# Patiromer faciliteert RAAS-remmer-optitratie bij HFrEF met hyperkaliëmie

*geplaatst 2024-10-01 · Hartfalen · Journal of the American College of Cardiology · doi 10.1016/j.jacc.2024.05.079 · https://hartvaat.nl/2024/10/01/patiromer-faciliteert-raas-remmer-optitratie-bij-hfref-met-hyperkaliemie/*

Studie bevestigde dat patiromer de RAAS-remmer- en MRA-therapie mogelijk maakt bij HFrEF-patiënten met hyperkaliëmie. Kaliumbinding is een effectieve strategie om hartfalenbehandeling te optimaliseren.

## English: Patiromer Facilitates Angiotensin Inhibitor and Mineralocorticoid Antagonist Therapies in Patients With Heart Failure and Hyperkalemia.

This study confirmed that patiromer enables optimization of RAAS inhibitor and MRA therapy in HFrEF patients with hyperkalemia, addressing the potassium barrier that limits guideline-directed heart failure treatment.

## Abstract (original, from the publication)

BACKGROUND: Hyperkalemia (HK) is associated with suboptimal renin-angiotensin system (RAS) inhibitor and mineralocorticoid receptor antagonist (MRA) use in heart failure with reduced ejection fraction (HFrEF). OBJECTIVES: This study sought to assess characteristics and RAS inhibitor/MRA use in patients receiving patiromer during the DIAMOND (Patiromer for the Management of Hyperkalemia in Subjects Receiving RAASi Medications for the Treatment of Heart Failure) run-in phase. METHODS: Patients with HFrEF and HK or past HK entered a run-in phase of ≤12 weeks with patiromer-facilitated RAS inhibitor/MRA optimization to achieve ≥50% recommended RAS inhibitor dose, 50 mg/d MRA, and normokalemia. Patients achieving these criteria (randomized group) were compared with the run-in failure group (patients not meeting the randomization criteria). RESULTS: Of 1,038 patients completing the run-in, 878 (84.6%) were randomized and 160 (15.4%) were run-in failures. Overall, 422 (40.7%) had HK entering run-in with a similar frequency in the randomized and run-in failure groups (40.3% vs 42.5%; P = 0.605). From start to the end of run-in, in the randomized group, an increase was observed in target RAS inhibitor and MRA use in patients with HK (RAS inhibitor: 76.8% to 98.6%; MRA: 35.9% to 98.6%) and past HK (RAS inhibitor: 60.5% to 98.1%; MRA: 15.6% to 98.7%). Despite not meeting the randomization criteria, an increase after run-in was observed in the run-in failure group in target RAS inhibitor (52.5% to 70.6%) and MRA use (15.0% to 48.1%). This increase was observed in patients with HK (RAS inhibitor: 51.5% to 64.7%; MRA: 19.1% to 39.7%) and past HK (RAS inhibitor: 53.3% to 75.0%; MRA: 12.0% to 54.3%). CONCLUSIONS: In patients with HFrEF and HK or past HK receiving suboptimal RAS inhibitor/MRA therapy, RAS inhibitor/MRA optimization increased during patiromer-facilitated run-in.

Auteurs: Bertram Pitt, Stefan D Anker, Lars H Lund, Andrew J S Coats, Gerasimos Filippatos, Patrick Rossignol, Matthew R Weir, Tim Friede, Mikhail N Kosiborod, Marco Metra, Michael Böhm, Justin A Ezekowitz, Antoni Bayes-Genis, Robert J Mentz, Piotr Ponikowski, Michele Senni, Ileana L Piña, Fausto J Pinto, Peter van der Meer, Cecilia Bahit, Jan Belohlavek, Jasper J Brugts, Amandine Perrin, Sandra Waechter, Jeffrey Budden, Javed Butler

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Bron: Journal of the American College of Cardiology, https://doi.org/10.1016/j.jacc.2024.05.079. Bijgewerkt 2026-07-03T13:30:15Z. 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.