ABSTRACT
Despite major technological advances in the past few decades, the frequency of restenosis still represents a vexing problem for the percutaneous approach to treating coronary artery disease. Unfavorable or negative vascular remodeling and neointimal hyperplasia represent the ultimate consequence of a puzzling healing process involving thrombosis, inflammation, cellular (smooth muscle cell and fibroblast) migration/proliferation and extracellular matrix formation/degradation. The ability of a given therapy to prevent both remodeling and intimal hyperplasia determines its potential to eradicate restenosis.
