Bilateral adrenal artery embolization for the treatment of idiopathic hyperaldosteronism: A proof-of-principle single center study.

Unilateral adrenal artery embolization (AAE) has emerged as an alternative treatment for patients with primary aldosteronism due to aldosterone-producing adenomas or idiopathic hyperaldosteronism with bilateral adrenal hyperplasia. This study aimed to investigate the effectiveness and safety of bilateral AAE in idiopathic hyperaldosteronism. We enrolled a total of 58 patients with idiopathic hyperaldosteronism who underwent successful bilateral AAE, and 55 of them completed 6-month follow-up. Bilateral AAE significantly lowered blood pressure of patients with IHA at 1, 3, and 6 months (all P < 0.01). Six months after the procedure, office, home, and 24-hour ambulatory blood pressure decreased by 20.3/13.5, 18.4/12.6, and 13.7/9.9 mmHg, respectively. Among them, 92.7%, 90.9%, and 89.1% had significant or moderate improvement in blood pressure control at 1, 3, and 6 months after the procedure. Bilateral AAE substantially decreased plasma aldosterone levels, reversed plasma renin suppression, decreased aldosterone-to-renin ratio, and corrected hypokalemia. Importantly, the procedure did not significantly change serum cortisol and plasma adrenocorticotropic hormone (ACTH) levels, and the cortisol and ACTH circadian rhythms remained intact three months after the procedure. Additionally, 16 patients underwent ACTH stimulation tests three months post-procedure and all of them had normal results except for one with a decreased response due to exogenous steroid therapy. Flank pain was the most common side effect which happened in 96.4% of the patients and resolved within 48 h. There were no long-term side effects in the 6 months. The present study provides evidence that bilateral AAE is an effective and safe alternative treatment for patients with IHA. Changes in office and 24h ambulatory blood pressure at 1, 3, and 6 months after bilateral adrenal artery embolization in patients with idiopathic hyperaldosteronism.