Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3720_Библиотеки_им_академика_М_И_Перельмана

Plaque rupture is defined by the presence of a disrupted thin fibrous cap with overlying thrombus and an underlying necrotic core. The underlying necrotic core in plaque rupture usually occupies >30% of the total plaque area [8e10] (Fig. 1.1A). The thin fibrous cap is made up of type I collagen with very few smooth muscle cells interspersed, but is infiltrated by varying numbers of macrophages and T lymphocytes. The mean fibrous cap thickness at the rupture site is 23  19 mm, and 95% of the fibrous caps are <64 mm [5]. The disrupted fibrous cap allows contact of flowing blood with the highly thrombogenic necrotic core. This blood allows large numbers of platelets to be activated and aggregate at the rupture site forming a white thrombus (Figs. 1.2 and 1.3). The thrombus may or may not lead to a complete obstruction of the coronary lumen. If there is obstruction and a side branch is present proximal to the obstruction site, the thrombus propagates to the side branch and consists of layers of fibrin (lines of Zahn) separated by red blood cells, classified as a red thrombus. Eventually, if the thrombus is not removed or crushed by angioplasty or thrombolysis, it will organize by infiltration of inflammatory cells, especially macrophages, releasing growth factors that attract endothelial cells and smooth muscle cells, which proliferate and deposit extracellular matrix consisting of proteoglycans and collagen, leading to or­ganization of the thrombus and chronic total occlusion of the coronary artery.