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This substantially reduces the lifetime risk of atherosclerotic cardiovascular disease (ASCVD) events.\u00a0In this context, plaque development and vulnerability result not only from lipid accumulation but also from inflammation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Changes in the composition of immune cells, including macrophages, dendritic cells, T cells, B cells, mast cells and neutrophils, along with altered cytokine and chemokine release, disrupt the equilibrium between inflammation and anti\u2010inflammatory mechanisms at plaque sites. Considering that it is not a competition between LDLc and inflammation, but instead that they are partners in crime, the present narrative review aims to give an overview of the main inflammatory molecular pathways linked to raised LDLc concentrations and to describe the impact of lipid\u2010lowering approaches on the inflammatory and lipid burden. Although remarkable changes in LDLc are driven by the most recent lipid lowering combinations, the relative reduction in plasma C\u2010reactive protein appears to be independent of the magnitude of LDLc lowering.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Identifying clinical biomarkers of inflammation (e.g. interleukin\u20106) and possible targets for therapy holds promise for monitoring and reducing the ASCVD burden in suitable patients.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/eci.14326","type":"journal-article","created":{"date-parts":[[2024,10,7]],"date-time":"2024-10-07T00:07:55Z","timestamp":1728259675000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":24,"title":["Hypercholesterolemia and inflammation\u2014Cooperative cardiovascular risk 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