Atherosclerotic Plaque Progression and Vulnerability to Rupture

Arteriosclerosis, Thrombosis, and Vascular Biology - Tập 25 Số 10 - Trang 2054-2061 - 2005
Renu Virmani1, Frank D. Kolodgie1, Allen Burke1, Aloke V. Finn1, Herman K. Gold1, Thomas N. Tulenko1, Steven P. Wrenn1, Jagat Narula1
1From 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.

Tóm tắt

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.

Từ khóa


Tài liệu tham khảo

10.1056/NEJMoa035655

10.1056/NEJM198405033101801

10.1097/00001573-200109000-00006

10.1161/atvb.20.5.1262

10.1136/hrt.2004.041798

10.1016/S0735-1097(03)00359-0

10.1161/circ.89.5.8181179

10.1161/circ.97.23.2307

1981, Am J Pathol, 103, 191

1992, J Biol Chem, 267, 4143, 10.1016/S0021-9258(19)50640-8

10.1161/01.atv.0000144951.08072.0b

10.1038/nm1102-1211

10.1016/S1388-1981(00)00146-3

10.1161/01.atv.0000148323.94021.e5

10.1161/atvb.19.8.1891

10.1172/JCI9021

10.1074/jbc.271.37.22773

10.1172/JCI108450

10.1161/atvb.17.7.1337

2002, Arch Pathol Lab Med, 126, 217, 10.5858/2002-126-0217-CGOTMS

Virmani R Roberts WC. Pulmonary arteries in congenital heart disease: a structure-function analysis. In: Roberts WC ed. Adult Congenital Heart Disease. Philadelphia Pa: F.A. Davis Company; 1987: 77–130.

Virmani R Burke AP Farb A. Non-neoplastic diseases of the pericardium. In: Atlas of Cardiovascular Pathology. Philadelphia Pa: W.B. Saunders Company; 1996: 103–110.

10.1016/0304-4157(85)90011-5

Bloch K. Cholesterol: evolution of structure and function. In: Vance DE Vance JE eds. Biochemistry of Lipids Lipoproteins and Membranes. Amsterdam The Netherlands: Elsevier Science; 1991: 363–381.

10.1161/circ.103.7.993

10.1007/s00228-002-0507-9

10.1161/atvb.19.11.2648

10.1161/atvb.21.6.884

1998, J Lipid Res, 39, 947, 10.1016/S0022-2275(20)33861-X

10.1016/S0002-8703(38)90300-X

Winternitz MC Thomas RM Le Compte PM. Thrombosis. In: Thomas CC ed. The Biology of Atherosclerosis. Springfield Ill; 1938: 94–103.

Patterson JC. The reaction of the arterial wall to intramural hemorrhage. In: Symposium of Atherosclerosis. Washington DC: National Academy of Sciences.; 1954: 65–73.

10.1161/circulationaha.104.504167

10.1001/jama.281.10.921

10.1016/S0741-5214(99)70136-9

10.1002/(SICI)1096-9896(199906)188:2<189::AID-PATH336>3.0.CO;2-N

10.1046/j.0007-1323.2001.01823.x

10.1161/01.atv.0000057807.28754.7f

10.1161/01.cir.0000146787.16297.e8

10.1136/hrt.53.4.363

1973, Bibl Anat, 11, 383

1972, Cancer Res, 32, 77

1876, Berl Klin Wochenschr, 13, 454

10.1172/JCI1568

1994, Am J Pathol, 145, 883

10.1056/NEJM198401193100307

10.1161/01.ATV.6.3.326

1993, Am J Pathol, 143, 164

10.1016/S0002-8703(98)70144-9

10.1016/S0002-9440(10)63214-2

10.1016/S0002-9440(10)63905-3

10.1083/jcb.153.3.543

1993, Am J Pathol, 143, 1377

10.1016/j.jvs.2004.06.032

10.1161/atvb.21.12.1876

10.1161/01.cir.0000079225.50817.71

10.1016/S0002-9440(10)65269-8

2000, Blood, 96, 3801, 10.1182/blood.V96.12.3801

10.4049/jimmunol.171.3.1534

10.4049/jimmunol.171.10.5489

10.1074/jbc.M300711200

10.4049/jimmunol.172.12.7503

10.2174/1568010043483881

10.1161/01.res.0000029784.15893.10

10.1111/j.0105-2896.2004.00202.x

10.1161/circ.105.10.1158

10.1161/01.cir.0000032146.75113.ee

10.1073/pnas.0403249101

10.1161/circ.104.25.3103

10.1016/S0002-9440(10)63698-X

10.1016/S0002-9440(10)61170-4

10.1161/atvb.20.12.2587

10.1073/pnas.0730843100