Effects of Aldosterone on the Heart

Abstract

As predicted by Laplace’s law, the ability of the left ventricle to compensate for increasing loading conditions requires the thickening of the ventricular wall and the growth of left ventricular mass (LVM), defined as left ventricular hypertrophy (LVH) when it exceeds partition values based on distribution in normal reference populations. The presence of LVH, however, does not discriminate between a compensatory and excessive increase in LVM. Therefore, the term “inappropriate LVM” (iLVM) has been applied to conditions in which the observed level of LVM exceeds the theoretical value predicted by sex, body size, and stroke work.1 iLVM is associated with clustered geometric and functional abnormalities of the left ventricle2 and appears to be a marker of adverse cardiovascular prognosis independent of LVH.3 Recent data suggest that changes in the appropriateness of LVM from baseline to follow-up during treatment may predict a subsequent cardiovascular event in hypertensive patients.4 It has been proposed that the pathophysiological process that yields iLVM is probably linked to the protracted activity over time of humoral mediators of LV growth, such as proto-oncogenes, growth factors, hormones, and cytokines, inducing modifications that initially compensate imposed overload but eventually change the structure of myocardial tissue (eg, remodeling) and, as a consequence, impair LV function.5 The study by Muiesan et al in this issue of Hypertension 6 points to aldosterone as one of the candidate hormones that may contribute to iLVM. The authors evaluated the inappropriateness of LVM in 125 patients with a diagnosis of primary aldosteronism (PA) and in 125 age-, sex-, and blood pressure–matched patients with essential hypertension. The prevalence of iLVM (defined by a ratio of observed:predicted LVM >135%) was greater in PA patients …