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Accelerated atherogenesis in these diseases is driven by persistent systemic inflammation, autoantibody-mediated endothelial injury, oxidative stress, and dysregulated lipid metabolism, resulting in premature vascular remodeling manifested by increased carotid intima\u2013media thickness, arterial stiffness, impaired flow-mediated dilation, and coronary artery calcification. This review synthesizes evidence regarding subclinical atherosclerosis and cardiometabolic risk across common RDs. In rheumatoid arthritis and systemic lupus erythematosus, vascular alterations correlate with inflammatory burden, disease duration, autoantibody profiles, renal involvement, and glucocorticoid exposure. Emerging biomarkers\u2014including apolipoprotein B48, FIB-4 index, asymmetric dimethylarginine, and adhesion molecules\u2014provide incremental prognostic value beyond traditional lipid parameters. Advanced imaging modalities, such as ^18F-sodium fluoride PET\/CT and vascular elastography, enhance early detection of arterial calcification and stiffness. Growing evidence in primary Sj\u00f6gren syndrome, Beh\u00e7et disease, systemic sclerosis, and ankylosing spondylitis similarly confirms increased subclinical atherosclerosis and endothelial dysfunction. Importantly, tight disease control and targeted immunomodulatory therapies\u2014including methotrexate, biologic agents, antimalarials, and cytokine-directed treatments\u2014are associated with improved vascular and metabolic profiles and attenuation of disease progression. Subclinical atherosclerosis represents a critical interface between autoimmunity and cardiovascular disease in RDs. Early vascular assessment integrated with disease-specific and metabolic risk stratification is essential to implement precision-based cardiovascular prevention in this high-risk population.<\/jats:p>","DOI":"10.1007\/s00296-026-06129-w","type":"journal-article","created":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T14:29:09Z","timestamp":1779200949000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Cardiometabolic risk and vascular changes in rheumatic diseases"],"prefix":"10.1007","volume":"46","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5042-1191","authenticated-orcid":false,"given":"Yuliya","family":"Fedorchenko","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0004-6967-4641","authenticated-orcid":false,"given":"Umida","family":"Khojakulova","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1229-2042","authenticated-orcid":false,"given":"Bekzhan A.","family":"Permenov","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9564-791X","authenticated-orcid":false,"given":"Mykhailo","family":"Fedorchenko","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2754-1232","authenticated-orcid":false,"given":"Ahmet","family":"Usen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,5,19]]},"reference":[{"issue":"1","key":"6129_CR1","doi-asserted-by":"publisher","first-page":"25","DOI":"10.1038\/nrrheum.2016.192","volume":"13","author":"F Navid","year":"2017","unstructured":"Navid F, Colbert RA (2017) Causes and consequences of endoplasmic reticulum stress in rheumatic disease. 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