ABSTRACT
Percutaneous coronary interventions (PCI) are the most common form of revascularization therapy for atherosclerotic coronary artery disease. Over 1.5 million PCI are performed annually in the USA. The major long-term limitation of PCI is restenosis, the recurrence of the treated blockage. Depending on the modality used and the lesion morphology treated, restenosis affects a substantial number of treated patients. The risk for restenosis is highest in patients with acute coronary syndromes, multivessel disease, and diabetes. The cellular and molecular changes that follow coronary intervention have been extensively characterized in animals and in humans.1,2 This chapter will describe what is currently known about the pathophysiology of restenosis associated with PCI. This continues to be an active area of research, focused on the identification of effective strategies to prevent or eliminate restenosis.
During balloon inflation in an atherosclerotic lesion, a combination of plaque displacement and vessel expansion result in lumen enlargement.3
Overdistention of the artery causes endothelial laceration, disruption of the internal elastic lamina, and tears of the medial layer. Stent placement compounds this acute injury by inflicting deeper tissue trauma. These insults provoke an immediate response by the vessel, which includes thrombosis, release of vasoactive agents, and inflammatory cell recruitment.4 As the acute response to injury abates, a chronic process of healing ensues, characterized by cell proliferation and remodeling of the vessel wall (Figure 2.1).
