TY - CHAP M1 - Book, Section TI - Atherothrombosis: Disease Initiation, Progression, and Treatment A1 - Mohler, Emile R. A1 - Schafer, Andrew I. A2 - Kaushansky, Kenneth A2 - Lichtman, Marshall A. A2 - Prchal, Josef T. A2 - Levi, Marcel M. A2 - Press, Oliver W. A2 - Burns, Linda J. A2 - Caligiuri, Michael PY - 2015 T2 - Williams Hematology, 9e AB - SUMMARYThe consequences of atherosclerotic vascular disease are the leading cause of morbidity and mortality in the developed countries of the world and are rapidly approaching that status in the developing world. This chapter reviews the pathologic mechanisms of atherosclerotic disease development and progression, and details the interaction of these processes with the coagulation system. The earliest morphologically visible lesion of arterial atherosclerosis, the fatty streak, already is an advanced metabolic and immunologic locus that manifests as abnormalities of vascular tone, inflammation, cellular growth, and endothelial cell dysfunction. After years to decades, the lesions advance to form plaques that grow and eventually either impinge on the arterial lumen or rupture. Rupture of a vulnerable plaque is a catastrophic event that, through activation of both platelets and the coagulation cascade, triggers thrombosis, which leads to complete occlusion, and unless collateral circulation has already been established, results in tissue ischemia. Based on an increased understanding of the pathogenesis and consequences of atheromatous plaque development and progression, medical management of atherothrombotic syndromes has improved and is reviewed for the coronary, cerebrovascular, and peripheral arteries. SN - PB - McGraw-Hill Education CY - New York, NY Y2 - 2024/11/08 UR - hemonc.mhmedical.com/content.aspx?aid=1121105346 ER -