Impact of aldosterone on left ventricular structure and function in young normotensive and mildly hypertensive subjects

Left ventricular (LV) hypertrophy is an independent risk factor for cardiov ascular morbidity and mortality. Experimental data revealed that elevated c irculating aldosterone is associated with increased collagen accumulation r esulting in myocardial fibrosis. To analyze whether aldosterone is also ass ociated with cardiac structural and functional changes in humans, we examin ed the effects of aldosterone on LV structure and function before and after suppression of aldosterone by Increasing oral salt intake. The study group comprised 26 normotensive male white healthy control subjects (age 26 +/- 3 years) and 31 male white subjects (age 25 +/- 3 years) with mild essentia l hypertension (World Health Organization stages I to II). Two-dimensional- guided M-mode echocardiography and 24-hour ambulatory blood pressure (BP) m onitoring was performed in each subject. Simultaneously, we measured 24-hou r urinary sodium excretion, 24-hour urinary aldosterone, and serum aldoster one concentration at baseline and after increasing oral salt intake to supp ress aldosterone secretion. In all subjects LV mass correlated with body ma ss index (r = 0.42, p <0.001) and both 24-hour ambulatory systolic: (r = 0. 28, p <0.05) and diastolic (r = 0.25, p <0.05) BP. Changes in urinary sodiu m excretion correlated inversely with changes in serum aldosterone concentr ation (r = -0.28; p <0.05). Urinary aldosterone concentration after salt lo ading decreased in normotensive (10.98 vs 7.44 mu g/24 hours; p <0.02) but not in hypertensive (9.34 vs 10.51 mu g/24 hours; p NS) subjects. Serum and urinary aldosterone levels at baseline were nat related to LV structure or function. In contrast, after increasing oral salt intake, urinary aldoster one concentration was related to LV mass (r = 0.43; p <0.01) and impaired m idwall fractional fiber shortening (r = -0.33; p <0.02) in all subjects, in dependent of 24-hour ambulatory BP. Subgroup analysis revealed that this wa s significant only in hypertensive (r = 0.46; p <0.01 and r = -0.44; p <0.0 2, respectively) but not in normotensive (r = 0.28 and -0.16; p NS for both , respectively) subjects. Consistently, the greater serum aldosterone remai ned after increasing oral salt intake, the greater was LV mass (r = 0.35; p <0.01). The latter was found in hypertensive subjects (r = 0.44; p <0.02), independent of 24-hour ambulatory BP, but not in normotensive subjects (r = 0.025; p = NS). Inadequate suppression of aldosterone in response to an i ncrease in oral salt intake is related to LV structural and functional chan ges in hypertensive subjects. Thus, our results support experimental data i ndicating that aldosterone affects LV structure and function in humans and that this effect is BP independent. (C) 2000 by Excerpta Medica, Inc.