{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,18]],"date-time":"2026-06-18T16:51:40Z","timestamp":1781801500174,"version":"3.54.5"},"reference-count":45,"publisher":"Springer Science and Business Media LLC","issue":"1","license":[{"start":{"date-parts":[[2026,2,3]],"date-time":"2026-02-03T00:00:00Z","timestamp":1770076800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"},{"start":{"date-parts":[[2026,2,5]],"date-time":"2026-02-05T00:00:00Z","timestamp":1770249600000},"content-version":"vor","delay-in-days":2,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"}],"funder":[{"DOI":"10.13039\/501100001734","name":"Copenhagen University","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100001734","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Cardiovasc Diabetol"],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background\/aims<\/jats:title>\n                    <jats:p>Current clinical risk tools in type 1 diabetes do not include left ventricular dysfunction or inflammation, potentially limiting early risk detection. We aimed to evaluate the associations and predictive value of combining echocardiography with inflammatory biomarkers for mortality and major adverse cardiovascular events (MACE).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>In a prospective cohort of individuals with type 1 diabetes without known cardiovascular disease, we evaluated whether subclinical left ventricular dysfunction, defined by an elevated ratio of early mitral inflow velocity to early diastolic mitral annular velocity (E\/e\u2032) or impaired global longitudinal strain (GLS), combined with elevated levels of an inflammatory biomarker (interleukin-6 [IL-6], soluble urokinase-plasminogen-activator-receptor [suPAR], or high-sensitivity C-reactive-protein [hsCRP]), was associated with all-cause mortality and MACE. Cox models were adjusted for all 10 variables included in the Steno T1 Risk Engine variables: age, sex, systolic blood pressure, duration of diabetes, HbA1c, low-density lipoprotein, estimated glomerular filtration rate, albuminuria status, smoking, and physical activity. C-statistics and net reclassification improvement were assessed.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Among 876 participants (51% male, median age 50 years), 114 deaths occurred over 14.5 years of follow-up. Elevated E\/e\u2019 combined with IL-6 or suPAR, but not hsCRP, was independently associated with mortality. Compared with individuals with E\/e\u2019 &lt;8 and non-elevated IL-6, the hazard ratio (HR) for E\/e\u2019 8\u201313 with elevated IL-6 was 2.5 (95% CI 1.4 to 4.6,\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u20090.01), and for E\/e\u2032 \u226513 with elevated IL-6 was 3.4 (1.5\u20137.6;\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u20090.01). Corresponding HRs for suPAR were 2.4 (1.2 to 4.7,\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u20090.01) and 3.9 (1.8 to 8.5,\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u20090.01). Adding E\/e\u2032 and an inflammatory biomarker increased the C-statistic from 0.839 (Steno T1 Risk Engine alone) to 0.887 (E\/e\u2019 and IL6) and 0.868 (E\/e\u2019 and suPAR). Findings were similar for GLS and with MACE as the outcome.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Echocardiography combined with inflammatory biomarkers synergistically identifies individuals with type 1 diabetes, without known cardiovascular disease, who are at high risk of mortality and MACE.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s12933-025-03071-2","type":"journal-article","created":{"date-parts":[[2026,2,3]],"date-time":"2026-02-03T06:15:41Z","timestamp":1770099341000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Echocardiography and inflammatory biomarkers for predicting mortality and major adverse cardiovascular events in type 1 diabetes"],"prefix":"10.1186","volume":"25","author":[{"given":"Hashmat Sayed Zohori","family":"Bahrami","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter Godsk","family":"J\u00f8rgensen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jens Dahlgaard","family":"Hove","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ulrik","family":"Dixen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Line Jee Hartmann","family":"Rasmussen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jesper","family":"Eugen-Olsen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter","family":"Rossing","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Magnus T.","family":"Jensen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,2,3]]},"reference":[{"key":"3071_CR1","doi-asserted-by":"publisher","first-page":"880","DOI":"10.1056\/NEJMc1415677","volume":"372","author":"DJ Magliano","year":"2015","unstructured":"Magliano DJ, Harding JL, Shaw JE. 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J.D.H. reports receiving honoraria for lectures from Novo Nordisk and support for attending two meetings from Novo Nordisk and AstraZeneca. J.E.O. is the Chief Scientific Officer and shareholder in ViroGates A\/S and is named as an inventor on patents using suPAR. Copenhagen University Hospital Hvidovre, Denmark, owns the patents. No patents are included in this manuscript. P.R. report grants to his institution from Astra Zeneca, Bayer, and Novo Nordisk; has received honoraria and consulting fees to his institution from Abbott, Astellas, Astra Zeneca, Bayer, Boehringer Ingelheim, Eli Lilly, Gilead, Novo Nordisk, and Sanofi. M.T.J. is the chief executive officer of Steno Diabetes Center Copenhagen, a public hospital funded through a partnership between the Capital Region of Denmark and the Novo Nordisk Foundation. All other authors have declared no conflict of interest.","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}],"article-number":"35"}}