Journal of Hypertension

Biological age acceleration in primary aldosteronism: associations with renin, aldosterone, aldosterone-to-renin ratio, and left ventricular mass index

Cross-sectional study of 1,201 peopleBiomarkers
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Abstract

OBJECTIVES: To investigate the associations of plasma aldosterone concentration (PAC), plasma renin activity (PRA), and aldosterone-to-renin ratio (ARR) with Gompertz law-based biological age difference (GOLD BioAgeDiff) in patients with primary aldosteronism versus essential hypertension (EHT), and to determine whether GOLD BioAgeDiff relates to cardiac mass. METHODS: We conducted a retrospective cross-sectional study of 1201 hypertensive adults (785 with primary aldosteronism and 416 with EHT). GOLD BioAgeDiff was defined as the calculated biological age minus chronological age. Multivariable linear regression was used to evaluate the associations of PAC, PRA, and ARR with GOLD BioAgeDiff. Furthermore, we assessed the relationship between GOLD BioAgeDiff and echocardiographic indices, including left ventricular mass index (LVMI) and excessive LVMI (eLVMI). RESULTS: Primary aldosteronism patients demonstrated significantly higher GOLD BioAgeDiff than EHT patients. In fully adjusted models, ARR was positively associated with GOLD BioAgeDiff in the primary aldosteronism group ( β = 0.292, P = 0.008) but not in the EHT group ( P for interaction = 0.032). PAC and postcaptopril PAC were also positively associated with GOLD BioAgeDiff in primary aldosteronism. Furthermore, higher GOLD BioAgeDiff was associated with greater eLVMI ( β = 0.591, P < 0.001) and LVMI ( β = 0.640, P = 0.001) in primary aldosteronism patients, suggesting a potential mediating role in the relationship between ARR and cardiac remodeling. CONCLUSION: Among patients with primary aldosteronism, elevated ARR and PAC were independently associated with GOLD BioAgeDiff, and GOLD BioAgeDiff was correlated with LVMI/eLVMI and may be involved in the association between ARR and eLVMI. Prospective studies are required to confirm causality and evaluate the clinical utility of this biological aging marker.