A pharmacogenomics study of atenolol found that heart rate response is genetically variable — but its own confirmed, replicated genes are not the ones tagged to this page's specific variants.
Beta blockers like atenolol are prescribed for high blood pressure partly because they slow heart rate — but exactly how much someone's heart rate drops on the same dose varies substantially from person to person. That variation has a genetic component, which pharmacogenomics research has tried to map.
Shahin et al. 2018, using the PEAR (Pharmacogenomic Evaluation of Antihypertensive Responses) study, ran four separate genome-wide association analyses for heart-rate response to atenolol: monotherapy and add-on therapy, analysed separately in 426 white and 273 black participants. Variants reaching a suggestive threshold were then tested for replication in a separate group of 200 white and 168 black participants treated with a different beta blocker, metoprolol. Two variants replicated and reached genome-wide significance in the combined analysis: rs17117817, near OR10P1 (effect size 5.53 beats per minute), and rs2364349, in SNX9 (effect size 3.5 beats per minute) — and the paper's own stated conclusion names only these two genes as its confirmed finding.
This page's own 9 variants are all in a different gene entirely, MARCHF1, and come from the "add-on therapy" arm of the four GWAS analyses specifically — the earlier, less strict discovery stage, not the genes the paper's replication and combined analysis actually confirmed. This page exists because the GWAS Catalog record ties these variants to this study and trait; readers should weigh OR10P1 and SNX9, the paper's own confirmed genes, more heavily than the MARCHF1 variants held here.
Heart rate response to beta blockers is monitored directly during treatment, not predicted from genotype, and no variant on this page is used clinically to choose or dose a beta blocker. This page is unusual in naming a limitation directly: its own variants are not the ones the source study's replication analysis confirmed.
Beta-blocker dosing is adjusted based on measured heart rate and blood pressure response in the clinic — not genotype. Nothing on this page changes that practice.
What a 23andMe/AncestryDNA export or raw VCF can and can't tell you about Heart Rate Response to Beta Blockers comes down to these specific, well-studied positions — not a diagnosis.
MARCHF1 · rs17044565
See detailed info →MARCHF1 · rs6822628
See detailed info →MARCHF1 · rs723730
See detailed info →MARCHF1 · rs10002082
See detailed info →MARCHF1 · rs11930019
See detailed info →MARCHF1 · rs17044630
See detailed info →MARCHF1 · rs6840738
See detailed info →MARCHF1 · rs985676
See detailed info →MARCHF1 · rs11931264
See detailed info →The studies behind these variants recruited participants from different ancestries — a result found in one population doesn't always transfer to another. Based on 10 of 10 linked studies with a resolved discovery ancestry.
Databases, guidelines and references
Part of the variation is genetic. A 2018 study found two genes, OR10P1 and SNX9, with replicated associations to heart-rate response to atenolol.
Its replication and combined analysis confirmed two genes: rs17117817 near OR10P1 and rs2364349 in SNX9. This page's own 9 variants, all in MARCHF1, come from an earlier discovery-stage analysis that was not part of that confirmed finding.
Because being direct about it matters: the GWAS Catalog record ties these MARCHF1 variants to this study and trait, but the paper's own replication only confirmed OR10P1 and SNX9. Readers should weigh those two genes more heavily.
No. Heart rate response is monitored directly during treatment. This page describes population-level research associations, not a predictive test.
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