Left ventricular remodeling and dysfunction in primary aldosteronism

Abstract

Primary aldosteronism (PA) is a common cause of secondary hypertension and is associated with worse cardiovascular outcomes. The elevated aldosterone in PA leads to left ventricular (LV) remodeling and dysfunction. In recent decades, clinical studies have demonstrated worse LV remodeling including increased LV mass and cardiac fibrosis in patients with PA compared to patients with essential hypertension. Several mechanisms may explain the process of aldosterone-induced LV remodeling, including directly profibrotic and hypertrophic effects of aldosterone on myocardium, increased reactive oxygen species and profibrotic molecules, dysregulation of extracellular matrix metabolism, endothelium dysfunction and circulatory macrophages activation. LV remodeling causes LV diastolic and systolic dysfunction, which may consequently lead to clinical complications such as heart failure, atrial fibrillation, ischemic heart disease, and other vascular events. Adequate treatment with adrenalectomy or medical therapy can improve LV remodeling and dysfunction in PA patients. In this review, we discuss the mechanisms of aldosterone-induced LV remodeling and provide an up-to-date review of clinical research about LV remodeling-related heart structural changes, cardiac dysfunction, and their clinical impacts on patients with PA.

Fig. 1. There are three major mechanisms of alsosterone induced LV remodeling including myocytes hyperthropathy, chronic inflammation and ECM dysregulation.

These detrimental effects will induce LV hypertrophy and fibrosis and then cause LV systolic and diastolic dysfunction. The salt will potentiate these effects. CT-1 cardiotrophin-1, ROS reactive oxygen species, ICAM intercellular adhesion molecule, IL-6 interleukin-6, MMP matrix metalloproteinase, TIMP-1 tissue inhibitor of metalloproteinases-1, LV left ventricle.