Abstract 5420: Suppression of Aldosterone Mediates Left Ventricular Hypertrophy Regression in Patients With Hypertension
Background. Although high circulating aldosterone levels stimulate myocardial fibrosis and left ventricular hypertrophy (LVH), it is less clear whether suppression of aldosterone is associated with LVH regression in hypertensive patients.
Methods. The Aliskiren in Left Ventricular Hypertrophy (ALLAY) trial randomized 465 hypertensive overweight subjects to the direct renin inhibitor aliskiren 300mg, losartan 100mg or the combination and followed patients for 9 months. All patients were treated to standard blood pressure targets. LV mass index (LVMI) and LV wall thickness (LVWT) were assessed by cardiac magnetic resonance. A subset of 135 patients with plasma aldosterone (ALDO) measured at baseline and study end was analyzed.
Results. At baseline, ALDO correlated poorly with systolic blood pressure (SBP) (r=0.2, p=0.02), LVMI (r=0.18, p=0.03) and LVWT (r=0.22, p=0.01). Mean blood pressure was 144±13/90±9mmHg, mean LVMI was 75±16 g/m2, and mean LVWT was 9.8±2.2mm. ALDO was reduced between baseline and end of the study in the aliskiren [244 (202–294) vs. 198 (161–243) pmol/L, p=0.03] and combination groups [209 (169–257) vs. 164 (138–196) pmol/L, p=0.0029], but not in the losartan group [223 (181–275) vs. 235 (199–278) pmol/L, p=0.63] [geometric means (95%CI)]. Reduction in ALDO was associated with regression of LVWT, even after adjustment for SBP reduction, treatment, baseline ALDO and baseline LVWT (p= 0.041).
Conclusion. In hypertensive patients with increased LVWT, regression of LVH was associated with suppression of ALDO, independently of the change in SBP, suggesting that ALDO, a known mediator of LVH, may be a particularly important target for suppression.