Key result
Patiromer enables ~99% target RAS inhibitor and MRA use in HFrEF patients with hyperkalemia.
Why the study?
Hyperkalemia is associated with suboptimal renin-angiotensin system inhibitor and mineralocorticoid receptor antagonist use in patients with HFrEF.
Does patiromer facilitate the optimization of RAS inhibitors and MRAs in patients with HFrEF and current or past hyperkalemia?
RCT (n=1,038)
Does patiromer facilitate the optimization of RAS inhibitors and MRAs in patients with HFrEF and current or past hyperkalemia?
Patiromer use during a run-in phase enabled significant optimization of RAS inhibitors and MRAs in HFrEF patients with current or past hyperkalemia.
Patiromer may enable near-complete RAS inhibitor and MRA optimization in HFrEF with hyperkalemia; leaves open effects on outcomes pending randomized trials.
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.
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Pitt et al. (2024) conducted an RCT in Heart failure with reduced ejection fraction (HFrEF) and hyperkalemia (n=1,038). Patiromer vs. Run-in failure group was evaluated on Target RAS inhibitor and MRA use. Patiromer-facilitated run-in optimization in patients with HFrEF and hyperkalemia increased target RAS inhibitor use to 98.6% and MRA use to 98.6% among those meeting randomization criteria.
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