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Pathobiology of the Human Atherosclerotic Plaque

Editat de Seymour Glagov, William P., III Newman, Sheldon A. Schaffer
en Limba Engleză Paperback – 29 sep 2011
Seymour Glagov The last meeting, devoted exclusively to an examination of the atherosclerotic plaque, took place in Chicago 25 years ago under the joint auspices of the Council on Arteriosclerosis of the American Heart Association and the Chicago Heart Association. The proceedings were published subsequently in a volume entitled "Evolution of the Atherosclerotic Plaque", edited by Richard J. Jones (1). Both experimental and human lesions were considered and several provocative new approaches to the disorder were discussed. The electron microscope was being applied systematically to the study of blood vessels at that time, so that details of the infrastructure and cellular composition of the artery wall and of atherosclerotic lesions were presented in some detail. There was, as one result of these explorations, considerable discussion of morphologic evidence suggesting that the principal cell involved in the atherogenic process was neither the fibroblast nor the macrophage, as had been supposed, but the smooth muscle cell. In particular, the findings indicated that this cell could incorporate lipid and become a foam cell.
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Specificații

ISBN-13: 9781461279686
ISBN-10: 1461279682
Pagini: 972
Ilustrații: XXXI, 923 p.
Dimensiuni: 155 x 235 x 51 mm
Greutate: 1.33 kg
Ediția:Softcover reprint of the original 1st ed. 1990
Editura: Springer
Colecția Springer
Locul publicării:New York, NY, United States

Public țintă

Research

Descriere

Seymour Glagov The last meeting, devoted exclusively to an examination of the atherosclerotic plaque, took place in Chicago 25 years ago under the joint auspices of the Council on Arteriosclerosis of the American Heart Association and the Chicago Heart Association. The proceedings were published subsequently in a volume entitled "Evolution of the Atherosclerotic Plaque", edited by Richard J. Jones (1). Both experimental and human lesions were considered and several provocative new approaches to the disorder were discussed. The electron microscope was being applied systematically to the study of blood vessels at that time, so that details of the infrastructure and cellular composition of the artery wall and of atherosclerotic lesions were presented in some detail. There was, as one result of these explorations, considerable discussion of morphologic evidence suggesting that the principal cell involved in the atherogenic process was neither the fibroblast nor the macrophage, as had been supposed, but the smooth muscle cell. In particular, the findings indicated that this cell could incorporate lipid and become a foam cell.

