Key result
Esaxerenone treatment is linked to improved FMD and ~11% lower baPWV in IHA patients.
Why the study?
Mineralocorticoid receptor antagonists are recommended for idiopathic hyperaldosteronism, but the effects of the nonsteroidal antagonist esaxerenone on vascular function and peripheral arterial stiffness were unknown.
Does esaxerenone improve vascular function and peripheral arterial stiffness in patients with idiopathic hyperaldosteronism?
Cohort (n=44)
No
Does esaxerenone improve vascular function and peripheral arterial stiffness in patients with idiopathic hyperaldosteronism?
p-value: p=<0.01
Esaxerenone treatment for 12 weeks significantly improves vascular function and reduces peripheral arterial stiffness in patients with idiopathic hyperaldosteronism.
Esaxerenone was associated with improved vascular function in IHA; hypothesis-generating and requires randomized confirmation.
OBJECTIVE: Primary aldosteronism is one of the most common types of secondary endocrine hypertension. Treatment with mineralocorticoid receptor antagonists is recommended for bilateral idiopathic hyperaldosteronism (IHA). The purpose of this study was to evaluate the effects of esaxerenone, a nonsteroidal mineralocorticoid receptor antagonist with high mineralocorticoid receptor-binding specificity, on vascular function and peripheral arterial stiffness in patients with IHA. METHODS: This study was a single-center, observational prospective cohort study. Forty-four patients with IHA (18 men and 26 women; 52 ± 11 years) were enrolled from Hiroshima University Hospital. Vascular function, including flow-mediated vasodilation (FMD) and nitroglycerine-induced vasodilation (NID) and peripheral arterial stiffness, including brachial-ankle pulse wave velocity (baPWV) and brachial artery intima-media thickness (bIMT) were measured before and after 12 weeks of treatment with esaxerenone. RESULTS: Esaxerenone treatment increased FMD (3.1 ± 2.0% to 5.7 ± 2.2%, P < 0.01) and NID (10.7 ± 3.8% to 15.7 ± 6.2%, P < 0.01) and decreased baPWV (1605 ± 263 to 1428 ± 241 cm/s, P < 0.01), while esaxerenone treatment did not significantly alter bIMT. The changes in FMD and NID posttreatment with esaxerenone were significantly correlated with the changes in plasma aldosterone concentration (PAC) and plasma renin activity (PRA). The change in baPWV was significantly correlated with the changes in PRA, aldosterone-to-renin ratio, and systolic blood pressure. CONCLUSION: Esaxerenone improved vascular function and peripheral arterial stiffness in patients with IHA. These findings suggest aldosterone inhibition is a potential mechanism governing improvement in cardiovascular health.
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Kishimoto et al. (2025) conducted a cohort in idiopathic hyperaldosteronism (n=44). esaxerenone vs. baseline was evaluated on Vascular function (FMD and NID) and peripheral arterial stiffness (baPWV and bIMT) (p=<0.01). Esaxerenone treatment for 12 weeks significantly improved flow-mediated vasodilation (3.1% to 5.7%, P<0.01) and decreased brachial-ankle pulse wave velocity (1605 to 1428 cm/s, P<0.01) in IHA patients.
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