) 65.8-55.5] and Lp(a) by 13.9% (95% CI 19.3-8.5). Among evolocumab-treated patients, the Week 16 mean (SD) LDL-C level was 1.6 (0.7) mmol/L [60.1 (28.1) mg/dL], and the median (IQR) Lp(a) level was 188.0 (140.0-268.0) nmol/L [75.2 (56.0-107.2) mg/dL]. Arterial wall inflammation [most diseased segment target-to-background ratio (MDS TBR)] in the index vessel (left carotid, right carotid, or thoracic aorta) was assessed by 18F-fluoro-deoxyglucose positron-emission tomography/computed tomography. Week 16 index vessel MDS TBR was not significantly altered with evolocumab (-8.3%) vs. placebo (-5.3%) [treatment difference -3.0% (95% CI -7.4% to 1.4%); P = 0.18]. CONCLUSION: Evolocumab treatment in patients with median baseline Lp(a) 200.0 nmol/L led to a large reduction in LDL-C and a small reduction in Lp(a), resulting in persistent elevated Lp(a) levels. The latter may have contributed to the unaltered arterial wall inflammation."}