Presence of Intraplaque Hemorrhage Stimulates Progression of Carotid Atherosclerotic Plaques A High-Resolution Magnetic Resonance Imaging Study
Background— Previous studies suggest that erythrocyte membranes from intraplaque hemorrhage into the necrotic core are a source of free cholesterol and may become a driving force in the progression of atherosclerosis. We have shown that MRI can accurately identify carotid intraplaque hemorrhage and...
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| Published in | Circulation (New York, N.Y.) Vol. 111; no. 21; pp. 2768 - 2775 |
|---|---|
| Main Authors | , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hagerstown, MD
Lippincott Williams & Wilkins
31.05.2005
|
| Subjects | |
| Online Access | Get full text |
| ISSN | 0009-7322 1524-4539 1524-4539 |
| DOI | 10.1161/CIRCULATIONAHA.104.504167 |
Cover
| Abstract | Background—
Previous studies suggest that erythrocyte membranes from intraplaque hemorrhage into the necrotic core are a source of free cholesterol and may become a driving force in the progression of atherosclerosis. We have shown that MRI can accurately identify carotid intraplaque hemorrhage and precisely measure plaque volume. We tested the hypothesis that hemorrhage into carotid atheroma stimulates plaque progression.
Methods and Results—
Twenty-nine subjects (14 cases with intraplaque hemorrhage and 15 controls with comparably sized plaques without intraplaque hemorrhage at baseline) underwent serial carotid MRI examination with a multicontrast weighted protocol (T1, T2, proton density, and 3D time of flight) over a period of 18 months. The volumes of wall, lumen, lipid-rich necrotic core, calcification, and intraplaque hemorrhage were measured with a custom-designed image analysis tool. The percent change in wall volume (6.8% versus −0.15%;
P
=0.009) and lipid-rich necrotic core volume (28.4% versus −5.2%;
P
=0.001) was significantly higher in the hemorrhage group than in controls over the course of the study. Furthermore, those with intraplaque hemorrhage at baseline were much more likely to have new plaque hemorrhages at 18 months compared with controls (43% versus 0%;
P
=0.006).
Conclusions—
Hemorrhage into the carotid atherosclerotic plaque accelerated plaque progression in an 18-month period. Repeated bleeding into the plaque may produce a stimulus for the progression of atherosclerosis by increasing lipid core and plaque volume and creating new destabilizing factors. |
|---|---|
| AbstractList | Previous studies suggest that erythrocyte membranes from intraplaque hemorrhage into the necrotic core are a source of free cholesterol and may become a driving force in the progression of atherosclerosis. We have shown that MRI can accurately identify carotid intraplaque hemorrhage and precisely measure plaque volume. We tested the hypothesis that hemorrhage into carotid atheroma stimulates plaque progression.BACKGROUNDPrevious studies suggest that erythrocyte membranes from intraplaque hemorrhage into the necrotic core are a source of free cholesterol and may become a driving force in the progression of atherosclerosis. We have shown that MRI can accurately identify carotid intraplaque hemorrhage and precisely measure plaque volume. We tested the hypothesis that hemorrhage into carotid atheroma stimulates plaque progression.Twenty-nine subjects (14 cases with intraplaque hemorrhage and 15 controls with comparably sized plaques without intraplaque hemorrhage at baseline) underwent serial carotid MRI examination with a multicontrast weighted protocol (T1, T2, proton density, and 3D time of flight) over a period of 18 months. The volumes of wall, lumen, lipid-rich necrotic core, calcification, and intraplaque hemorrhage were measured with a custom-designed image analysis tool. The percent change in wall volume (6.8% versus -0.15%; P=0.009) and lipid-rich necrotic core volume (28.4% versus -5.2%; P=0.001) was significantly higher in the hemorrhage group than in controls over the course of the study. Furthermore, those with intraplaque hemorrhage at baseline were much more likely to have new plaque hemorrhages at 18 months compared with controls (43% versus 0%; P=0.006).METHODS AND RESULTSTwenty-nine subjects (14 cases with intraplaque hemorrhage and 15 controls