neointima

Neointima is a new, thickened intimal layer that forms within arteries or veins after vascular injury, surgery, or device implantation. It primarily arises from vascular smooth muscle cells that proliferate and migrate from the media into the intima, accompanied by deposition of extracellular matrix. The neointimal response can be observed after procedures such as angioplasty, stenting, or bypass grafting and is distinct from primary atherosclerotic plaque formation.

Mechanistically, endothelial denudation exposes subendothelial structures and initiates a cascade of growth factors and cytokines (for example PDGF, TGF-β, and FGF) that stimulate smooth muscle cells to switch from a contractile to a synthetic phenotype. Migratory SMCs proliferate within the intima and produce collagen and proteoglycans, sometimes with inflammatory cells and new microvessels contributing to the matrix. The resulting hyperplastic intima narrows the vessel lumen.

Clinical relevance: Neointimal hyperplasia is the principal cause of restenosis after percutaneous coronary interventions and can limit long-term graft patency. In-stent restenosis is more common with bare-metal stents, while drug-eluting stents release antiproliferative agents to reduce neointimal growth and improve lumen size.

Diagnosis and management: Neointimal formation is typically assessed with intravascular imaging modalities such as intravascular ultrasound or optical coherence tomography and histology in research. Treatment of restenosis may involve repeat angioplasty, atherectomy, or surgical revision. Prevention focuses on lipid lowering, antiplatelet therapy, optimized device selection, and use of antiproliferative drug-eluting devices when appropriate.