Abstract
BACKGROUND: The loss of physiological nocturnal blood pressure (BP) decline is a major contributor to cardiovascular risk, yet its endocrine underpinnings in primary aldosteronism (PA) remain underexplored. This study aimed to elucidate the dose-dependent relationship between aldosterone excess and circadian BP rhythm disruption and assess whether targeted aldosterone suppression could ameliorate nocturnal dipping. METHODS: We prospectively analyzed 24-hour ambulatory BP data from 681 patients with confirmed PA, stratified by plasma aldosterone concentration. A subset of 99 patients with adrenal vein sampling-confirmed unilateral PA received targeted, minimally invasive vascular intervention for aldosterone suppression and were evaluated for changes in BP rhythm on the basis of treatment response. RESULTS: In multivariable-adjusted models, both log-transformed plasma aldosterone concentration and aldosterone-to-renin ratio were inversely associated with the proportion of nocturnal systolic BP decline (log plasma aldosterone concentration: β=-0.054 [95% CI, -0.087 to -0.020]; P=0.002; log aldosterone-to-renin ratio: β=-0.016 [95% CI, -0.025 to -0.006]; P=0.001). In patients achieving biochemical remission after selective suppression, nighttime systolic BP decreased significantly (mean reduction=-33 mm Hg; Cohen's d_z=2.113). The prevalence of the dipper pattern increased from 14.5% to 39.1% (P<0.001), while no rhythm improvement was observed in nonresponders. Multivariable regression confirmed biochemical success as an independent predictor of nocturnal dip amelioration (P=0.045), irrespective of adrenal imaging phenotype. CONCLUSIONS: Aldosterone excess contributes directly to circadian BP rhythm disruption in PA. Selective hormonal suppression can ameliorate physiological BP dipping in responsive patients. These findings highlight the value of rhythm-based end points and support aldosterone-targeted modulation as a strategic goal in PA management. Registration: URL: https://www.chictr.org.cn/; Unique Identifier: ChiCTR2200057297.