with comparably sized plaques without intraplaque hemorrhage at baseline) underwent serial carotid MRI examination with a multicontrast weighted protocol (T1, T2, proton density, and 3D time of flight) over a period of 18 months. The volumes of wall, lumen, lipid-rich necrotic core, calcification, and intraplaque hemorrhage were measured with a custom-designed image analysis tool. The percent change in wall volume (6.8% versus -0.15%; P=0.009) and lipid-rich necrotic core volume (28.4% versus -5.2%; P=0.001) was significantly higher in the hemorrhage group than in controls over the course of the study. Furthermore, those with intraplaque hemorrhage at baseline were much more likely to have new plaque hemorrhages at 18 months compared with controls (43% versus 0%; P=0.006).Hemorrhage into the carotid atherosclerotic plaque accelerated plaque progression in an 18-month period. Repeated bleeding into the plaque may produce a stimulus for the progression of atherosclerosis by increasing lipid core and plaque volume and creating new destabilizing factors.CONCLUSIONSHemorrhage into the carotid atherosclerotic plaque accelerated plaque progression in an 18-month period. Repeated bleeding into the plaque may produce a stimulus for the progression of atherosclerosis by increasing lipid core and plaque volume and creating new destabilizing factors. Background— Previous studies suggest that erythrocyte membranes from intraplaque hemorrhage into the necrotic core are a source of free cholesterol and may become a driving force in the progression of atherosclerosis. We have shown that MRI can accurately identify carotid intraplaque hemorrhage and precisely measure plaque volume. We tested the hypothesis that hemorrhage into carotid atheroma stimulates plaque progression. Methods and Results— Twenty-nine subjects (14 cases with intraplaque hemorrhage and 15 controls with comparably sized plaques without intraplaque hemorrhage at baseline) underwent serial carotid MRI examination with a multicontrast weighted protocol (T1, T2, proton density, and 3D time of flight) over a period of 18 months. The volumes of wall, lumen, lipid-rich necrotic core, calcification, and intraplaque hemorrhage were measured with a custom-designed image analysis tool. The percent change in wall volume (6.8% versus −0.15%; P =0.009) and lipid-rich necrotic core volume (28.4% versus −5.2%; P =0.001) was significantly higher in the hemorrhage group than in controls over the course of the study. Furthermore, those with intraplaque hemorrhage at baseline were much more likely to have new plaque hemorrhages at 18 months compared with controls (43% versus 0%; P =0.006). Conclusions— Hemorrhage into the carotid atherosclerotic plaque accelerated plaque progression in an 18-month period. Repeated bleeding into the plaque may produce a stimulus for the progression of atherosclerosis by increasing lipid core and plaque volume and creating new destabilizing factors. Previous studies suggest that erythrocyte membranes from intraplaque hemorrhage into the necrotic core are a source of free cholesterol and may become a driving force in the progression of atherosclerosis. We have shown that MRI can accurately identify carotid intraplaque hemorrhage and precisely measure plaque volume. We tested the hypothesis that hemorrhage into carotid atheroma stimulates plaque progression. Twenty-nine subjects (14 cases with intraplaque hemorrhage and 15 controls with comparably sized plaques without intraplaque hemorrhage at baseline) underwent serial carotid MRI examination with a multicontrast weighted protocol (T1, T2, proton density, and 3D time of flight) over a period of 18 months. The volumes of wall, lumen, lipid-rich necrotic core, calcification, and intraplaque hemorrhage were measured with a custom-designed image analysis tool. The percent change in wall volume (6.8% versus -0.15%; P=0.009) and lipid-rich necrotic core volume (28.4% versus -5.2%; P=0.001) was significantly higher in the hemorrhage group than in controls over the course of the study. Furthermore, those with intraplaque hemorrhage at baseline were much more likely to have new plaque hemorrhages at 18 months compared with controls (43% versus 0%; P=0.006). Hemorrhage into the carotid atherosclerotic plaque accelerated plaque progression in an 18-month period. Repeated bleeding into the plaque may produce a stimulus for the progression of atherosclerosis by increasing lipid core and plaque volume and creating new destabilizing factors. |
