TY - CHAP M1 - Book, Section TI - CORONARY BLOOD FLOW AND MYOCARDIAL ISCHEMIA A1 - Gould, K. Lance A1 - Gewirtz, Henry A1 - Narula, Jagat 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 pathophysiology of coronary thrombus formation (see accompanying Hurst’s Central Illustration), which constitutes the basis of acute coronary events. The luminal thrombus in up to three fourths of cases may be secondary to plaque rupture, and in the remaining cases it may result from plaque erosion; very infrequently calcific nodules may induce luminal thrombosis. Upon plaque rupture, components of deeper layers of the plaque are exposed to the circulating blood, which leads to marked platelet aggregation. The nature of the substrate exposed after plaque rupture likely determines whether a nonocclusive mural thrombus persists or whether the thrombus progresses to become occlusive. Indeed, the atheromatous core of a plaque is substantially more active than other substrates at triggering thrombosis and, therefore, ruptured plaques with large atheromatous core are at high risk of leading to acute coronary syndromes. The local geometry at the site of damage (degree of stenosis) and local hemodynamic conditions, as well as the presence of circulating systemic factors, also influence the mechanisms of thrombus formation. SN - PB - McGraw-Hill Education CY - New York, NY Y2 - 2024/10/10 UR - accesscardiology.mhmedical.com/content.aspx?aid=1191187602 ER -