Evidence for Abnormal Left Ventricular Structure and Function in Normotensive Individuals with Familial Hyperaldosteronism Type I

TLDR

The study aimed to determine whether aldosterone excess causes cardiovascular abnormalities in normotensive patients with primary aldosteronism. Eight FH‑I patients and 24 matched normotensive controls were compared on blood pressure, biochemical markers, pulse wave velocity, and echocardiographic parameters. FH‑I patients had higher aldosterone levels yet similar blood pressure, but displayed concentric left‑ventricular remodeling with increased wall thickness and impaired diastolic function, despite unchanged pulse wave velocity and ejection fraction.

Abstract

Objectives: To explore whether aldosterone excess can induce adverse cardiovascular effects independently of effects on blood pressure (BP), we sought evidence of disturbed cardiovascular structure or function in normotensive individuals with primary aldosteronism. Methods: Eight normotensive subjects with genetically proven familial hyperaldosteronism type I (FH-I) were compared with 24 age- and sex-matched normotensive controls in terms of BP, biochemical parameters, pulse wave velocity, and echocardiographic characteristics. Results: Subjects with FH-I demonstrated higher serum aldosterone levels and aldosterone/renin ratios than controls, as expected. Despite having similar 24-h ambulatory BPs, subjects with FH-I demonstrated evidence of concentric remodeling with greater septal (mean ± sd, 9.4 ± 1.1 vs. 7.9 ± 0.9 mm; P < 0.001), posterior wall (9.2 ± 1.7 vs. 7.7 ± 1.0 mm; P < 0.01), and relative wall (0.29 ± 0.03 vs. 0.24 ± 0.02; P < 0.001) thicknesses, and lower mitral early peak velocities (0.74 ± 0.10 vs. 0.90 ± 0.16 m/sec; P < 0.05), ratios of early to late peak diastolic transmitral flow velocity (1.56 ± 0.24 vs. 2.06 ± 0.41; P < 0.01), and myocardial early peak velocities (8.3 ± 1.8 vs. 10.3 ± 2.6 cm/sec; P < 0.05). There were no significant differences in pulse wave velocity or left ventricular ejection fraction, long axis strain rate, peak systolic strain, cyclic variation of integrated backscatter, or posterior wall calibrated integrated backscatter. Conclusions: Aldosterone excess is associated with increased left ventricular wall thicknesses and reduced diastolic function, even in the absence of hypertension.