on July 21, 2005
Arteriosclerosis, Thrombosis, and Vascular Biology. 2005
Published online before print July 21, 2005, doi: 10.1161/01.ATV.0000178991.71605.18
Published online before print July 21, 2005, doi: 10.1161/01.ATV.0000178991.71605.18
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Submitted on February 22, 2005
Accepted on June 9, 2005
Atherosclerotic Plaque Progression and Vulnerability to Rupture Angiogenesis as a Source of Intraplaque Hemorrhage
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, Irvine.
* To whom correspondence should be addressed. E-mail: rvirmani{at}cvpath.org.
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.
Key words: angiogenesis • plaque rupture • sudden coronary death • free cholesterol • hemorrhage
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H. Qiu, A. Gabrielsen, H. E. Agardh, M. Wan, A. Wetterholm, C.-H. Wong, U. Hedin, J. Swedenborg, G. K. Hansson, B. Samuelsson, et al. Expression of 5-lipoxygenase and leukotriene A4 hydrolase in human atherosclerotic lesions correlates with symptoms of plaque instability PNAS, May 23, 2006; 103(21): 8161 - 8166. [Abstract] [Full Text] [PDF]
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M. Sata Role of Circulating Vascular Progenitors in Angiogenesis, Vascular Healing, and Pulmonary Hypertension: Lessons From Animal Models Arterioscler Thromb Vasc Biol, May 1, 2006; 26(5): 1008 - 1014. [Abstract] [Full Text] [PDF]
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E. Falk Pathogenesis of atherosclerosis. J. Am. Coll. Cardiol., April 18, 2006; 47(8 Suppl): C7 - C12. [Abstract] [Full Text] [PDF]
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F. A. Jaffer, P. Libby, and R. Weissleder Molecular and Cellular Imaging of Atherosclerosis: Emerging Applications J. Am. Coll. Cardiol., April 4, 2006; 47(7): 1328 - 1338. [Abstract] [Full Text] [PDF]
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F. J. Byfield, S. Tikku, G. H. Rothblat, K. J. Gooch, and I. Levitan OxLDL increases endothelial stiffness, force generation, and network formation J. Lipid Res., April 1, 2006; 47(4): 715 - 723. [Abstract] [Full Text] [PDF]
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A. C. Langheinrich, A. Michniewicz, D. G. Sedding, G. Walker, P. E. Beighley, W. S. Rau, R. M. Bohle, and E. L. Ritman Correlation of Vasa Vasorum Neovascularization and Plaque Progression in Aortas of Apolipoprotein E-/-/Low-Density Lipoprotein-/- Double Knockout Mice Arterioscler Thromb Vasc Biol, February 1, 2006; 26(2): 347 - 352. [Abstract] [Full Text] [PDF]
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