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Refractory hyperaldosteronism in heart failure is associated with plasma renin activity and angiotensinogen polymorphism

Authors :
Patrick Rossignol
Gian Franco Gensini
Andrea Ripoli
Michele Emdin
Cinzia Fatini
Rosanna Abbate
Elena Sticchi
Giuseppe Vergaro
Claudio Passino
Cristina Vassalle
Fondazione Toscana Gabriele Monasterio
Centre d'investigation clinique plurithématique Pierre Drouin [Nancy] (CIC-P)
Centre d'investigation clinique [Nancy] (CIC)
Université de Lorraine (UL)-Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lorraine (UL)-Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Institut National de la Santé et de la Recherche Médicale (INSERM)
Défaillance Cardiovasculaire Aiguë et Chronique (DCAC)
Université de Lorraine (UL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)
Institute of Clinical Physiology
Source :
Journal of Cardiovascular Medicine, Journal of Cardiovascular Medicine, Lippincott, Williams & Wilkins, 2015, 16 (6), pp.416-422. ⟨10.2459/JCM.0000000000000156⟩
Publication Year :
2015
Publisher :
HAL CCSD, 2015.

Abstract

International audience; AIMS:Refractory hyperaldosteronism is frequently observed in heart failure patients on up-to-date treatment, and holds prognostic value. Our aim was to identify which factors, either genetic or nongenetic, are associated with refractory hyperaldosteronism.METHODS:We enrolled 109 consecutive patients with left ventricular systolic dysfunction [left ventricular ejection fraction (LVEF) 32 ± 10%; 86% males; age 65 ± 13 years (mean ± standard deviation)] on optimized adrenergic and renin-angiotensin-aldosterone system (RAAS) antagonism, undergoing clinical and neuroendocrine characterization, and genotyping for six polymorphisms in key RAAS-regulating genes [angiotensinogen (AGT M235T), angiotensin-converting enzyme (ACE-240A>T and I/D), angiotensin II type I receptor (AGTR1 1166A>C), aldosterone synthase (CYP11B2-344C>T) and renin (REN rs7539596)].RESULTS:Patients with refractory hyperaldosteronism (n = 41, 38%, with plasma concentration >180 ng/l, URL, median 283 ng/l, interquartile range 218-433), when compared with those without (106 ng/l, 74-144; P

Details

Language :
English
ISSN :
15582027
Database :
OpenAIRE
Journal :
Journal of Cardiovascular Medicine, Journal of Cardiovascular Medicine, Lippincott, Williams & Wilkins, 2015, 16 (6), pp.416-422. ⟨10.2459/JCM.0000000000000156⟩
Accession number :
edsair.doi.dedup.....ec8fdab1e1a520e99678a1678e523ea9
Full Text :
https://doi.org/10.2459/JCM.0000000000000156⟩