TY - CHAP M1 - Book, Section TI - ATHEROTHROMBOSIS: DISEASE BURDEN, ACTIVITY, AND VULNERABILITY A1 - Falk, Erling A1 - Fuster, Valentin A2 - Fuster, Valentin A2 - Harrington, Robert A. A2 - Narula, Jagat A2 - Eapen, Zubin J. PY - 2017 T2 - Hurst's The Heart, 14e AB - SummaryThis chapter discusses the pathophysiological development of atherothrombosis. Atherothrombosis is the chronic, lipid-driven, multifocal inflammatory process of atherosclerotic plaque development (see accompanying Hurst’s Central Illustration) and subsequent thrombosis. Individual susceptibility to well-known risk factors for atherothrombosis varies considerable, and better detection of at-risk individuals may be achieved by visualizing the arterial wall. Plaques are very heterogeneous in size and composition. Many plaques remain asymptomatic, some become obstructive, and a few, if any, become vulnerable to plaque rupture or erosion. The major determinants of plaque vulnerability seem to be the size of the necrotic core and the thickness of the fibrous cap. However, because of the complexity of the processes leading to plaque vulnerability and susceptibility to thrombosis, trying to predict the fate and clinical impact of a particular plaque may be futile. Combining knowledge of risk factors and detection of overall disease burden, and treating patients who are at highest risk, may be the best strategy for this systemic disease. Inflammatory activity is present in most, or all, atherosclerotic lesions within the body and might therefore be a useful marker of systemic disease activity. Additionally, focal calcifications are very common in atherosclerotic plaques, and the total amount of coronary artery calcium correlates strongly with plaque burden and is a strong predictor of coronary events. SN - PB - McGraw-Hill Education CY - New York, NY Y2 - 2024/04/20 UR - accessmedicine.mhmedical.com/content.aspx?aid=1191187295 ER -