{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,16]],"date-time":"2026-06-16T03:43:48Z","timestamp":1781581428778,"version":"3.54.5"},"reference-count":41,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2025,5,19]],"date-time":"2025-05-19T00:00:00Z","timestamp":1747612800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2025,5,19]],"date-time":"2025-05-19T00:00:00Z","timestamp":1747612800000},"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":["Cathet Cardio Intervent"],"published-print":{"date-parts":[[2025,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>The association between lipoprotein(a) [Lp(a)] levels and progression of non\u2010culprit atherosclerosis (NSA) in patients with acute coronary syndrome (ACS) who underwent percutaneous coronary intervention (PCI) is unknown.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>This study enrolled 177 patients with ACS who underwent OCT\u2010guided PCI and follow\u2010up OCT examinations of non\u2010culprit lesions between 2013 and 2018. Lesion characteristics including fibrous tissue, calcium, lipid, and macrophage content were assessed using quantitative plaque analysis. High Lp(a) levels were defined as Lp(a)\u2009\u2265\u200930\u2009mg\/dL. The association between Lp(a) levels and NSA progression was investigated using linear effect models adjusted for clinical risk factors. A discordance analysis was also performed.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      At 1\u2010year follow\u2010up, individuals with Lp(a) levels\u2009\u2265\u200930\u2009mg\/dL had increased total atheroma volume and lipid component, and higher incidence of thin\u2010cap fibroatheroma (TCFA) (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.021;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.006;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.025, respectively). After adjusted, multivariable linear regression model revealed an association between Lp(a) and plaque progression in NSA (7.22 for each 1\u2009SD increase, 95% CI: 0.96\u201313.48;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.025) and increased lipid component (3.60 for each 1\u2009SD increase, 95% CI: 0.63\u20136.56;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.019). Discordance analyses showed that individuals with discordantly low Lp(a) levels had the lightest plaque progression and increase in lipid plaque burden (17.34 [10.22, 28.21] vs. 28.73 [14.88, 45.88] versus 25.73 [13.85, 45.70],\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.017).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Among patients with ACS, elevated Lp(a) levels were related to the progression of coronary plaques in non\u2010culprit lesions, including increased total atheroma volume and lipid component, and a higher prevalence of TCFA at follow\u2010up.<\/jats:p>\n                  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