{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,8]],"date-time":"2026-01-08T02:53:37Z","timestamp":1767840817476,"version":"3.49.0"},"reference-count":42,"publisher":"Oxford University Press (OUP)","issue":"13","license":[{"start":{"date-parts":[[2024,7,17]],"date-time":"2024-07-17T00:00:00Z","timestamp":1721174400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001659","name":"German Research Foundation","doi-asserted-by":"publisher","award":["DFG-BR2107\/4-1"],"award-info":[{"award-number":["DFG-BR2107\/4-1"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003246","name":"Netherlands Organization for Scientific Research","doi-asserted-by":"publisher","award":["09150171910029"],"award-info":[{"award-number":["09150171910029"]}],"id":[{"id":"10.13039\/501100003246","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,11,5]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Aims<\/jats:title>\n                  <jats:p>Short QT syndrome type 1 (SQT1) is a genetic channelopathy caused by gain-of-function variants in human-ether-a-go-go (HERG) underlying the rapid delayed-rectifier K+ current (IKr), leading to QT-shortening, ventricular arrhythmias, and sudden cardiac death. Data on efficient pharmacotherapy for SQT1 are scarce. In patients with primary carnitine-deficiency, acquired-short QT syndrome (SQTS) has been observed and rescued by carnitine supplementation. Here, we assessed whether carnitine exerts direct beneficial (prolonging) effects on cardiac repolarization in genetic SQTS.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods and results<\/jats:title>\n                  <jats:p>Adult wild-type (WT) and transgenic SQT1 rabbits (HERG-N588K, gain of IKr) were used. In vivo electrocardiograms (ECGs), ex vivo monophasic action potentials (APs) in Langendorff-perfused hearts, and cellular ventricular APs and ion currents were assessed at baseline and during L-Carnitine\/C16-Carnitine-perfusion. Two-dimensional computer simulations were performed to assess re-entry-based ventricular tachycardia-inducibility. L-Carnitine\/C16-Carnitine prolonged QT-intervals in WT and SQT1, leading to QT-normalization in SQT1. Similarly, monophasic and cellular AP duration (APD) was prolonged by L-Carnitine\/C16-Carnitine in WT and SQT1. As underlying mechanisms, we identified acute effects on the main repolarizing ion currents: IKr-steady, which is pathologically increased in SQT1, was reduced by L-Carnitine\/C16-Carnitine and deactivation kinetics were accelerated. Moreover, L-Carnitine\/C16-Carnitine decreased IKs-steady and IK1. In silico modelling identified IKr changes as the main factor for L-Carnitine\/C16-Carnitine-induced APD-prolongation. 2D simulations revealed increased sustained re-entry-based arrhythmia formation in SQT1 compared to WT, which was decreased to the WT-level when adding carnitine-induced ion current changes.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>L-Carnitine\/C16-Carnitine prolong\/normalize QT and whole-heart\/cellular APD in SQT1 rabbits. These beneficial effects are mediated by acute effects on IKr. L-Carnitine may serve as a potential future QT-normalizing, anti-arrhythmic therapy in SQT1.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/cvr\/cvae149","type":"journal-article","created":{"date-parts":[[2024,7,16]],"date-time":"2024-07-16T17:07:32Z","timestamp":1721149652000},"page":"1550-1561","source":"Crossref","is-referenced-by-count":4,"title":["Beneficial normalization of cardiac repolarization by carnitine in transgenic short QT syndrome type 1 rabbit models"],"prefix":"10.1093","volume":"120","author":[{"given":"Ilona","family":"Bodi","sequence":"first","affiliation":[{"name":"Department of Cardiology and Angiology I, Medical Faculty, Heart Center University of Freiburg , Hugstetter Str. 55, 79106 Freiburg ,","place":["Germany"]},{"name":"Institute of Experimental Cardiovascular Medicine , Medical Faculty, Heart Center University of Freiburg, Hugstetter Str. 55, 79106 Freiburg ,","place":["Germany"]},{"name":"Translational Cardiology, Department of Cardiology, 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