Ticagrelor to Prevent Restenosis

Abstract

Neointimal proliferation after stent implantation remains a concern even if local delivery of various antimitotic drugs has led to a significant reduction in smooth cell proliferation and a subsequent reduction in the rate of target vessel revascularization. The prevention of arterial restenosis in those treated by percutaneous coronary intervention using such new-generation stents fails in approximately 10% of patients, contributing to recurrent ischemic events and new revascularization procedures. Thus far, the systemic approach with statins, pioglitazone, angiotensin-converting enzyme inhibitors, and various antiproliferative drugs has not been successful in further reducing in-stent stenosis, raising the question of whether the aim included the right targets. See accompanying article on page 2385 Histopathologic studies in humans have demonstrated that after coronary stent placement, thrombus formation and acute inflammation are followed by vascular smooth cell proliferation, resulting in neointimal growth and leading to restenosis.1,2 Platelets play a key role in early thrombus generation and in the late neointima formation that results from arterial injury, such as after percutaneous coronary intervention or as a consequence of vessel wall inflammation, as occurs with atherosclerosis. Indeed, once recruited to or in the proximity of the vessel wall and exposed to thrombin, collagen, or thromboxane A2, platelets may release or express a plethora of growth factors …