TY - CHAP M1 - Book, Section TI - Inflammation and Atherosclerosis A1 - Siddiqi, Hasan K. A1 - Ridker, Paul M A2 - Fuster, Valentin A2 - Narula, Jagat A2 - Vaishnava, Prashant A2 - Leon, Martin B. A2 - Callans, David J. A2 - Rumsfeld, John A2 - Poppas, Athena Y1 - 2022 N1 - T2 - Fuster and Hurst's The Heart, 15e AB - Chapter SummaryThis chapter discusses the role of inflammation in the development of atherosclerotic disease, with lessons from basic science and clinical studies informing future strategies for prevention and treatment. Historically considered a disease driven by dyslipidemia, the central role of inflammation in atherosclerosis has been elucidated in recent years with the concept of residual inflammatory risk as an important contributor to atherosclerotic disease. Various stimuli and insults converge on the immune system leading to activation of multiple immune effectors, including the innate and adaptive immune system, that have key roles in the development of atherosclerosis (see Fuster and Hurst’s Central Illustration). The use of biomarkers and inflammatory intermediaries including C-reactive protein (CRP), interleukin (IL)-1, and IL-6 for risk stratification and mechanistic elucidation is of key interest. Recent therapies targeting inflammatory pathways, including the NLRP3 inflammasome and IL-1 pathway, have shown promise in reducing this residual inflammatory risk for atherosclerosis in high-risk populations, with positive results seen in multiple large clinical trials. In addition, public health efforts to improve nutrition, reduce obesity, and combat environmental pollution will play a role in reducing the inflammatory contribution to atherosclerosis. SN - PB - McGraw-Hill Education CY - New York, NY Y2 - 2022/05/20 UR - accesscardiology.mhmedical.com/content.aspx?aid=1191371087 ER -