| Author | Saam, Tobias Polissar, Nayak L. Isaac, Carol Small, Randy Ferguson, Marina S. Jarvik, Gail P. Hatsukami, Thomas S. Natiello, Cynthia McDonough, Judith Takaya, Norihide Yuan, Chun Chu, Baocheng |
| Author_xml | – sequence: 1 givenname: Norihide surname: Takaya fullname: Takaya, Norihide organization: From the Departments of Radiology (N.T., C.Y., B.C., T.S., M.S.F.), Pathology (R.S.), and Medicine, Division of Medical Genetics (G.P.J.), University of Washington, Seattle; Department of Cardiology, Juntendo University School of Medicine, Tokyo, Japan (N.T.); Mountain-Whisper-Light Statistical Consulting, Seattle, Wash (N.L.P.); and Department of Surgery, University of Washington, and Veterans Affairs Puget Sound Health Care System, Seattle, Wash (C.I., J.M., C.N., T.S.H.) – sequence: 2 givenname: Chun surname: Yuan fullname: Yuan, Chun organization: From the Departments of Radiology (N.T., C.Y., B.C., T.S., M.S.F.), Pathology (R.S.), and Medicine, Division of Medical Genetics (G.P.J.), University of Washington, Seattle; Department of Cardiology, Juntendo University School of Medicine, Tokyo, Japan (N.T.); Mountain-Whisper-Light Statistical Consulting, Seattle, Wash (N.L.P.); and Department of Surgery, University of Washington, and Veterans Affairs Puget Sound Health Care System, Seattle, Wash (C.I., J.M., C.N., T.S.H.) – sequence: 3 givenname: Baocheng surname: Chu fullname: Chu, Baocheng organization: From the Departments of Radiology (N.T., C.Y., B.C., T.S., M.S.F.), Pathology (R.S.), and Medicine, Division of Medical Genetics (G.P.J.), University of Washington, Seattle; Department of Cardiology, Juntendo University School of Medicine, Tokyo, Japan (N.T.); Mountain-Whisper-Light Statistical Consulting, Seattle, Wash (N.L.P.); and Department of Surgery, University of Washington, and Veterans Affairs Puget Sound Health Care System, Seattle, Wash (C.I., J.M., C.N., T.S.H.) – sequence: 4 givenname: Tobias surname: Saam fullname: Saam, Tobias organization: From the Departments of Radiology (N.T., C.Y., B.C., T.S., M.S.F.), Pathology (R.S.), and Medicine, Division of Medical Genetics (G.P.J.), University of Washington, Seattle; Department of Cardiology, Juntendo University School of Medicine, Tokyo, Japan (N.T.); Mountain-Whisper-Light Statistical Consulting, Seattle, Wash (N.L.P.); and Department of Surgery, University of Washington, and Veterans Affairs Puget Sound Health Care System, Seattle, Wash (C.I., J.M., C.N., T.S.H.) – sequence: 5 givenname: Nayak L. surname: Polissar fullname: Polissar, Nayak L. organization: From the Departments of Radiology (N.T., C.Y., B.C., T.S., M.S.F.), Pathology (R.S.), and Medicine, Division of Medical Genetics (G.P.J.), University of Washington, Seattle; Department of Cardiology, Juntendo University School of Medicine, Tokyo, Japan (N.T.); Mountain-Whisper-Light Statistical Consulting, Seattle, Wash (N.L.P.); and Department of Surgery, University of Washington, and Veterans Affairs Puget Sound Health Care System, Seattle, Wash (C.I., J.M., C.N., T.S.H.) – sequence: 6 givenname: Gail P. surname: Jarvik fullname: Jarvik, Gail P. organization: From the Departments of Radiology (N.T., C.Y., B.C., T.S., M.S.F.), Pathology (R.S.), and Medicine, Division of Medical Genetics (G.P.J.), University of Washington, Seattle; Department of Cardiology, Juntendo University School of Medicine, Tokyo, Japan (N.T.); Mountain-Whisper-Light Statistical Consulting, Seattle, Wash (N.L.P.); and Department of Surgery, University of Washington, and Veterans Affairs Puget Sound Health Care System, Seattle, Wash (C.I., J.M., C.N., T.S.H.) – sequence: 7 givenname: Carol surname: Isaac fullname: Isaac, Carol organization: From the Departments of Radiology (N.T., C.Y., B.C., T.S., M.S.F.), Pathology (R.S.), and Medicine, Division of Medical Genetics (G.P.J.), University of Washington, Seattle; Department of Cardiology, Juntendo University School of Medicine, Tokyo, Japan (N.T.); Mountain-Whisper-Light Statistical Consulting, Seattle, Wash (N.L.P.); and Department of Surgery, University of