A prospective study of the impact of

To evaluate the impact of A1166C (rs5186) on the response to candesartan in patients with heart failure. Prospective, multicentre, open-label study. We studied 299 symptomatic patients with heart failure presenting a left ventricular ejection fraction ≤40%. Reductions in the primary end points of na...

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Bibliographic Details
Published in:Pharmacogenomics 2018-04
Main Authors: Denus, Simon de, Dubé, Marie-Pierre, Fouodjio, René, Huynh, Thao, LeBlanc, Marie-Hélène, Lepage, Serge, Sheppard, Richard, Giannetti, Nadia, Lavoie, Joël, Mansour, Asmaa, Provost, Sylvie, Normand, Valérie, Mongrain, Ian, Langlois, Mathieu, O'Meara, Eileen, Ducharme, Anique, Racine, Normand, Guertin, Marie-Claude, Turgeon, Jacques, Phillips, Michael S, Rouleau, Jean-Lucien, Tardif, Jean-Claude, White, Michel
Format: Article
Language:English
Subjects:
biomarkers
cardiovascular diseases
pharmacodynamics
pharmacogenomics
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Summary:To evaluate the impact of A1166C (rs5186) on the response to candesartan in patients with heart failure. Prospective, multicentre, open-label study. We studied 299 symptomatic patients with heart failure presenting a left ventricular ejection fraction ≤40%. Reductions in the primary end points of natriuretic peptides were not significantly associated with A1166C. Nevertheless, carrying the 1166C allele was associated with a greater compensatory increase in renin activity (p = 0.037) after 16 weeks of treatment with candesartan and a more modest effect on aldosterone concentrations (p = 0.022). 1166C carriers may experience a greater long-term compensatory renin-angiotensin-aldosterone system activation following treatment with candesartan. Whether these associations ultimately influence clinical outcomes requires investigation. : NCT00400582
ISSN:1462-2416
1744-8042
DOI:10.2217/pgs-2018-0004