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Is interleukin-1 beta a triggering factor for restenosis?

Cardiovascular Research , Volume 44 (1): 17 – Oct 1, 1999


Oxford University Press
Copyright © 2010 European Society of Cardiology
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Is interleukin-1 beta a triggering factor for restenosis?


Is interleukin-1 beta a triggering factor for restenosis? See article by Chamberlain et al. 9 (pages 156–165) in this issue. Today, more than 20 years after percutaneous transluminal coronary angioplasty (PTCA) was introduced into the clinic by Andreas Grüntzig 1 , PTCA has become a well-established and routine procedure for myocardial revascularization of patients with coronary heart disease (CHD). However, restenosis occurs in these patients at a rate between 30 and 50%, despite a successful initial procedure (for an extensive reviews see Refs. 2–5 ). More than 60 large-scale clinical trials later, we are still struggling to understand why restenosis occurs in some but not in others, and why after 20 years the rate of restenosis is virtually unchanged, despite the availability of modern therapeutics and extensive knowledge in vascular biology 6–8 . The paper presented in this issue 9 intriguingly puts interleukin-1β (IL-1β) onto center stage as a possible triggering factor in the initiation process of restenosis, and may provide us with a handle for successful therapeutic intervention. According to current concepts, three processes (phases) have been postulated to lead to post PTCA restenosis in patients 10 . Phase I is the acute lumen loss which occurs in some patients, and is termed elastic ‘recoil’. Recoil develops within hours of the intervention and appears to be the consequence of overstretching. Phase II is the mural thrombus formation which results from endothelium removal, and the exposure of deep vascular structures and induction of procoagulant factors. These thrombi are rich in cytokines and growth factors, including interleukin-1β, platelet-derived growth factor (PDGF), and transforming growth factor-β (TGF-β) 11 . Finally, … Full Text of this Article * Tel.: +1-203-401-3330, ext. 325; fax: +1-203-401-3337
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