ArticleCirculation. Genomic and precision medicine2026
Polygenic Prediction of Nongoal Response to Statin Therapy.
Article in Circulation. Genomic and precision medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundGenetic differences may contribute to interindividual variability in LDL-C (low-density lipoprotein cholesterol) lowering with statin therapy. Polygenic risk scores may help identify individuals unlikely to achieve guideline-concordant LDL-C targets on statins, enabling earlier therapy intensification.
methodsWe developed a multiancestry polygenic risk score for statin nongoal response (PRS-NGR) and evaluated its association with failure to achieve an on-statin LDL-C level of ≤70 mg/dL and with percent LDL-C reduction. This longitudinal cohort study used genotyping and electronic health record-linked data from the All of Us Research Program (2018-2025), the UK Biobank (2014-2023), and the Biobank Japan (2003-2008). Participants were statin users with at least 1 prestatin and 1 on-statin LDL-C measurement. Associations were assessed overall and by genetic ancestry, with replication in the UK Biobank and Biobank Japan.
resultsThe study included 46 564 participants from All of Us, 37 009 from the UK Biobank, and 3613 from Biobank Japan. In All of Us, higher PRS-NGR was associated with increased odds of nongoal response (odds ratio per SD, 1.43 [95% CI, 1.37-1.49]). Compared with the middle quintile, individuals in the top 1% had a higher risk, whereas those in the bottom 1% had a lower risk of nongoal response. Associations of PRS-NGR were consistent across African, European, and Latin American ancestry groups. Each SD increase in PRS-NGR corresponded to a 1.2-percentage-point smaller LDL-C reduction. Findings were replicated in the UK Biobank (odds ratio per SD, 2.39 [95% CI, 2.23-2.57]) and in Biobank Japan (odds ratio per SD, 1.31 [95% CI, 1.17-1.46]). Integration of PRS-NGR with guideline-based criteria identified individuals who derived a higher LDL-C% change and increased identification of statin-eligible individuals.
conclusionsWe developed and validated a multiancestry polygenic risk score that estimates the risk of nongoal LDL-C response to statin therapy. Incorporation of polygenic risk into lipid-lowering treatment paradigms may improve risk stratification and support more tailored therapy intensification strategies.
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