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FOCUS ISSUE: PLAQUE NEOVASCULARIZATION, HEMORRHAGE, AND VULNERABILITY: STATE-OF-THE-ART PAPER

Plaque Neovascularization and Antiangiogenic Therapy for Atherosclerosis

Brendan Doyle, MD^_* and Noel Caplice, MD, PhD^,_*

^_* Division of Cardiovascular Diseases, Molecular Medicine Program, Mayo Clinic, Rochester, Minnesota
Centre for Research in Vascular Biology, Biosciences Institute, University College Cork, Cork, Ireland

Manuscript received May 24, 2006; revised manuscript received December 12, 2006, accepted January 18, 2007.

^_* Reprint requests and correspondence: Dr. Noel Caplice, Centre for Research in Vascular Biology, Biosciences Institute, University College Cork, Co. Cork, Ireland. (Email: n.caplice{at}ucc.ie).

The concept that neovascularization of the vessel wall may play a fundamental role in the pathophysiology of atherosclerosis was proposed more than a century ago. In recent years, supportive experimental evidence for this hypothesis (such as the finding that neointimal microvessels may increase delivery of cellular and soluble lesion components to the vessel wall) has been underscored by clinical studies associating plaque angiogenesis with more rapidly progressive high-grade disease. Attention has also focused on a possible role for microvessel-derived intraplaque hemorrhage in the development of acute lesion instability. The interest of clinicians in this phenomenon has been spurred by the potential to target vessel wall neovascularization with angiogenesis inhibitors, a therapeutic approach that has been associated with impressive reductions in plaque progression in animal models of vascular disease. The rationale for pursuing an "antiangiogenic" strategy in the treatment of patients with vascular disease, and a framework for further preclinical evaluation of such therapy, is presented here.

Abbreviations and Acronyms   HIF = hypoxia inducible factor   VEGF = vascular endothelial growth factor

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