Washington, and Veterans Affairs Puget Sound Health Care System, Seattle, Wash (C.I., J.M., C.N., T.S.H.) – sequence: 8 givenname: Judith surname: McDonough fullname: McDonough, Judith organization: From the Departments of Radiology (N.T., C.Y., B.C., T.S., M.S.F.), Pathology (R.S.), and Medicine, Division of Medical Genetics (G.P.J.), University of Washington, Seattle; Department of Cardiology, Juntendo University School of Medicine, Tokyo, Japan (N.T.); Mountain-Whisper-Light Statistical Consulting, Seattle, Wash (N.L.P.); and Department of Surgery, University of Washington, and Veterans Affairs Puget Sound Health Care System, Seattle, Wash (C.I., J.M., C.N., T.S.H.) – sequence: 9 givenname: Cynthia surname: Natiello fullname: Natiello, Cynthia organization: From the Departments of Radiology (N.T., C.Y., B.C., T.S., M.S.F.), Pathology (R.S.), and Medicine, Division of Medical Genetics (G.P.J.), University of Washington, Seattle; Department of Cardiology, Juntendo University School of Medicine, Tokyo, Japan (N.T.); Mountain-Whisper-Light Statistical Consulting, Seattle, Wash (N.L.P.); and Department of Surgery, University of Washington, and Veterans Affairs Puget Sound Health Care System, Seattle, Wash (C.I., J.M., C.N., T.S.H.) – sequence: 10 givenname: Randy surname: Small fullname: Small, Randy organization: From the Departments of Radiology (N.T., C.Y., B.C., T.S., M.S.F.), Pathology (R.S.), and Medicine, Division of Medical Genetics (G.P.J.), University of Washington, Seattle; Department of Cardiology, Juntendo University School of Medicine, Tokyo, Japan (N.T.); Mountain-Whisper-Light Statistical Consulting, Seattle, Wash (N.L.P.); and Department of Surgery, University of Washington, and Veterans Affairs Puget Sound Health Care System, Seattle, Wash (C.I., J.M., C.N., T.S.H.) – sequence: 11 givenname: Marina S. surname: Ferguson fullname: Ferguson, Marina S. organization: From the Departments of Radiology (N.T., C.Y., B.C., T.S., M.S.F.), Pathology (R.S.), and Medicine, Division of Medical Genetics (G.P.J.), University of Washington, Seattle; Department of Cardiology, Juntendo University School of Medicine, Tokyo, Japan (N.T.); Mountain-Whisper-Light Statistical Consulting, Seattle, Wash (N.L.P.); and Department of Surgery, University of Washington, and Veterans Affairs Puget Sound Health Care System, Seattle, Wash (C.I., J.M., C.N., T.S.H.) – sequence: 12 givenname: Thomas S. surname: Hatsukami fullname: Hatsukami, Thomas S. organization: From the Departments of Radiology (N.T., C.Y., B.C., T.S., M.S.F.), Pathology (R.S.), and Medicine, Division of Medical Genetics (G.P.J.), University of Washington, Seattle; Department of Cardiology, Juntendo University School of Medicine, Tokyo, Japan (N.T.); Mountain-Whisper-Light Statistical Consulting, Seattle, Wash (N.L.P.); and Department of Surgery, University of Washington, and Veterans Affairs Puget Sound Health Care System, Seattle, Wash (C.I., J.M., C.N., T.S.H.) |
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Previous studies suggest that erythrocyte membranes from intraplaque hemorrhage into the necrotic core are a source of free cholesterol and may... Previous studies suggest that erythrocyte membranes from intraplaque hemorrhage into the necrotic core are a source of free cholesterol and may become a... |
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| SubjectTerms | Aged Aged, 80 and over Atherosclerosis (general aspects, experimental research) Atherosclerosis - etiology Atherosclerosis - pathology Biological and medical sciences Blood and lymphatic vessels Blood Vessels - pathology Calcinosis - pathology Cardiology. Vascular system Carotid Artery Diseases - etiology Carotid Artery Diseases - pathology Case-Control Studies Disease Progression Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Female Hemorrhage - complications Hemorrhage - etiology Humans Imaging, Three-Dimensional Lipids Magnetic Resonance Imaging - methods Male Medical sciences Middle Aged Neurology Vascular diseases and vascular malformations of the nervous system |
| Subtitle | A High-Resolution Magnetic Resonance Imaging Study |
| Title | Presence of Intraplaque Hemorrhage Stimulates Progression of Carotid Atherosclerotic Plaques |
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