Neovascularization and Plaque Rupture: A Key Link in Acute Stroke

Acute stroke events often result from the rupture of vulnerable plaques, which release embolic materials and cause blood clots to form. Plaque rupture is the most common complication of plaques, and vulnerable plaques are those that have a high risk of rupture and thrombosis formation. Neovascularization within plaques has been found to be closely linked to plaque rupture and clinical symptoms.

The histopathological characteristics of vulnerable plaques include active inflammation, a large lipid core, a thin fibrous cap, and intraplaque hemorrhage. Studies have shown that the area of increased neovascularization within plaques is the primary site of the inflammatory response. CEUS also indicates that the grading of neovascularization within the plaque is positively correlated with the size of the macrophage infiltration area. These findings suggest that neovascularization within plaques is associated with inflammatory reactions.

Some studies propose that inflammatory cells promote the formation of neovessels within plaques, which in turn induce blood flow. However, these neovessels are also vulnerable to damage from cytotoxic substances produced within the plaque, thereby promoting plaque rupture.