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(Circulation. 2002;105:2932.)
© 2002 American Heart Association, Inc.

Editorial

What Is "The Matter" With Restenosis in 2002?

J. Eduardo Sousa, MD, PhD; Marco A. Costa, MD, PhD; Amanda G.M.R. Sousa, MD, PhD

From the Institute Dante Pazzanese of Cardiology (J.E.S., A.G.M.R.S.), São Paulo, Brazil; and the University of Florida-Shands (M.A.C.), Jacksonville, Fla.

Correspondence to Prof J. Eduardo Sousa, MD, PhD, Director of the Institute Dante Pazzanese of Cardiology, Av. Dr Dante Pazzanese, 500 - Ibirapuera 04012180, São Paulo, SP, Brazil. E-mail jesousa@uol.com.br

Key Words: Editorials • restenosis • stents

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Undoubtedly, we have come a long way since the introduction of intracoronary stents, but restenosis continues to plague cardiologists. Much research has been devoted to the pathophysiology and treatment of in-stent restenosis. However, we still do not yet fully understand the "matter" of restenosis, and it is possible that we never will. The detailed pathological investigation by Farb et al¹ published in this issue of Circulation elegantly portrays a putative novel mechanism related to the initiation of restenosis.

See p 2974

Farb and colleagues¹ previously described recognized mechanisms of in-stent restenosis,² disruption of the internal elastic lamina, and protrusion of stent struts into lipid-laden portions of the plaque, as well as the presence of neovascularization in the neointima, which had not previously been defined. Peri-strut neoangiogenesis was weakly correlated with mean in-stent neointimal thickness but was strongly correlated with inflammation. Because the time course of neovascularization and neointimal hyperplasia is unknown, a causal relationship between the development of new blood vessels and clinical restenosis cannot be firmly established. In addition, angiogenic properties of vascular endothelial growth factors may have the dual role of inhibiting the formation of intimal hyperplasia³ and promoting its growth.⁴

The findings of Farb et al¹ challenge the clinical paradigm that "bigger is better" in percutaneous coronary interventions, in which a larger lumen after angioplasty diminishes angiographic and clinical restenosis.⁵ The "bigger is better" adage may also reflect a rather simple, but still important, aspect of the pathophysiology of restenosis, which is the idea of "the bigger . . . [Full Text of this Article]

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