{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T21:10:26Z","timestamp":1789593026625,"version":"build-2803163510"},"reference-count":40,"publisher":"Springer Science and Business Media LLC","license":[{"start":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T00:00:00Z","timestamp":1789516800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"},{"start":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T00:00:00Z","timestamp":1789516800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"}],"funder":[{"name":"Centermed"},{"name":"eLab Laboratories"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Hepatol Int"],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Metabolic dysfunction\u2013associated steatotic liver disease (MASLD) and coronary artery disease (CAD) share common pathophysiologic pathways. However, the relationship between different stages of MASLD and distinct coronary atherosclerosis phenotypes remains unclear. We evaluated the association of hepatic steatosis and fibrosis with coronary artery disease outcomes using paired vibration-controlled transient elastography (VCTE) and coronary computed tomography angiography (CCTA).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>425 adults who underwent both VCTE and CCTA within a three-month interval were included. MASLD was defined as controlled attenuation parameter (CAP) \u2265248\u00a0dB\/m, and significant fibrosis was defined as Liver Stiffness Measurement (LSM) \u22658\u00a0kPa. Coronary outcomes were assessed according to Coronary Artery Disease Reporting and Data System guidance. The primary outcome was plaque presence; secondary outcomes included obstructive stenosis, calcified plaque, high segment involvement, and CAD severity. Multivariable logistic regression models were progressively adjusted for demographic, lifestyle, and cardiometabolic factors.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>MASLD was present in 47.3% of participants. Individuals with MASLD had a higher prevalence of overall plaque than those without (81.6% vs 60.7%, p&lt;0.001), whereas obstructive stenosis did not differ between groups. MASLD was independently associated with higher odds of overall plaque presence after full adjustment (OR 2.22, 95% CI 1.04\u20134.73; p=0.038). In exploratory analyses, MASLD did not increase the odds of obstructive stenosis, calcified plaque, or CAD severity. In contrast, 1\u00a0kPa increase in LSM was associated with higher odds of obstructive stenosis (OR 1.14, 95% CI 1.00\u20131.30) and calcified plaque (OR 1.18, 95% CI 1.04\u20131.34), but not CAD presence and severity.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>MASLD was independently associated with the presence of coronary atherosclerotic plaque. Exploratory analyses further suggested that greater liver stiffness may be associated with obstructive stenosis and calcified plaque, raising the possibility that more advanced liver disease relates to specific features of advanced coronary artery disease. Confirmation in larger prospective studies is warranted.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s12072-026-11147-8","type":"journal-article","created":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T20:44:28Z","timestamp":1789591468000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Coronary atherosclerosis across stages of metabolic dysfunction\u2013associated steatotic liver disease: a VCTE\u2013CCTA study"],"prefix":"10.1007","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0313-8673","authenticated-orcid":false,"given":"Gediz","family":"Dogay Us","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Francesco","family":"Innocenti","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ozgur Muhammet","family":"Koc","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sevval \u0130lke","family":"Ebeoglu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Baris","family":"Okcun","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"\u0130hsan Nuri","family":"Akpinar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melih Hulusi","family":"Us","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ger H.","family":"Koek","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,9,16]]},"reference":[{"issue":"11","key":"11147_CR1","doi-asserted-by":"publisher","first-page":"2462","DOI":"10.1016\/j.cgh.2021.09.021","volume":"20","author":"JZK Toh","year":"2022","unstructured":"Toh JZK, et al. 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