{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T20:04:40Z","timestamp":1792785880810,"version":"4.5.0"},"reference-count":39,"publisher":"Oxford University Press (OUP)","issue":"36","license":[{"start":{"date-parts":[[2026,5,13]],"date-time":"2026-05-13T00:00:00Z","timestamp":1778630400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/501100001674","name":"Fondation Leducq","doi-asserted-by":"publisher","award":["18CVD05"],"award-info":[{"award-number":["18CVD05"]}],"id":[{"id":"10.13039\/501100001674","id-type":"DOI","asserted-by":"publisher"}]},{"name":"\u2018Towards Precision Medicine with Human iPSCs for Cardiac Channelopathies\u2019","award":["EJPRD19-187"],"award-info":[{"award-number":["EJPRD19-187"]}]},{"DOI":"10.13039\/100031478","name":"NextGenerationEU","doi-asserted-by":"publisher","award":["H45E22001210006"],"award-info":[{"award-number":["H45E22001210006"]}],"id":[{"id":"10.13039\/100031478","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003196","name":"Italian Ministry of Health","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100003196","id-type":"DOI","asserted-by":"publisher"}]},{"name":"\u2018Ricerca Corrente\u2019","award":["08064017"],"award-info":[{"award-number":["08064017"]}]},{"name":"\u2018Ricerca Corrente\u2019","award":["2022RZCWWH_001"],"award-info":[{"award-number":["2022RZCWWH_001"]}]},{"DOI":"10.13039\/501100003793","name":"Swedish Heart-Lung Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100003793","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,9,22]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background and Aims<\/jats:title>\n                    <jats:p>Modifier genes may cause different clinical phenotypes in patients with long QT syndrome (LQTS) carrying the same pathogenic variant. Variants in the MTMR4 gene have been previously associated, via patient-specific cardiomyocytes derived from induced pluripotent stem cells, with variable arrhythmic risk in a family with the p.Y111C-LQT1 mutation. This study aimed to evaluate the broader clinical impact of MTMR4 variants in patients with LQT1 and LQT2.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>A total of 1192 LQTS patients were analysed: 638 with LQT1, 432 with LQT2, and 122 Swedish carriers of the p.Y111C-LQT1 variant. The association between MTMR4 variants and clinical severity was assessed by comparing patients with severe symptoms (cardiac arrest or syncope on beta-blockers) vs asymptomatic or mildly symptomatic individuals. ECG parameters, including Tpeak-Tend and T-wave heterogeneity, were also evaluated.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>In the LQT1 cohort, there was a significant decreasing pattern for cardiac events across MTMR4 genotypes (AA:15.9%, Aa:11.6%, aa:6.3%), while an opposite trend was apparent in the LQT2 cohort (AA:16.5%, Aa:18.2%, aa:27.6%). No pattern was apparent in the Swedish cohort. In the combined LQT1 cohort, the aa genotype was found in 15% of 702 mild\/asymptomatic vs 1.7% of 58 with severe symptoms (P = .002). Vice versa, in LQT2, aa was more frequent in severe cases (24.1% vs 11.9%, P = .014). QTc was not associated with MTMR4, but the repolarization markers supported a gene-specific directionality of arrhythmic risk.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>The MTMR4 minor allele in homozygosis exerts a gene-specific and opposite impact on arrhythmic risk in LQTS. This finding should influence risk stratification in clinical practice.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/eurheartj\/ehag294","type":"journal-article","created":{"date-parts":[[2026,4,8]],"date-time":"2026-04-08T11:54:45Z","timestamp":1775649285000},"page":"5189-5199","source":"Crossref","is-referenced-by-count":3,"title":["<i>MTMR4<\/i>\n                    variants have opposite gene-specific impact on life-threatening arrhythmic risk in type 1 and 2 long QT syndrome"],"prefix":"10.1093","volume":"47","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0367-1048","authenticated-orcid":false,"given":"Peter J","family":"Schwartz","sequence":"first","affiliation":[{"name":"Center for Cardiac Arrhythmias of Genetic Origin and Laboratory of Cardiovascular Genetics, IRCCS Istituto Auxologico Italiano , Via Pier Lombardo, 22, Milan 20135 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