Neointimal hyperplasia

Neointimal Hyperplasia is the body's response to vascular injury, characterized by the proliferation and migration of smooth muscle cells (SMCs) from the tunica media to the intima, leading to the thickening of the vascular wall. This process is a common pathological mechanism underlying various vascular diseases, including restenosis following percutaneous coronary interventions, such as angioplasty and stent placement, as well as in vascular grafts and arteriovenous fistulas used for hemodialysis.

Etiology

Neointimal hyperplasia is primarily triggered by endothelial injury. The disruption of the endothelial layer exposes the underlying SMCs to factors that promote their proliferation and migration. These factors include platelet-derived growth factor (PDGF), fibroblast growth factor (FGF), and transforming growth factor-beta (TGF-β). Mechanical stress, such as that caused by blood flow disturbance and hypertension, also contributes to the development of neointimal hyperplasia.

Pathophysiology

Following vascular injury, the endothelial layer is compromised, leading to platelet adhesion and the release of growth factors that stimulate SMC proliferation and migration. SMCs migrate from the media to the intima, where they proliferate and secrete extracellular matrix proteins, leading to intimal thickening. This process not only narrows the vascular lumen but also alters vascular reactivity, contributing to the progression of vascular diseases.

Clinical Significance

Neointimal hyperplasia is a significant cause of morbidity in patients undergoing vascular interventions. In coronary arteries, it can lead to restenosis, a condition where the artery narrows again after treatment. In peripheral arteries, it can cause graft failure in bypass surgeries. In arteriovenous fistulas, it can lead to stenosis, affecting hemodialysis efficacy.

Prevention and Treatment

Current strategies to prevent and treat neointimal hyperplasia focus on minimizing vascular injury during interventions, using drug-eluting stents that release antiproliferative agents, and pharmacological treatments targeting the molecular pathways involved in SMC proliferation and migration. Research is ongoing to develop more effective therapies, including gene therapy and regenerative medicine approaches.

See Also

• Vascular disease
• Restenosis
• Percutaneous coronary intervention
• Angioplasty
• Stent
• Vascular graft
• Arteriovenous fistula
• Hemodialysis

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