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.

Effect of RGOs on the Efficacy of Nkx2.5 Transfected Bone Marrow Mesenchymal Stem Cells Transplantation in Treatment Heart Failure in Rats

“…Left ventricular remodeling including increased LV mass and cardiac brosis causes left ventricular diastolic and systolic dysfunction, which may consequently lead to clinical complications such as heart failure, atrial brillation, ischemic heart disease, and other vascular events [40]. Our In vivo studies found that RGOs improved heart systolic and pumping function.…”

New-Onset Atrial Fibrillation in Patients With Primary Aldosteronism Receiving Different Treatment Strategies: Systematic Review and Pooled Analysis of Three Studies

“…In addition, left ventricular remodeling, which is also strongly correlated to atrial fibrillation. Some clinical studies have shown that aldosterone induces left ventricular hypertrophy and fibrosis which is associated with left ventricular diastolic dysfunction (8,(36)(37)(38)(39)(40). The left ventricular diastolic dysfunction has a prominent influence on atrial structure and function which also contributed to the atrial fibrillation genesis (8,12,41).…”

“…The prevalence of PA has been reported to be 4.3 to 9.5% in all patients with hypertension and 17 to 23% in PA patients with resistant hypertension (2,3). Compared to essential hypertension, PA is associated with higher risks of cardiovascular, renal, and metabolic complications (4)(5)(6)(7)(8). The excess aldosterone in PA will cause atrial structural and electrical remodeling which induce atrial fibrillation genesis.…”

CMR-Verified Myocardial Fibrosis Is Associated With Subclinical Diastolic Dysfunction in Primary Aldosteronism Patients

“…The aldosterone promotes LV hypertrophy by activating mineralocorticoid receptors (MRs), extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and protein kinase C-a (PKC-a) (29). Basic and clinical studies found that aldosterone-induced cardiac fibrosis is associated with the activation of MRs and glucocorticoid receptors (GRs) through genomic and non-genomic pathways (30). Previous echocardiography studies showed a decreased global longitudinal strain in PA patients compared with EH (31,32).…”