# Arteriële stijfheid en endotheeldysfunctie bij ANCA-geassocieerde vasculitis

*geplaatst 2022-11-01 · Preventie · Kidney international · doi 10.1016/j.kint.2022.07.026 · https://hartvaat.nl/2022/11/01/arteriele-stijfheid-en-endotheeldysfunctie-bij-anca-geassocieerde-vasculitis/*

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.

## English: Arterial stiffness, endothelial dysfunction and impaired fibrinolysis are pathogenic mechanisms contributing to cardiovascular risk in ANCA-associated vasculitis.

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.

## Abstract (original, from the publication)

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.

Auteurs: 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

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Bron: Kidney international, https://doi.org/10.1016/j.kint.2022.07.026. Bijgewerkt 2026-07-03T13:29:08Z. 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.