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Primary aldosteronism is the most common secondary endocrine form of hypertension and causes many cardiovascular injuries. KCNJ5 somatic mutations have recently been identified in aldosterone-producing adenoma. However, their impacts on left ventricular remodeling precluding the interference of age, sex, and blood pressure are still uncertain. We enrolled 184 aldosterone-producing adenoma patients who received adrenalectomy. Clinical, biochemical, and echocardiographic data were analyzed preoperatively and 1 year postoperatively. KCNJ5 gene sequencing of aldosterone-producing adenoma was performed. After propensity score matching for age, sex, body mass index, blood pressure, hypertension duration, and number of hypertensive medications, there were 60 patients in each group with and without KCNJ5 mutations. The mutation carriers had higher left ventricular mass index (LVMI) and inappropriately excessive LVMI (ieLVMI) and lower e′ than the noncarriers. After adrenalectomy, the mutation carriers had greater decreases in LVMI and ieLVMI than the noncarriers. In addition, only mutation carriers had a significant decrease in E/e′ after surgery. In multivariate analysis, baseline LVMI correlated with KCNJ5 mutations, the number of hypertensive medications, and systolic blood pressure. Baseline ieLVMI correlated with KCNJ5 mutations and the number of hypertensive medications. The regression of both LVMI and ieLVMI after surgery was mainly correlated with KCNJ5 mutations and changes in systolic blood pressure. Aldosterone-producing adenoma patients with KCNJ5 mutations had higher LVMI and ieLVMI and a greater regression of LVMI and ieLVMI after adrenalectomy than those without mutations. The patients with KCNJ5 mutations also benefited from adrenalectomy with regard to left ventricular diastolic function, whereas noncarriers did not.

Background/aim: Primary aldosteronism (PA) patients are correlated to higher cardiovascular events, endothelial function, and altered cardiac structure. Macrophage-mediated low grade inflammation plays important role of aldosterone-induced myocardial and vascular fibrosis. However, theeffect of aldosterone on macrophage movementis still unclear. Methods: We investigated the effect of aldosterone on macrophage movement and its mechanism. We used THP-1 as cell model of macrophage, and transwell assay to evaluate the migration and infiltration of cell. Two periods (16 hour and 48 hour) wereused to evaluate the migration and infiltration of macrophage. Results: Aldosterone increased THP-1 migration and infiltrationsince 10−8 M at 48 hours but not 16 hours. Aldosterone induced both galectin-3 and IL-6 production in THP-1 cell. In contrast, aldosterone does not affect the production of matrix metalloproteinase-2 and tissue inhibitor of metalloproteinase-1in THP-1. The increased migration and infiltrationby aldosterone was inhibited partially by IL-6 siRNA but not galectin-3 siRNA. Aldosterone also induced Rho-ROCK up-regulation but also partially inhibited by IL-6 siRNA. The aldosterone induced cell migration and infiltration was blocked by Y27632 (Rho-ROCK inhibitor). Conclusions: Aldosterone increased microphage migration and infiltration. The process was partially involved IL-6/Rho-ROCK pathway.