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Cardiac Structure and Function Across the Spectrum of Aldosteronism: the Atherosclerosis Risk in Communities Study.

TitleCardiac Structure and Function Across the Spectrum of Aldosteronism: the Atherosclerosis Risk in Communities Study.
Publication TypeJournal Article
Year of Publication2022
AuthorsBrown JM, Wijkman MO, Claggett BL, Shah AM, Ballantyne CM, Coresh J, Grams ME, Wang Z, Yu B, Boerwinkle E, Vaidya A, Solomon SD
Date Published2022 Sep
KeywordsAldosterone, Atherosclerosis, Atrial Fibrillation, Heart Atria, Heart Failure, Humans, Hyperaldosteronism, Renin

BACKGROUND: Aldosterone production and mineralocorticoid receptor activation are implicated in myocardial fibrosis and cardiovascular events.

METHODS: Cardiac structure and function were assessed in 4547 participants without prevalent heart failure (HF) in the ARIC study (Atherosclerosis Risk in Communities), with echocardiography, aldosterone, and plasma renin activity measurement (2011-2013). Subjects were characterized by plasma renin activity as suppressed (≤0.5 ng/mL per hour) or unsuppressed (>0.5 ng/mL per hour). Cross-sectional relationships with cardiac structure and function, and longitudinal relationships with outcomes (HF hospitalization; HF and all-cause death; HF, death, myocardial infarction, and stroke; and incident atrial fibrillation) were assessed. Models were adjusted for demographic and anthropometric characteristics and additively, for blood pressure and antihypertensives.

RESULTS: Evidence of primary aldosteronism physiology was prevalent (11.6% with positive screen) and associated with echocardiographic parameters. Renin suppression was associated with greater left ventricular mass, left ventricular volumes, and left atrial volume index, and a lower E/A ratio (adjusted

CONCLUSIONS: Renin suppression and aldosterone excess, consistent with primary aldosteronism pathophysiology, were associated with cardiac structural and functional alterations and may represent an early target for mitigation of fibrosis with mineralocorticoid receptor antagonists.

Alternate JournalHypertension
PubMed ID35582954