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Percutaneous transluminal coronary angioplasty (PTCA) has become the treatment of choice for severe cases of coronary artery atherosclerosis, and currently, >1 million PTCA interventions are performed each year worldwide.1 However, despite its overall value in achieving an immediate increase in lumen diameter, PTCA often triggers local arterial renarrowing (restenosis). This occurs in 20% to 50% of cases within 3 to 6 months and represents a major clinical and economic problem.2 Although several drugs have been shown capable of preventing or reducing the proliferative healing response after arterial injury in experimental animal models, only stenting has proved effective in reducing postinterventional restenosis in humans.3 Prevention of restenosis is therefore a major challenge, which highlights the need to better understand the interplay of the various components responsible for restenotic lesions.Arterial restenosis after balloon angioplasty is a complex and multifactorial wound healing process that involves several redundant and overlapping mechanisms. Schematically, one distinguishes 4 interrelated issues.4 5 First, a vessel wall “ elastic recoil ” (vasoconstriction due to endothelial disruption) occurs, which tends to present within 24 hours of PTCA and which may be of predictive value for subsequent restenosis. Second, a mural thrombus forms, which occurs within 2 to 3 weeks and involves local platelet activation and thrombin secretion; an increase in smooth muscle cell activation, proliferation, and migration; and leukocyte recruitment at the site of balloon injury. This complex process then induces neointimal hyperplasia. Already beginning 48 hours after balloon injury, …

Toward New Therapeutic Strategies Against Neointimal Formation in Restenosis