Primary aldosteronism was independently associated with higher cIMT and AIx@75 compared to essential hypertension, an effect not entirely mediated by central systolic blood pressure.
Cohort (n=158)
No
Is vascular damage in primary aldosteronism mediated by central systolic blood pressure compared to essential hypertension?
Primary aldosteronism is associated with greater vascular damage than essential hypertension, which is not entirely explained by increased central blood pressure, suggesting aldosterone-specific vascular toxicity.
Objective: Primary aldosteronism (PA) is the most common form of secondary hypertension and is associated with a greater burden of hypertension-mediated organ damage (HMOD) than essential hypertension (EH). This study aimed to assess whether different vascular HMOD phenotypes are partially or fully mediated by increased central systolic blood pressure (BP) in patients with PA. Design and method: In this monocentric cohort study, hypertensive patients (n=158; age 47 ± 14.6 years; 43.7% females) referred to the ESH Excellence Centre of Verona underwent a comprehensive diagnostic work-up for secondary hypertension. Vascular assessment was performed using the SphygmoCor Xcel system and vascular ultrasound integrated with the Cardiovascular Suite to measure carotid intima–media thickness (cIMT), carotid distensibility coefficient (cDC), augmentation index normalized to a heart rate of 75 bpm (AIx@75), and carotid–femoral pulse wave velocity (cf-PWV), along with peripheral and central BP. Results: The final analysis included 121 patients with EH and 37 with PA. The two groups did not differ significantly in age, sex, body mass index, or peripheral systolic BP. In contrast, central systolic BP was significantly higher in PA patients, despite a higher number of antihypertensive drugs. Patients with PA also exhibited higher cIMT, AIx@75, and cf-PWV, but similar cDC, compared with EH patients. In multivariable regression analyses adjusted for age, sex, body mass index, hypercholesterolemia, diabetes, smoking status, number of antihypertensive drugs, and central systolic BP, PA remained independently associated with cIMT and AIx@75, but not with cf-PWV or cDC. Mediation analyses using Hayes’ framework with bias-corrected bootstrap confidence intervals showed that central systolic BP significantly mediated the association between PA and cDC and partially mediated the association with AIx@75, whereas no mediation effect was observed for cIMT or cf-PWV. Conclusions: In patients referred to a tertiary hypertension center, PA was associated with a greater burden of vascular damage compared with EH. Although limited by its cross-sectional design, mediation analysis suggests that these adverse vascular effects are not entirely explained by increased BP, supporting a role for BP-independent, aldosterone-related mechanisms.
Sabba’ et al. (Fri,) conducted a cohort in Hypertension (Primary aldosteronism vs Essential hypertension) (n=158). Primary aldosteronism vs. Essential hypertension was evaluated on Vascular hypertension-mediated organ damage (cIMT, cDC, AIx@75, and cf-PWV). Primary aldosteronism was independently associated with higher cIMT and AIx@75 compared to essential hypertension, an effect not entirely mediated by central systolic blood pressure.