{"id":"cbff4fa58eac","type":"article","url":"https://hartvaat.nl/2022/11/01/arteriele-stijfheid-en-endotheeldysfunctie-bij-anca-geassocieerde-vasculitis/","title":"Arteriële stijfheid en endotheeldysfunctie bij ANCA-geassocieerde vasculitis","title_en":"Arterial stiffness, endothelial dysfunction and impaired fibrinolysis are pathogenic mechanisms contributing to cardiovascular risk in ANCA-associated vasculitis.","category":"preventie","category_label":"Preventie","professions":["cardioloog","internist"],"tags":["perifeer-vaatlijden"],"journal":"Kidney international","doi":"10.1016/j.kint.2022.07.026","source_url":"https://doi.org/10.1016/j.kint.2022.07.026","authors":["Tariq E Farrah","Vanessa Melville","Alicja Czopek","Henry Fok","Lorraine Bruce","Nicholas L Mills","Matthew A Bailey","David J Webb","James W Dear","Neeraj Dhaun"],"significance":5,"published":"2022-11-01","source_date":"2022-11-01","image":"","kennis":["https://hartvaat.nl/kennis/lipiden/lpa-meten-wanneer-waarom/","https://hartvaat.nl/kennis/cardiometabool/diabetes-en-cardiovasculair-risico/"],"congress":"","summary_en":"This study showed that patients with ANCA-associated vasculitis have increased arterial stiffness and endothelial dysfunction, identifying vascular pathogenic mechanisms that contribute to their elevated cardiovascular risk.","created":"2026-07-03T10:30:02Z","updated":"2026-07-03T13:29:08Z","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 toonde dat patiënten met ANCA-geassocieerde vasculitis verhoogde arteriële stijfheid en endotheeldysfunctie hebben, wat bijdraagt aan hun verhoogde cardiovasculaire risico. Chronische inflammatie is een belangrijke driver van vaatschade bij deze populatie.","abstract_original":"Cardiovascular disease is a complication of systemic inflammatory diseases including anti-neutrophil cytoplasm antibody-associated vasculitis (AAV). The mechanisms of cardiovascular morbidity in AAV are poorly understood, and risk-reduction strategies are lacking. Therefore, in a series of double-blind, randomized case-control forearm plethysmography and crossover systemic interventional studies, we examined arterial stiffness and endothelial function in patients with AAV in long-term disease remission and in matched healthy volunteers (32 each group). The primary outcome for the case-control study was the difference in endothelium-dependent vasodilation between health and AAV, and for the crossover study was the difference in pulse wave velocity (PWV) between treatment with placebo and selective endothelin-A receptor antagonism. Parallel in vitro studies of circulating monocytes and platelets explored mechanisms. Compared to healthy volunteers, patients with AAV had 30% reduced endothelium-dependent vasodilation and 50% reduced acute release of endothelial active tissue plasminogen activator (tPA), both significant in the case-control study. Patients with AAV had significantly increased arterial stiffness (PWV: 7.3 versus 6.4 m/s). Plasma endothelin-1 was two-fold higher in AAV and independently predicted PWV and tPA release. Compared to placebo, both selective endothelin-A and dual endothelin-A/B receptor blockade reduced PWV and increased tPA release in AAV in the crossover study. Mechanistically, patients with AAV had increased platelet activation, more platelet-monocyte aggregates, and altered monocyte endothelin receptor function, reflecting reduced endothelin-1 clearance. Patients with AAV in long-term remission have elevated cardiovascular risk and endothelin-1 contributes to this. Thus, our data support a role for endothelin-blockers to reduce cardiovascular risk by reducing arterial stiffness and increasing circulating tPA activity."}