ABSTRACT
Since the late 1970s percutaneous transluminal coronary angioplasty (PTCA) has found widespread application in the therapy of coronary artery stenosis. Although the immediate success rate of PTCA has increased to more than 95%, long-term success remains limited by significant renarrowing of the artery (restenosis) in 20-50% of patients within 6 months of intervention. Finding effective therapies to combat restenosis has been difficult.1-3 At first, research was focused on inhibition of intimal thickening, often referred to as neointima formation. Commonly studied models involve gentle withdrawal of an inflated low pressure Fogarty balloon along normal rat carotid or rabbit femoral arteries to create a modest injury of smooth muscle cells (SMCs) in the media.4 The SMCs start to proliferate and migrate to the intima, where cell division continues and matrix components are deposited. This healing process leads to formation of a neointima that replaces the original intima consisting solely of a monolayer of endothelial cells.
