Intimal hyperplasia is not a true disease, but a physiologic healing response to injury to the blood vessel wall. It is the bane of endovascular intervention and vascular surgery.
When the endothelium is injured, endothelial cells release inflammatory mediators that trigger platelet aggregation, fibrin deposition and recruitment of leukocytes to the area. These cells express growth factors that promote smooth muscle cells migration from the media to the intima. The smooth muscle cells proliferate in the intima and deposit extracellular matrix, in a process analogous to scar formation. This typically occurs over a period of a few months.
The result is formation of a neo-intima over the site of injury. An exuberant healing response leads to intimal hyperplasia (thickening) that encroaches on the vessel lumen and causes stenosis. This process is analogous to keloid formation in epithelial wounds. It seems to be accelerated by the presence of prosthetic material in the vessel.
Intimal hyperplasia may result from endovascular intervention, vascular surgical procedures, long term vascular catheters and devices, or turbulent flow. It is not infrequently seen after angioplasty, stent insertion, around long term venous catheters, and at surgical vascular and graft anastomoses. Re-stenosis occurring 3 to 12 months after angioplasty is typically due to intimal hyperplasia.
Intimal hyperplasia can be minimised by limiting the extent of endothelial injury; such as minimising trauma to adjacent normal vessel during angioplasty and the judicious use of stents and prosthetic devices.
Stenosis from intimal hyperplasia is often difficult to treat. Unlike soft atheromatous plaques, these stenoses are firm and require prolonged high inflation pressures to dilate with a balloon. The stenoses often recur; repeated dilatation causes repeated intimal injury and perpetuates the intimal healing response.
A stent may be inserted to hold the stenosis open but this is also not without issues. The stent itself will stimulate further intimal hyperplasia. The hyperplastic intimal tissue can grow through the interstices of a bare stent and re-stenose the vessel. A covered stent will prevent this from happening but intimal hyperplasia can still occur at the ends of the stent where there is most irritation of the vessel wall.
A number of strategies are under investigation to reduce intimal hyperplasia. These include coating of angioplasty balloons, drug-eluting stents, intravascular brachytherapy, systemic low-dose low molecular weight heparin, and systemic low-dose warfarin.
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