Journal
NATURE CLINICAL PRACTICE CARDIOVASCULAR MEDICINE
Volume 4, Issue 9, Pages 491-502Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncpcardio0979
Keywords
angiogenesis; atherosclerosis; cancer; hemorrhage; vascular normalization
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Funding
- NCI NIH HHS [P01 CA080124] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [P01CA080124] Funding Source: NIH RePORTER
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Angiogenesis within human atherosclerotic plaques has an important role in plaque progression as immature blood vessels leak red blood cells and inflammatory mediators into the plaque center. Accumulation of free cholesterol from red blood cell membranes potentially increases the size of the necrotic core and triggers a chain of events that promote plaque destabilization. Antiangiogenic agents have been shown to prune some tumor vessels and 'normalize' the structure and function of the remaining vasculature, thereby improving the access of chemotherapeutic agents to tumors. We propose that antiangiogenic therapy can similarly stabilize vulnerable 'rupture-prone' plaques by pruning and normalizing immature intraplaque vessels, preventing further intraplaque hemorrhage. This normalization would limit necrotic core enlargement, further luminal narrowing and the degree of inflammation. Such normalization has been realized using vascular endothelial growth factor antagonists for the treatment of cancer and age-related macular degeneration. The development of this novel approach to prevent plaque progression might add to the armamentarium of preventive measures for acute myocardial infarction, stroke and sudden cardiac death.
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