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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2009;29:439.)
© 2009 American Heart Association, Inc.

Editorials

VEGF and Restenosis

The Rest of the Story

Michael Simons

From the Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, Conn.

Correspondence to Michael Simons, Section of Cardiovascular Medicine, Yale University School of Medicine, 333 Cedar Street, P.O. Box 208017, New Haven, CT 06520-8017. E-mail michael.simons@yale.edu

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

The challenge of restenosis has been with us since the dawn of intravascular percutaneous interventions. Much effort has been spent on developing strategies designed to effectively treat it. These ranged from mechanical means such as minimal plaque removal with an idea of not "disturbing" the media (directional atherectomy), to extensive debulking (rotational atherectomy), to creating the largest possible lumen and then preventing the recoil (stenting), to systemic and local use of numerous drug classes including antithrombotic, antiplatelet, antiproliferative drugs, calcium channel blockers, statins, steroids, and other antiinflammatory agents among the others.

See accompanying article on page 458

While most of these failed, as frequently happens in medicine, the effective therapy was arrived at much earlier than any glimmer of understanding of the biology of the process that was treated became apparent. Bare metal stents offered a major reduction in restenosis, largely by preventing arterial recoil despite a markedly increased stress on the media and unappreciated at the time damage to the adventitia. Interestingly, whereas angiographically defined restenosis was substantially reduced, intimal proliferation was actually increased,¹ emphasizing that bare metal stenting was a purely mechanical means for dealing with the problem and that the fundamental biology was not affected. The first truly significant reduction in intimal formation was achieved using drug eluting stents with either paclitaxel- or sirolimus-like compounds. The effect was ascribed to their antiproliferative effect on smooth muscle cells (SMC) even though multiple other antiproliferative drugs showed no comparable activity, suggesting there was something special about these 2 classes . . . [Full Text of this Article]

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