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We analyzed these metabolites using liquid chromatography\u2013tandem mass spectrometry in patients with atrial fibrillation (AF) (<jats:italic>n<\/jats:italic>\u2009=\u2009241) with a focus on heart rhythm at blood withdrawal, AF progression phenotypes, and successful sinus rhythm (SR) restoration (<jats:italic>n<\/jats:italic>\u2009=\u200922). AF progression phenotypes were defined as paroxysmal AF with\/without low voltage areas (LVA) and persistent AF with\/without LVA. While arginine, ADMA, and hArg were within reference limits for healthy controls, SDMA was higher in the AF cohort (0.57\u2009\u00b1\u20090.12 vs. 0.53\u00a0\u03bcmol\/L (97.5th percentile in reference cohort)). SR restoration in AF patients resulted in normalization of SDMA concentrations (0.465\u2009\u00b1\u20090.082 vs. 0.570\u2009\u00b1\u20090.134\u00a0\u03bcmol\/L at baseline, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.001). Patients with AF at the time of blood sampling had significantly lower hArg (1.65\u2009\u00b1\u20090.51 vs. 1.85\u2009\u00b1\u20090.60\u00a0\u03bcmol\/L, <jats:italic>p<\/jats:italic>\u2009=\u20090.006) and higher ADMA concentrations (0.526\u2009\u00b1\u20090.08 vs. 0.477\u2009\u00b1\u20090.08\u00a0\u03bcmol\/L, p\u2009&lt;\u20090.001) compared with AF patients in SR. hArg concentrations were lower in patients with advanced AF progression phenotypes (persistent AF with LVA (<jats:italic>p<\/jats:italic>\u2009=\u20090.046)) independent of heart rhythm at blood sampling. Summarizing, arginine metabolism imbalance is associated with AF in general and AF progression and may contribute to associated risk.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Key messages<\/jats:title>\n                <jats:p>\u2022 Heart rhythm at blood withdrawal affects ADMA and hArg level in AF patients.<\/jats:p>\n                <jats:p>\u2022 SDMA is higher in AF patients.<\/jats:p>\n                <jats:p>\u2022 SDMA levels normalize after sinus rhythm restoration.<\/jats:p>\n                <jats:p>\u2022 hArg levels decrease in advanced AF progression phenotypes.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1007\/s00109-020-01932-9","type":"journal-article","created":{"date-parts":[[2020,6,6]],"date-time":"2020-06-06T00:02:45Z","timestamp":1591401765000},"page":"999-1008","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Arginine derivatives in atrial fibrillation progression phenotypes"],"prefix":"10.1007","volume":"98","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0799-4725","authenticated-orcid":false,"given":"Petra","family":"B\u00fcttner","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin","family":"Bahls","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rainer H.","family":"B\u00f6ger","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gerhard","family":"Hindricks","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Holger","family":"Thiele","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Edzard","family":"Schwedhelm","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jelena","family":"Kornej","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2020,6,6]]},"reference":[{"issue":"1","key":"1932_CR1","first-page":"191","volume":"2","author":"J Pillarisetti","year":"2009","unstructured":"Pillarisetti J, Patel A, Boc K, Bommana S, Sawers Y, Vanga S, Sayana H, Chen W, Nath J, Vacek J et al (2009) Evolution of paroxysmal atrial fibrillation to persistent or permanent atrial fibrillation. 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