Cuprins

1. Questions About the Natural History of Human Atherosclerosis.- Cellular Contents.- 2. Arterial Endothelial Structure and Permeability as It Relates to Susceptibility to Atherogenesis.- 3. Second Messengers in Human Vascular Endothelial Cells: Regulation of Endothelial Monolayer Formation and Repair.- 4. Cytoskeletal Characterization of Smooth Muscle Cells of Human and Experimental Atherosclerotic Plaques.- 5. Phenotypic Changes in Smooth Muscle Cells of Human Atherosclerotic Plaques.- 6. Changes in the Cells of Atherosclerotic Lesions as Advanced Lesions Evolve in Coronary Arteries of Children and Young Adults.- 7. Inflammatory Components of the Human Atherosclerotic Plaque.- 8. The Role of Macrophages in Human Atherosclerosis.- 9. Recent Observations on Human Atherosclerotic Lesions, and their Possible Significance.- Tissue Organization and Architecture.- 10. Intimal Lipids and Associated Changes in Intimal Composition.- 11. Evolution of the Atherosclerotic Plaque—A Physicochemical Approach to Lipid Deposition.- 12. Modification of Collagen and Elastin in the Human Atherosclerotic Plaque.- 13. Nature and Importance of Proteoglycans in the Atherosclerotic Plaque.- 14. Biochemical and Immunological Evidence for the Presence of Lipoprotein-Antilipoprotein Immune Complexes in Human Atherosclerotic Plaques.- 15. Mechanisms of Calcification in Atherosclerosis.- 16. Characterization of Nucleating Proteolipids from Calcified and Non-Calcified Atherosclerotic Lesions.- Pathobiologic Processes.- 17. The Problems of Procedures for the Study of the Pathological Processes of Human Atherosclerosis.- 18. Problems and Progress in Understanding “Endothelial Permeability” and Mass Transport in Human Arteries.- 19. Accumulating Evidence from Human Artery Studies of What Gets Transported and What Accumulates Relative to Atherogenesis.- 20. How Hemodynamic Forces in the Human Affect the Topography and Development of Atherosclerosis.- 21. What Do We Find in Human Atherosclerosis that Provides Insight into the Hemodynamic Factors in Atherogenesis?.- 22. Cell Births and Cell Deaths in the Human Atherosclerotic Plaque as Evaluated from Human Studies.- 23. Immunocytochemical Analysis of the Cellular Composition of Atherosclerotic Lesions in the Human Aorta.- 24. An Overview of Thrombosis and Platelet Involvement in the Development of the Human Atherosclerotic Plaque.- 25. Observations Regarding the Thrombotic Process in Human Subjects.- 26. Plaque Hemorrhages, Their Genesis and Their Role in Supra-Plaque Thrombosis and Atherogenesis.- 27. Mechanical Properties of Human Atherosclerotic Lesions.- 28. Cinemicrographic Studies of the Vasa Vasorum of Human Coronary Arteries.- 29. Atherosclerosis Regression and Arterial Repair.- 30. Adaptive Responses of the Artery Wall as Human Atherosclerosis Develops.- 31. Hemodynamic Consequences of Changes in the Artery Wall During Atherogenesis.- 32. Lipoproteins and Pathogenesis of Atherosclerosis.- 33. A Cellular Basis for the Potential Atherogenicity of Triglycer-ide-Rich Lipoproteins.- Response of Human Lesions to Direct Intervention and Risk Factor Control.- 34. Strategies for Statistical Analysis of Angiographic Data: Individual Lesions Versus Individual Patients.- 35. Quantitative Arteriography in Coronary Intervention Trials: Rationale, Study Design, and Lipid Response in the University of Washington Familial Atherosclerosis Treatment Study (FATS).- 36. Measured Coronary Lesion Change in Relation to Blood Lipid Levels in the Leiden Intervention Trial and a View of the Atherosclerotic Process.- 37. The Repetitive Plasma Exchange/Drug Trial in Familial Hypercholesterolemia: Very Early Results from Two-Year Coronary Angiograms.- 38. Histologic and Functional Basis for Ameliorating Plaques by Percutaneous Translumial Angioplasty.- 39. Angioplasty, Laser Probes and Atherectomy.- Evaluation of Lesion Status in Major Arterial Beds.- 40. Late Changes in Saphenous Vein Aorto-Coronary Bypass Grafts: Clinical, Angiographic, Lipid and Pathological Correlations.- 41. Atherosclerosis of Saphenous Vein Coronary Artery Bypass Grafts in Relation to Risk Factors.- 42. Femoral Lesion Change in Relation to Measured Risk Factors in the Stockholm-Uppsala Trial.- 43. Arteriography of Patients Included in a Regression Study.- 44. Ultrasound Lesions of the Carotid Artery and Risk Factors in Men.- 45. Clinical Trials in Atherosclerosis: Summary and Overview.- Current and Prospective Methods for Detecting Plaque Change.- 46. Ultrasonic Evaluation of Arterial Wall Dynamics.- 47. Role of Doppler Ultrasound in Monitoring Atherosclerotic Disease Progression.- 48. Ultrasonic Evaluation of Arterial Intima and Media Thickness: Development and Validation of Methodology.- 49. Multicenter Validation Study of Real Time (B Mode) Ultrasound, Arteriography, and Pathology: I. Methods and Materials.- 50. Multicenter Validation Study of Real Time (B Mode) Ultrasound, Arteriography, and Pathology: II. Repeatability/Variability Assessment.- 51 Multicenter Validation Study of Real Time (B Mode) Ultrasound Arteriography, and Pathology: III. Sensitivity and Specificity Assessment.- 52. Multicenter Validation Study of Real Time (B Mode) Ultrasound, Arteriography, and Pathology: IV. Comparison of B Mode Ultrasonic Imaging with Arteriography in Lower Extremity Arteries.- 53. Multicenter Validation Study of Real Time (B Mode) Ultrasound, Arteriography, and Pathology: V. Pathologic Evaluation of Endarteroctomy Specimens and of Perfusion Fixed Carotid Arteries.- 54. Lessons Learned, Unresolved Problems and Future Opportunities. U.S. Multicenter Assessment of B Mode Ultrasound Imaging.- 55. Computer Image Processing Methods to Quantify Atherosclerosis Change: Problems and Prospects.- 56. External Imaging of Active Atherosclerosis with 99mTc-LDL.- 57. Magnetic Resonance Imaging for the Visualization of Vasculature and Atherosclerosis.- 58. Plaque Characterization—An Integrated Approach.- 59. Atherosclerosis Risk in Communities (ARIC): A Follow-up Study of Early Arterial Lesions in the General Population.- 60. Atherosclerosis Risk in Communities—Ultrasound Reading Center: Quantitative B Mode Scanning Protocol.- 61. Ultrasound Measurement of Atherosclerosis: Directions for Epidemiology.- 62. Ultrasound Studies of Factors Associated with Early Athero-mata: Design Considerations.- Summary.- 63. Conclusions: Perspectives for Future Study of Human Plaques.