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.

Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology

“…A principal hormone contributing to ECM deposition is ANG II, which has been implicated in both reparative fibrosis of scar tissue that is seen post-MI (835,1130) and reactive fibrosis that occurs for example with hypertension or aortic valve stenosis (256,723). Some of the pro-fibrotic effects of ANG II on the left ventricle may be mediated by aldosterone, particularly in the presence of a high-salt diet (131). In fact, high salt may activate the mineralocorticoid receptor, due to increased Rac1 activity, independent of aldosterone (101).…”

Zi Shen Huo Luo Formula Enhances the Therapeutic Effects of Angiotensin-Converting Enzyme Inhibitors on Hypertensive Left Ventricular Hypertrophy by Interfering With Aldosterone Breakthrough and Affecting Caveolin-1/Mineralocorticoid Receptor Colocalization and Downstream Extracellular Signal-Regulated Kinase Signaling

“…These finding also provide guidance for our subsequent definitive constituent analysis. Experimental and clinical evidence indicates that protracted exposure to inappropriately elevated ALD levels causes significant changes in left ventricular structure and function (Catena et al, 2015). Although the use of ACEIs and ARBs may initially decrease plasma ALD levels, chronic therapy with these drugs may lead to ABT, in which ALD levels return to or exceed the baseline levels (Struthers and MacDonald, 2004).…”

Dilated cardiomyopathy and aldosteronoma: a causal link?

“…In addition, animal experiments demonstrated the damage leading to tissue hypertrophy and fibrosis of aldosterone on left ventricle. [8][9][10] Through this case, we propose hyperaldosteronism as…”