Journal article
Atherosclerotic Plaque Progression and Vulnerability to Rupture: Angiogenesis as a Source of Intraplaque Hemorrhage
Arteriosclerosis, thrombosis, and vascular biology, v 25(10), pp 2054-2061
Oct 2005
PMID: 16037567
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
Observational studies of necrotic core progression identify intraplaque hemorrhage as a critical factor in atherosclerotic plaque growth and destabilization. The rapid accumulation of erythrocyte membranes causes an abrupt change in plaque substrate characterized by increased free cholesterol within the lipid core and excessive macrophage infiltration. Neoangiogenesis is associated closely with plaque progression, and microvascular incompetence is a likely source of intraplaque hemorrhage. Intimal neovascularization is predominantly thought to arise from the adventitia, where there are a plethora of pre-existing vasa vasorum. In lesions that have early necrotic cores, the majority of vessels invading from the adventitia occur at specific sites of medial wall disruption. A breech in the medial wall likely facilitates the rapid in-growth of microvessels from the adventitia, and exposure to an atherosclerotic environment stimulates abnormal vascular development characterized by disorganized branching and immature endothelial tubes with “leaky” imperfect linings. This network of immature blood vessels is a viable source of intraplaque hemorrhage providing erythrocyte-derived phospholipids and free cholesterol. The rapid change in plaque substrate caused by the excessive accumulation of erythrocytes may promote the transition from a stable to an unstable lesion. This review discusses the potential role of intraplaque vasa vasorum in lesion instability as it relates to plaque rupture.
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Details
- Title
- Atherosclerotic Plaque Progression and Vulnerability to Rupture: Angiogenesis as a Source of Intraplaque Hemorrhage
- Creators
- Renu Virmani - From the CVPath, International Registry of Pathology (R.V., F.D.K.), Gaithersburg, Md; Department of Pathology (A.P.B.), University of Maryland, Baltimore; Cardiac Unit (H.K.G., A.V.F.), Department of Internal Medicine, Massachusetts General Hospital, Boston; Department of Surgery (T.N.T.), Thomas Jefferson University, Philadelphia, Pa; Department of Chemical Engineering (S.P.W.), Drexel University, Philadelphia, Pa; and Department of Cardiology (J.N.), University of California, IrvineFrank KolodgieAllen BurkeAloke FinnHerman GoldThomas TulenkoSteven WrennJagat Narula
- Publication Details
- Arteriosclerosis, thrombosis, and vascular biology, v 25(10), pp 2054-2061
- Publisher
- American Heart Association, Inc
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Chemical and Biological Engineering
- Web of Science ID
- WOS:000232231500007
- Scopus ID
- 2-s2.0-26244463577
- Other Identifier
- 991014878367104721
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InCites Highlights
Data related to this publication, from InCites Benchmarking & Analytics tool:
- Collaboration types
- Domestic collaboration
- Web of Science research areas
- Hematology
- Peripheral Vascular Disease