The global burden of atherosclerotic cardiovascular disease has risen from 271 million people in 1990 to more than 600 million people in 2023. Atherosclerotic vascular disease results not only from lipid accumulation within the arterial walls but also from acute and chronic inflammatory changes in response to arterial endothelial injury. Inflammation together with cytokines, chemokines, and acute-phase reactants play a pivotal role in atherosclerotic vascular plaque formation, progression, rupture, and thrombogenesis that lead to an acute coronary syndrome (ACS) or stroke. In addition, individuals who have previously sustained an ACS frequently have evidence of residual arterial inflammation as indicated by increased blood concentrations of the inflammatory biomarker C-reactive protein (CRP). As a consequence, chronic arterial inflammatory disease contributes to more than 15% of all global deaths from myocardial infarction, cerebral vascular events (transient ischemic attacks or strokes), and peripheral vascular disease. This Review Article discusses the important mechanisms by which inflammation contributes to the initiation and progression of coronary artery atherosclerosis, the biologic measurements which indicate arterial inflammation in individuals, the diagnostic techniques useful in the detection of arterial inflammation and atherosclerosis, and the clinical studies that have been performed and are currently being performed to limit the contributions of acute and chronic inflammation to the morbidity and mortality from coronary artery atherosclerosis.
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