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

Hypertension Unit (M.S., R.D.G., D.C.) and Cardiovascular Imaging and Research Group (J.S., R.L., T.H.M.), University of Queensland Department of Medicine, and Queensland Health Pathology and Scientific Services (G.W.), Princess Alexandra Hospital, Brisbane, Queensland 4102, Australia

Address all correspondence and requests for reprints to: Assoc. Prof. Michael Stowasser, Hypertension Unit, University of Queensland Department of Medicine, Princess Alexandra Hospital, Ipswich Road, Woolloongabba, Brisbane, Queensland 4102, Australia. E-mail: m.stowasser{at}uq.edu.au.

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.

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