Biochemical success after selective adrenal arterial embolization predicts long-term regression of aldosterone-mediated cardiac remodeling.

BACKGROUND

Selective adrenal arterial embolization (SAAE) is a minimally invasive, vascular intervention targeting aldosterone-producing tissue in primary aldosteronism (PA). While surgery and mineralocorticoid receptor antagonists are standard therapies, long-term cardiac outcomes after SAAE remain poorly defined.

METHODS

In this prospective cohort study, 129 patients with adrenal vein sampling-confirmed unilateral PA who declined adrenalectomy underwent SAAE. Biochemical outcomes were classified by Primary Aldosteronism Surgical Outcome (PASO) criteria as complete (CS, n = 71) or incomplete (non-CS, n = 58) success. Echocardiography was performed at baseline and at a median of 25 months post-SAAE. Left ventricular remodeling was evaluated using LVMI, predicted LVMI (pLVMI), and inappropriately excessive LVMI (ieLVMI).

RESULTS

SAAE significantly reduced both office and 24-h blood pressure in all patients (mean Δ24-h SBP: -19.3 mmHg; Δ24-h DBP: -9.8 mmHg; all P < .001). The CS group demonstrated greater improvement in plasma aldosterone concentration, aldosterone-to-renin ratio, and serum potassium (all P < .001). Both groups showed reductions in LVMI and pLVMI, but only the CS group had significant regression in ieLVMI (-5.77 vs +2.36 g/m2; P = .010), indicating reversal of aldosterone-specific myocardial injury. This association remained significant after adjustment. Subgroup analyses showed consistent trends across age, sex, BMI, and adenoma status. Left ventricular hypertrophy prevalence declined from 31.8% to 17.1% overall (P < .001). Adverse events were mild and comparable between groups.

CONCLUSIONS

In unilateral PA, sustained biochemical normalization after SAAE is associated with meaningful regression of aldosterone-mediated cardiac remodeling. These findings support SAAE may serve as a potential alternative for selected patients and highlight ieLVMI as a mechanistic treatment marker.