FIGURE 2.

The pathophysiology of intimal hyperplasia. IH is triggered by endothelial injury, which activates platelets aggregation, and recruitment and activation of immune cells in the arterial wall (early inflammatory phase). The platelets and immune cells release cytokines, chemokines and growth factors, which stimulate a wound healing response mediated by SMC-like cells (mostly synthetic SMC derived from medial VSMC and myofibroblasts derived from adventitial fibroblasts). These synthetic SMC-like cells proliferate and migrate under the internal elastic lamina (IEL), forming the neointima layer. Long after inflammation is resolved and the endothelium is repaired (chronic phase), these cells continue to secrete extracellular matrix (ECM), leading to the progressive narrowing of the lumen.