Aldosterone induces left ventricular subclinical systolic dysfunction

Chen, Zheng-Wei; Huang, Kuo‐Feng; Lee, Jen‐Kuang; Lin, Lung‐Chun; Chen, Ching-Way; Chang, Yuan‐Jen; Liao, Che‐Wei; Wu, Vin-Cent; Hung, Chi-Shen; Lin, Yen‐Hung

doi:10.1097/hjh.0000000000001534

Cited by 35 publications

(29 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, whether this LV dysfunction was caused by an excess of aldosterone or merely the effect of blood pressure was unclear [71]. In our previous study, we found that PA patients had a lower magnitude of global longitudinal strain compared to EH patients with comparable blood pressure, which indicated subclinical systolic dysfunction in PA patients [9]. This finding suggested that the effect of aldosterone on systolic function impairment was independent of hemodynamics.…”

Section: Systolic Function Evaluation In Pa: Strain Echocardiographymentioning

confidence: 88%

“…Subsequently, the excess aldosterone can cause more cardiovascular complications, including coronary artery disease, myocardial infarction, stroke, transient ischemic attack, atrial fibrillation and heart failure than in patients with essential hypertension (EH) [2][3][4][5][6][7][8]. In addition, it can also lead to cardiovascular remodeling and dysfunction [9][10][11]. Clinical studies have demonstrated that patients with PA have more left ventricular (LV) remodeling including increased LV mass and cardiac fibrosis than patients with EH [12][13][14][15][16][17].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Left ventricular remodeling and dysfunction in primary aldosteronism

et al. 2020

Self Cite

View full text Add to dashboard Cite

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.

show abstract

Section: Systolic Function Evaluation In Pa: Strain Echocardiographymentioning

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Left ventricular remodeling and dysfunction in primary aldosteronism

et al. 2020

Self Cite

View full text Add to dashboard Cite

show abstract

“…In 2017, Yang et al reported a higher LAVI among 100 PA patients compared to 100 EH controls [60]. Our previous investigation of left ventricular subclinical systolic dysfunction using strain analysis also showed a higher left atrial diameter and LAVI among PA patients compared to those among matched EH controls, although the difference did not reach statistical significance [61]. Wang et al recently reported increased left atrial stiffness in 107 PA patients with lower left atrial velocity, strain, and strain rate, and higher left atrial stiffness index compared to 50 EH controls [62].…”

Section: Left Atrium Structure and Functionmentioning

confidence: 76%

Atrial Fibrillation in Primary Aldosteronism

et al. 2020

Self Cite

View full text Add to dashboard Cite

Primary aldosteronism (PA) is the most common cause of secondary hypertension. Increasing evidence has demonstrated an increased cardiovascular risk in patients with PA compared to those with essential hypertension (EH), including atrial fibrillation (AF), the most prevalent arrhythmia among adults that is associated with an elevated risk of subsequent cerebro-cardiovascular adverse events. The mechanisms of increased prevalence of AF in PA patients are complex. Excessive aldosterone production is regarded to be a key component in the pathogenesis of AF, in addition to arterial hypertension and electrolyte imbalance. In addition, several translational and clinical studies have reported that structural remodeling with atrial fibrosis and electrical remodeling with arrhythmogenicity induced by an excess of aldosterone also play major roles in AF genesis. Clinical studies from several registries and meta-analysis have reported an increased prevalence and risk of AF in PA patients compared to EH patients. Recent trials have further demonstrated a reduction in the risk of new-onset atrial fibrillation (NOAF) after adrenalectomy, while the results of medical treatment with mineralocorticoid receptor antagonists (MRAs) have been inconsistent. This review outlines the current evidence of the relationship between PA and AF, and highlights recent progress in the management of PA with regards to the development of AF.

show abstract

“…We calculated adjusted HR (aHR) values after adjusting for age, sex, Charlson comorbidity index, and propensity covariates. Death before the occurrence of diabetes was considered a competing risk event in the Fine and Gray model (12,15). To assess the difference in the diabetes-free probability curve and survival curve between the two patient groups, we analyzed competing regression plots.…”

Section: Discussionmentioning

confidence: 99%

“…New-onset diabetes was defined as one of the following conditions in those who had no history of diabetes at baseline: records of greater than three consecutive outpatient visits with the codes of prescriptions of oral antidiabetic drugs or insulin (12). Patients were monitored from the index date until death, diabetes diagnosis, 5-year follow-up period, or 31 December 2011, whichever occurred first.…”

Section: Study Outcome and Follow-upmentioning

confidence: 99%