Key result
The AGTR1 1166C allele was not significantly associated with reductions in natriuretic peptides but was associated with a greater compensatory increase in renin activity (p=0.037).
Why the study?
Does the AGTR1 A1166C genotype impact the biomarker response to candesartan in symptomatic patients with heart failure and LVEF ≤40%?
Cohort (n=299)
Open-label
Yes
Does the AGTR1 A1166C genotype impact the biomarker response to candesartan in symptomatic patients with heart failure and LVEF ≤40%?
In patients with HFrEF, the AGTR1 1166C allele is associated with greater compensatory RAAS activation following candesartan treatment, though it does not significantly affect natriuretic peptide reduction.
Should not guide candesartan use by AGTR1 genotype in HFrEF; hypothesis-generating for compensatory renin activation.
AIM: To evaluate the impact of AGTR1 A1166C (rs5186) on the response to candesartan in patients with heart failure. MATERIALS & METHODS: Prospective, multicentre, open-label study. We studied 299 symptomatic patients with heart failure presenting a left ventricular ejection fraction ≤40%. RESULTS: 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). CONCLUSION: 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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Denus et al. (2018) conducted a cohort in heart failure (n=299). AGTR1 1166C allele vs. Non-carriers was evaluated on reductions in natriuretic peptides. The AGTR1 1166C allele was not significantly associated with reductions in natriuretic peptides but was associated with a greater compensatory increase in renin activity (p=0.037).
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