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A prospective study of the impact of AGTR1 A1166C on the effects of candesartan in patients with heart failure

De Denus, S.; Dubé, M.-P.; Fouodjio, R.é; Huynh, T.; LeBlanc, M.-H.él.èn.; Lepage, S.; Sheppard, R.; Giannetti, N.; Lavoie, J.ël.; Mansour, A.; Provost, S.; Normand, V.ér.; Mongrain, I.; Langlois, M.; O'Meara, E.; Ducharme, A.; Racine, N.; Guertin, M.-C.; Turgeon, J.; Phillips, M.S.; Rouleau, J.-L.; Tardif, J.-C.; White, M.

Pharmacogenomics 19(7): 599-612

2018


ISSN/ISBN: 1744-8042
PMID: 29701105
DOI: 10.2217/pgs-2018-0004
Accession: 049313295

To evaluate the impact of AGTR1 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 AGTR1 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). AGTR1 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. Clinicaltrials.gov : NCT00400582.

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