Patiromer reduced potassium levels by 0.21 mEq/L (P<.0001) in heart failure patients at risk of hyperkalemia, but RASi/mineralocorticoid receptor antagonist optimization remained at ≤40%.
Observational
Does patiromer facilitate RASi/MRA optimization in heart failure patients at increased risk of hyperkalemia?
In a real-world registry, patiromer effectively lowered potassium levels in HF patients at risk of hyperkalemia, but this did not translate into increased optimization of RASi/MRA therapy, highlighting ongoing clinical inertia.
Effect estimate: 0.21 mEq/L decline (95% CI 0.30-0.12)
p-value: p=< .0001
BACKGROUND: ) concentrations and HK, potentially enabling RASi optimization. We sought to assess the real-world effectiveness of patiromer in facilitating RASi optimization in HF patients at increased risk of HK. METHODS AND RESULTS: was 5.5 mEq/L (interquartile range 5.4-5.7 mEq/L) and declined by 0.21 mEq/L (95% confidence interval 0.30-0.12 mEq/L) (P < .0001). However, RASi/mineralocorticoid receptor antagonist optimization within 2 years remained at ≤40% and did not increase with patiromer. CONCLUSIONS: but rates of RASi/mineralocorticoid receptor antagonist optimization remain low. Overcoming clinical inertia, including the addition of patiromer when appropriate, is required to optimize RASi/mineralocorticoid receptor antagonist therapy in patients with HF at high risk of HK.
Martinez et al. (Sun,) conducted a observational in Heart failure at risk of hyperkalemia. Patiromer was evaluated on Potassium decline (0.21 mEq/L decline, 95% CI 0.30-0.12, p=< .0001). Patiromer reduced potassium levels by 0.21 mEq/L (P<.0001) in heart failure patients at risk of hyperkalemia, but RASi/mineralocorticoid receptor antagonist optimization remained at ≤40%.