Abstract

Left ventricular dysfunction (LVD) is a harmful condition leading to increased cardiovascular morbidity and mortality. Among the complex pathophysiological factors contributing to the development of LVD, the renin–angiotensin–aldosterone system (RAAS) has been recognized to play a pivotal role. Hyperactivation of RAAS promotes structural and functional changes leading to myocardial fibrosis, stiffness and left ventricular hypertrophy [1–4]. A large proportion of patients with altered RAAS homeostasis presents with isolated increase in plasma renin activity (PRA) or aldosterone concentrations (PAC). However, data about the impact of isolated hyperreninemia or hyperaldosteronism on LV geometry and function are not exhaustive. Moreover, it remains unclearwhether the coexistence of high renin and aldosterone has a synergic effect on cardiac damage. LV mass (LVM) exceeding compensatory values for individual cardiac load has been recently described as inappropriate left ventricular mass (ILVM). This adverse phenotype of cardiac hypertrophy is emerging as a key determinant of cardiovascular risk [5]. In the present study we investigated the individual contribution of isolated PRA and PAC elevations on ILVM and LVD. PRA and PAC were measured in 133 young newly diagnosed hypertensive subjectswho had never been treatedwith RAAS blockers or other antihypertensive drugs. The study population was stratified as follows: 1) normal PRA and PAC (N) [n = 45]; 2) high PRA and normal PAC (hyperreninemia, HR)

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