Neovascularization in Vulnerable Plaques: A Key Driver of Stroke Risk

Acute stroke events are frequently caused by vulnerable plaques that rupture, releasing embolic materials and leading to the formation of blood clots. Plaque rupture is the most common complication of plaque, and vulnerable plaques are those that have a risk of rupture and thrombosis formation. Neovascularization within plaques has been shown to be closely related to plaque rupture and clinical symptoms. The histopathological features of vulnerable plaques include active inflammation, a large lipid core, a thin fibrous cap, and intraplaque hemorrhage. Research has demonstrated that the area of increased neovascularization within plaques is the main 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 studies 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 susceptible to damage from cytotoxic substances produced within the plaque, thereby promoting plaque rupture.