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=== Atherosclerosis === {{main|Atherosclerosis}} Atherosclerosis, formerly considered a [[lipid]] storage disorder, is now understood as a chronic inflammatory condition involving the arterial walls.<ref name="libby2021">{{cite journal |vauthors=Libby P |title=Inflammation during the life cycle of the atherosclerotic plaque |journal=Cardiovascular Research |volume=117 |issue=13 |pages=2525β2536 |date=November 2021 |pmid=34550337 |pmc=8783385 |doi=10.1093/cvr/cvab303}}</ref> Research has established a fundamental role for inflammation in mediating all stages of atherosclerosis from initiation through progression and, ultimately, the thrombotic complications from it.<ref name=libby2021/> These new findings reveal links between traditional risk factors like cholesterol levels and the underlying mechanisms of [[atherogenesis]]. Clinical studies have shown that this emerging biology of inflammation in atherosclerosis applies directly to people.<ref name="libby2021" /> For instance, elevation in markers of inflammation predicts outcomes of people with [[acute coronary syndrome]]s, independently of myocardial damage. In addition, low-grade chronic inflammation, as indicated by levels of the inflammatory marker [[C-reactive protein]], prospectively defines risk of atherosclerotic complications, thus adding to prognostic information provided by traditional risk factors, such as LDL levels.<ref>{{cite journal | vauthors = Spagnoli LG, Bonanno E, Sangiorgi G, Mauriello A | title = Role of inflammation in atherosclerosis | journal = Journal of Nuclear Medicine | volume = 48 | issue = 11 | pages = 1800β1815 | date = November 2007 | pmid = 17942804 | doi = 10.2967/jnumed.107.038661 }}</ref><ref name=libby2021/> Moreover, certain treatments that reduce coronary risk also limit inflammation. Notably, lipid-lowering medications such as [[statin]]s have shown anti-inflammatory effects, which may contribute to their efficacy beyond just lowering LDL levels.<ref>{{cite journal | vauthors = Morofuji Y, Nakagawa S, Ujifuku K, Fujimoto T, Otsuka K, Niwa M, Tsutsumi K | title = Beyond Lipid-Lowering: Effects of Statins on Cardiovascular and Cerebrovascular Diseases and Cancer | journal = Pharmaceuticals | volume = 15 | issue = 2 | pages = 151 | date = January 2022 | pmid = 35215263 | pmc = 8877351 | doi = 10.3390/ph15020151 | doi-access = free }}</ref> This emerging understanding of inflammation's role in atherosclerosis has had significant clinical implications, influencing both risk stratification and therapeutic strategies. ==== Emerging treatments ==== Recent developments in the treatment of atherosclerosis have focused on addressing inflammation directly. New anti-inflammatory drugs, such as monoclonal antibodies targeting IL-1Ξ², have been studied in large clinical trials, showing promising results in reducing cardiovascular events.<ref>{{cite journal | vauthors = Szekely Y, Arbel Y | title = A Review of Interleukin-1 in Heart Disease: Where Do We Stand Today? | journal = Cardiology and Therapy | volume = 7 | issue = 1 | pages = 25β44 | date = June 2018 | pmid = 29417406 | pmc = 5986669 | doi = 10.1007/s40119-018-0104-3 }}</ref> These drugs offer a potential new avenue for treatment, particularly for patients who do not respond adequately to statins. However, concerns about long-term safety and cost remain significant barriers to widespread adoption. ==== Connection to depression ==== Inflammatory processes can be triggered by negative cognition or their consequences, such as stress, violence, or deprivation. Negative cognition may therefore contribute to inflammation, which in turn can lead to depression. A 2019 meta-analysis found that chronic inflammation is associated with a 30% increased risk of developing [[major depressive disorder]], supporting the link between inflammation and [[mental health]].<ref>{{cite journal | vauthors = Osimo EF, Pillinger T, Rodriguez IM, Khandaker GM, Pariante CM, Howes OD | title = Inflammatory markers in depression: A meta-analysis of mean differences and variability in 5,166 patients and 5,083 controls | journal = Brain, Behavior, and Immunity | volume = 87 | pages = 901β909 | date = July 2020 | pmid = 32113908 | pmc = 7327519 | doi = 10.1016/j.bbi.2020.02.010 }}</ref>
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