CHENG-HSUAN TSAICHIEN-TING PANChang Y.-Y.ZHENG-WEI CHENVIN-CENT WUCHI-SHENG HUNGYEN-HUNG LIN2022-02-152022-02-1520210950-9240https://www.scopus.com/inward/record.uri?eid=2-s2.0-85092668678&doi=10.1038%2fs41371-020-00426-y&partnerID=40&md5=cae40b8583f9e16284adb25338ff042ahttps://scholars.lib.ntu.edu.tw/handle/123456789/594549Primary 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. ? 2020, The Author(s), under exclusive licence to Springer Nature Limited.[SDGs]SDG3aldosterone; hydrocortisone; mineralocorticoid antagonist; reactive oxygen metabolite; spironolactone; aldosterone; adrenalectomy; adverse outcome; atrial fibrillation; cardiac patient; cell metabolism; chronic inflammation; clinical assessment tool; clinical research; diastolic dysfunction; disease association; disease course; Doppler echocardiography; drug effect; endothelial dysfunction; essential hypertension; extracellular matrix; functional assessment; heart failure; heart hypertrophy; heart left ventricle; heart left ventricle failure; heart left ventricle mass; heart left ventricle remodeling; heart muscle fibrosis; heart ventricle hypertrophy; heart ventricle remodeling; human; ischemic heart disease; macrophage activation; medical research; metabolic disorder; nonhuman; nuclear magnetic resonance imaging; pathogenesis; primary hyperaldosteronism; Review; systolic dysfunction; tissue Doppler imaging; treatment response; vascular disease; heart left ventricle function; heart left ventricle hypertrophy; heart ventricle remodeling; hyperaldosteronism; hypertension; Aldosterone; Humans; Hyperaldosteronism; Hypertension; Hypertrophy, Left Ventricular; Ventricular Dysfunction, Left; Ventricular Remodelingreview10.1038/s41371-020-00426-y330675542-s2.0-85092668678