{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,23]],"date-time":"2026-07-23T12:00:41Z","timestamp":1784808041442,"version":"3.55.0"},"reference-count":30,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2026,7,16]],"date-time":"2026-07-16T00:00:00Z","timestamp":1784160000000},"content-version":"vor","delay-in-days":15,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T00:00:00Z","timestamp":1782864000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Eur J Clin Investigation"],"published-print":{"date-parts":[[2026,7]]},"abstract":"ABSTRACT<\/jats:title>\n \n Background<\/jats:title>\n Growth differentiation factor\u201015 (GDF\u201015) is upregulated in coronary artery disease (CAD). The relationship of intensive statin therapy with circulating GDF\u201015 levels has not been explored yet. In the current secondary analysis of an observational cohort, we investigated whether high\u2010intensity statin treatment is associated with GDF\u201015 in patients with advanced CAD.<\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n In 102 CAD patients we measured GDF\u201015 levels before and after median 7 [6\u20138] months from initiation atorvastatin 80\u2009mg\/day (\n n<\/jats:italic>\n \u2009=\u200963, 61.8%) or rosuvastatin 40\u2009mg\/day (\n n<\/jats:italic>\n \u2009=\u200939, 38.2%). At the two time points we also determined C\u2010reactive protein (CRP), thrombin generation and fibrinolysis inhibitors. There was no concurrent control group.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n At baseline GDF\u201015 levels (median 942; interquartile range 639\u20131284\u2009pg\/mL) were associated solely with age (\n R<\/jats:italic>\n \u2009=\u20090.567,\n p<\/jats:italic>\n \u2009<\u20090.001) and CRP (\n R<\/jats:italic>\n \u2009=\u20090.464,\n p<\/jats:italic>\n \u2009<\u20090.001), but not with lipid profile. On high\u2010intensity statin therapy GDF\u201015 reduction by 17.8% was observed (\n p<\/jats:italic>\n \u2009=\u20090.006), which was associated with CRP lowering by 46.4% (\n R<\/jats:italic>\n \u2009=\u20090.788,\n p<\/jats:italic>\n \u2009<\u20090.001), but not with changes in total cholesterol (by 17.6%) and low\u2010density lipoprotein cholesterol (LDL\u2010C) (by 28.1%). However, GDF\u201015 levels were lower by 28.5% (\n p<\/jats:italic>\n \u2009<\u20090.001) and 18.9% (\n p<\/jats:italic>\n \u2009=\u20090.013) in 43 patients (42.2%) who achieved the target LDL\u2010C\u2009<\u20091.8\u2009mmol\/L and 19 (18.6%) with LDL\u2010C\u2009<\u20091.4\u2009mmol\/L, respectively, as compared to the remainder. The type of statin was not associated with follow\u2010up GDF\u201015. Age (\n p<\/jats:italic>\n \u2009=\u20090.029), baseline GDF\u201015 (\n p<\/jats:italic>\n \u2009<\u20090.001) and CRP (\n p<\/jats:italic>\n \u2009<\u20090.001), but not LDL\u2010C, were independently associated with follow\u2010up GDF\u201015.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n We demonstrated that high\u2010dose statin therapy is associated with lower GDF\u201015 in CAD patients and this effect is largely related to the anti\u2010inflammatory properties of statins.<\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/eci.70241","type":"journal-article","created":{"date-parts":[[2026,7,16]],"date-time":"2026-07-16T11:45:54Z","timestamp":1784202354000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["High\u2010Intensity Statin Treatment Is Associated With Reduced Growth Differentiation Factor\u201015 in Patients With Coronary Artery Disease"],"prefix":"10.1111","volume":"56","author":[{"given":"Konrad","family":"St\u0119pie\u0144","sequence":"first","affiliation":[{"name":"Department of Thromboembolic Disorders Institute of Cardiology, Jagiellonian University Medical College Krak\u00f3w Poland"},{"name":"Department of Coronary Artery Disease and Heart Failure St. John Paul II Hospital Krak\u00f3w Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1762-308X","authenticated-orcid":false,"given":"Micha\u0142","family":"Z\u0105bczyk","sequence":"additional","affiliation":[{"name":"Department of Thromboembolic Disorders Institute of Cardiology, Jagiellonian University Medical College Krak\u00f3w Poland"},{"name":"Krakow Center for Medical Research and Technologies St. John Paul II Hospital Krak\u00f3w Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joanna","family":"Natorska","sequence":"additional","affiliation":[{"name":"Department of Thromboembolic Disorders Institute of Cardiology, Jagiellonian University Medical College Krak\u00f3w Poland"},{"name":"Krakow Center for Medical Research and Technologies St. John Paul II Hospital Krak\u00f3w Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jaros\u0142aw","family":"Zalewski","sequence":"additional","affiliation":[{"name":"Department of Coronary Artery Disease and Heart Failure St. John Paul II Hospital Krak\u00f3w Poland"},{"name":"Department of Coronary Artery Disease and Heart Failure Institute of Cardiology, Jagiellonian University Medical College Krak\u00f3w Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jacek","family":"Jawie\u0144","sequence":"additional","affiliation":[{"name":"Department of Pharmacology Jagiellonian University Medical College Krak\u00f3w Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anetta","family":"Undas","sequence":"additional","affiliation":[{"name":"Department of Thromboembolic Disorders Institute of Cardiology, Jagiellonian University Medical College Krak\u00f3w Poland"},{"name":"Krakow Center for Medical Research and Technologies St. John Paul II Hospital Krak\u00f3w Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,7,16]]},"reference":[{"key":"e_1_2_11_2_1","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/cvae214"},{"key":"e_1_2_11_3_1","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.2200641"},{"key":"e_1_2_11_4_1","doi-asserted-by":"publisher","DOI":"10.1038\/s41574-021-00529-7"},{"key":"e_1_2_11_5_1","doi-asserted-by":"publisher","DOI":"10.1093\/eurheartj\/ehac577"},{"key":"e_1_2_11_6_1","doi-asserted-by":"publisher","DOI":"10.1177\/10760296211063875"},{"key":"e_1_2_11_7_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00441-004-0986-3"},{"key":"e_1_2_11_8_1","doi-asserted-by":"publisher","DOI":"10.3389\/fcvm.2023.1054187"},{"key":"e_1_2_11_9_1","article-title":"High\u2010Dose Atorvastatin and Rosuvastatin Reduce the Levels of Neutrophil Extracellular Trap\u2010Related Proteins in Coronary Artery Disease: Association With Prothrombotic 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