ABSTRACT
It has long been considered that restenosis following balloon angioplasty is the result of the formation of excessive neointima. More recently, both animal and human studies have shown that constrictive arterial remodeling is the major determinant of restenosis after balloon angioplasty, and it is responsible for up to 70% of late lumen loss. Arterial remodeling in this context means a structural change of the vessel wall, where reorganization of cells and matrix at sites of injury leads to decreased lumen diameter. At the heart of this remodeling process is the degradation of the extracellular matrix by a group of enzymes known as matrix metalloproteinases (MMPs), secreted predominately by vascular smooth muscle cells (VSMCs) but also macrophages and monocytes.
