What is the pathophysiology of plaque rupture?

Updated: Dec 30, 2019
  • Author: Elena R Ladich, MD; Chief Editor: Allen Patrick Burke, MD  more...
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Answer

Answer

Plaque rupture is defined as a lesion consisting of a lipid-rich necrotic core with an overlying thin, ruptured, fibrous cap heavily infiltrated by macrophages and T lymphocytes (see the image below). Although the precise mechanisms of plaque rupture are poorly understood, most researchers agree that disruption of a fibrous cap rich in macrophages and T lymphocytes in addition to the necrotic core coming in contact with circulating blood are events that lead to the development of thrombi in fatal plaques. [6, 7]

Vulnerable plaque pathology. Gross photograph and Vulnerable plaque pathology. Gross photograph and composition of plaque rupture. A: Gross photograph of a coronary artery cut in cross-section showing the site of a plaque rupture (arrow) with an underlying necrotic core (NC) and luminal thrombus (Th). B: Histologic section of the artery seen in Image A showing rupture site, necrotic core, and luminal thrombus (Movat, ×20). C: High-power view of the area of the fibrous cap disruption (arrow) showing communication of the thrombus (Th) with the underlying necrotic core (NC) (×200). D: High-power view of the area of the fibrous cap showing a paucity of smooth muscle cells—actin (x 200). E and F: The fibrous cap is heavily infiltrated by macrophages and T-lymphocytes (CD68 and CD45Ro, respectively) (×200). G: Shows the strong expression of human leukocyte antigen (HLA)–DR antigens, particularly in macrophages and T-cells of the fibrous cap. (Farb et al, Circulation. 1996;93:1354-63, with permission)

Thrombosis occurs when platelets and inflammatory cells in the circulating blood come into contact with the thrombogenic necrotic core. Previously, the necrotic core was thought to be the major source of tissue factor. It is now believed that circulating monocytes as well as plaque macrophages support the development of acute thrombi in unstable coronary plaques. [8]

The incidence of plaque rupture varies with each decade of life, and the highest incidence of rupture is seen in the 40s in men, whereas in women the incidence increases beyond age 50 years. Plaque rupture is a more frequent cause of coronary thrombosis in men than in women, and there is a strong association with circulating total cholesterol. The incidence of rupture beyond 50 years is similar for both sexes.


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