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.