{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T12:48:24Z","timestamp":1792068504033,"version":"4.4.0"},"reference-count":41,"publisher":"Oxford University Press (OUP)","license":[{"start":{"date-parts":[[2026,8,3]],"date-time":"2026-08-03T00:00:00Z","timestamp":1785715200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Horizon Europe under grant agreements","award":["101057639"],"award-info":[{"award-number":["101057639"]}]},{"name":"Horizon Europe under grant agreements","award":["101060011"],"award-info":[{"award-number":["101060011"]}]},{"DOI":"10.13039\/501100002301","name":"Estonian Research Council","doi-asserted-by":"publisher","award":["PRG2625"],"award-info":[{"award-number":["PRG2625"]}],"id":[{"id":"10.13039\/501100002301","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100010114","name":"Yrj\u00f6 Jahnsson Foundation","doi-asserted-by":"publisher","award":["20247848"],"award-info":[{"award-number":["20247848"]}],"id":[{"id":"10.13039\/100010114","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100008723","name":"Finnish Medical Foundation","doi-asserted-by":"publisher","award":["8466"],"award-info":[{"award-number":["8466"]}],"id":[{"id":"10.13039\/100008723","id-type":"DOI","asserted-by":"publisher"}]},{"name":"EMBO postdoctoral fellowship","award":["ALTF 267-2025"],"award-info":[{"award-number":["ALTF 267-2025"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background and Aims<\/jats:title>\n                    <jats:p>Up to half of patients switch or discontinue antihypertensive medications within the first year, but underlying mechanisms remain elusive. This study aimed to identify genetic predictors of antihypertensive medication use trajectories within the first year.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Using longitudinal medication data from &amp;gt;400 000 genotyped antihypertensive medication users across three cohorts (FinnGen, the UK Biobank, and the Estonian Biobank), short-term antihypertensive medication use trajectories were classified as Continue, Switch, or Discontinue. Genome-wide association studies were performed across five medication classes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>In total, 14 genome-wide significant loci were identified for switching from angiotensin-converting enzyme inhibitors (ACEI) and dihydropyridine calcium channel blockers (dCCB) to other antihypertensive medications. For ACEI switching, evidence converged on the neurotensin-NTSR1 pathway, including a 320-fold Finnish-enriched protective missense variant in the neurotensin receptor gene NTSR1 (rs148569146 [G301R], odds ratio [OR] 0.49, P = 3.3 \u00d7 10\u221243) and a variant near RASSF9 (rs181941187, OR = 0.74, P = 1.2 \u00d7 10\u221249) tagging the neurotensin gene NTS. In drug\u2013gene interaction analyses, NTSR1 G301R was associated with reduced ACEI-induced cough risk (OR 0.39, P = 8.1 \u00d7 10\u22124). The dCCB switching locus at CYP3A43 was in near-complete linkage (r2 = 0.99) with the functional CYP3A4*22 allele (rs35599367, OR 1.23, P = 6.1 \u00d7 10\u221210). A polygenic risk score (PRS) for ACEI switching predicted two-fold ACEI cough risk in the top 10% PRS compared with the middle 20% in an independent sample of the Estonian Biobank.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>These findings extend the bradykinin hypothesis of ACEI-induced cough by implicating neurotensin-NTSR1 signalling, pinpoint CYP3A4*22 as a novel functional predictor of dCCB switching with potential for genotype-guided prescribing, and validate medication use trajectories as a framework for pharmacogenetic discovery.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/eurheartj\/ehag575","type":"journal-article","created":{"date-parts":[[2026,7,7]],"date-time":"2026-07-07T11:39:44Z","timestamp":1783424384000},"source":"Crossref","is-referenced-by-count":2,"title":["Side effects in hypertension treatment: a pharmacogenomic analysis"],"prefix":"10.1093","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6036-889X","authenticated-orcid":false,"given":"Felix","family":"Vaura","sequence":"first","affiliation":[{"name":"Institute for Molecular Medicine Finland (FIMM), HiLIFE, University of Helsinki , P.O. 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Box 20, Helsinki FI-00014 ,","place":["Finland"]},{"name":"Cardiovascular Disease Initiative, Broad Institute of MIT and Harvard , Cambridge, MA ,","place":["USA"]},{"name":"Division of Cardiology, Heart and Vascular Institute, Mass General Brigham , Boston, MA ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2249-0971","authenticated-orcid":false,"given":"Max","family":"Tamlander","sequence":"additional","affiliation":[{"name":"Institute for Molecular Medicine Finland (FIMM), HiLIFE, University of Helsinki , P.O. 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