Neointimal Hyperplasia

Atherosclerosis is a leading cause of morbidity and mortality globally. Currently, many procedures are performed by interventionists and vascular surgeons to treat atherosclerosis, such as balloon angioplasty with or without stenting, endarterectomy, or surgical bypass grafting. However, despite the benefits, these interventions fail from restenosis due to neointimal hyperplasia (NIH). In a normal vasculature, smooth muscle cells (SMC) are found in the tunica media, and they are quiescent with minimal turnover and contractile phenotype. Neointimal hyperplasia refers to post-intervention, pathological, vascular remodeling due to the proliferation and migration of vascular smooth muscle cells into the tunica intima layer, resulting in vascular wall thickening and the gradual loss of luminal patency which may lead to the return of vascular insufficiency symptoms. SMC in neointimal hyperplasia lose contractile phenotype, and they differentiate into secretory phenotype predominantly. These modified SMC secrete the growth factors, growth factor receptors, extracellular matrix, proteinases, and inflammatory mediators responsible for neointimal hyperplasia. Many vascular interventions put vessels at risk of injury, leading to restenosis due to activation of the inflammatory cascade and cellular recruitment. It is most evident in "in-stent restenosis" after the plain old balloon angioplasty (POBA) without stenting and percutaneous coronary intervention with bare-metal stenting. Metallic stents were necessary to counteract acute vascular recoil after POBA, but after serving this purpose, long-term in situ metallic platform injure the vascular wall and sets in chronic inflammation and hyperplasia of the vascular intimal layer. Other vascular manipulation also may result in vessel injury, leading to neointimal hyperplasia.

There are two types of neointimal hyperplasia.

1. Arterial neointimal hyperplasia secondary to arterial manipulation in endarterectomy or angioplasty.

2. Venous graft associated neointimal hyperplasia secondary to coronary artery bypass grafting or arteriovenous grafting/ fistula formation.