RT Book, Section A1 Gould, K. Lance A1 Gewirtz, Henry A1 Narula, Jagat A2 Fuster, Valentin A2 Harrington, Robert A. A2 Narula, Jagat A2 Eapen, Zubin J. SR Print(0) ID 1191187602 T1 CORONARY BLOOD FLOW AND MYOCARDIAL ISCHEMIA T2 Hurst's The Heart, 14e YR 2017 FD 2017 PB McGraw-Hill Education PP New York, NY SN 9780071843249 LK accesscardiology.mhmedical.com/content.aspx?aid=1191187602 RD 2024/10/10 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.