title: Aldosterone and Left Ventricular Remodeling.
abstract: Experimental and clinical evidence obtained in the last 2 decades clearly indicates that protracted exposure to inappropriately elevated aldosterone levels causes significant changes in left ventricular structure and function. Animal studies have demonstrated that aldosterone induces myocardial inflammatory changes and fibrosis in the presence of a high salt diet. Moreover, the effects of aldosterone on the heart have been investigated in different clinical conditions. These conditions include systolic and diastolic heart failure, essential hypertension, and primary aldosteronism that offers a unique clinical model to study the cardiac effects of excess aldosterone because these effects are isolated from those of the renin-angiotensin axis. A relatively clear picture is emerging from these studies with regard to aldosterone-related changes in left ventricular mass and geometry. Conversely, no direct effect of aldosterone on left ventricular diastolic function can be demonstrated and improvement of diastolic function obtained in some studies that have employed mineralocorticoid receptor blockers could result from left ventricular mass reduction. Animal experiments demonstrate that effects of aldosterone on the left ventricle require high salt intake to occur, but the evidence of this contribution of salt to aldosterone-induced cardiac changes in humans remains weaker and needs further research. The article reviews the results of clinical studies addressing the role of aldosterone in regulation of LV remodeling and diastolic function, and focuses on the possible relevance of salt intake.
authors.affiliation: Hypertension Unit, Internal Medicine, Department of Experimental and Clinical Medical Science, University of Udine, Udine, Italy.
authors.forename: C
authors.initials: C
authors.lastname: Catena
authors.affiliation: Hypertension Unit, Internal Medicine, Department of Experimental and Clinical Medical Science, University of Udine, Udine, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Colussi
authors.affiliation: Hypertension Unit, Internal Medicine, Department of Experimental and Clinical Medical Science, University of Udine, Udine, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Brosolo
authors.affiliation: Hypertension Unit, Internal Medicine, Department of Experimental and Clinical Medical Science, University of Udine, Udine, Italy.
authors.forename: M
authors.initials: M
authors.lastname: Novello
authors.affiliation: Hypertension Unit, Internal Medicine, Department of Experimental and Clinical Medical Science, University of Udine, Udine, Italy.
authors.forename: L A
authors.initials: LA
authors.lastname: Sechi
mesh_terms: D000450:Aldosterone / Q000378:metabolism*; D000075222:Essential Hypertension; D006352:Heart Ventricles / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D006929:Hyperaldosteronism / Q000503:physiopathology; D006973:Hypertension / Q000503:physiopathology; D016277:Ventricular Function, Left; D020257:Ventricular Remodeling
chemical_list: D000450:Aldosterone