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The thrombotic process in atherogenesis : [proceedings of the Workshop on the Thrombotic Process in Atherogenesis, held in Reston, Virginia, October 16-19, 1977]

Author: A Bleakley Chandler; Council on Thrombosis (American Heart Association)
Publisher: New York : Plenum Press, ©1978.
Series: Advances in experimental medicine and biology, v. 104.
Edition/Format:   Print book : Conference publication : EnglishView all editions and formats
Database:WorldCat
Summary:
The Workshop on the Thrombotic Process in Atherogenesis has explored many aspects of this emerging field. In view of current interest and significant new developments, it was considered timely to hold a broad-based, in-depth meeting of scientists representing the disciplines involved. In a series of conceptual review papers, the subject is placed in perspective, while other reviews provide background for the  Read more...
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Genre/Form: Congresses
Conference papers and proceedings
Additional Physical Format: Online version:
Workshop on the Thrombotic Process in Atherogenesis (1977 : Reston, Va.).
Thrombotic process in atherogenesis.
New York : Plenum Press, ©1978
(OCoLC)610147860
Material Type: Conference publication
Document Type: Book
All Authors / Contributors: A Bleakley Chandler; Council on Thrombosis (American Heart Association)
ISBN: 0306400227 9780306400223
OCLC Number: 3933009
Notes: Sponsored by the Council of Thrombosis, American Heart Association and others.
Description: xvi, 546 pages : illustrations ; 26 cm.
Series Title: Advances in experimental medicine and biology, v. 104.
Responsibility: edited by A. Bleakley Chandler [and others].

Abstract:

The Workshop on the Thrombotic Process in Atherogenesis has explored many aspects of this emerging field. In view of current interest and significant new developments, it was considered timely to hold a broad-based, in-depth meeting of scientists representing the disciplines involved. In a series of conceptual review papers, the subject is placed in perspective, while other reviews provide background for the individual workshop sessions, which concentrate on recent work. Special note should be taken of an extensive survey on endothelium, the focal point of interaction between the constituents of the blood and vascular wall. Over a number of years, much evidence has accrued from experimental studies and from observations in man that thrombi can contribute to the growth of atherosclerotic plaques, and at times, may initiate the lesions. The organization and incorporation of thrombi into atherosclerotic plaques is a direct, clear-cut mechanism for plaque growth. This concept has not previously been given substantial recognition as a factor in atherogenesis, in part because of the paradoxical nature of the process: recent thrombi that have formed on established atherosclerotic lesions are readily identified; but once formed, the thrombi may undergo organization and conversion by the arterial wall into plaque tissue no longer recognizable as thrombotic in origin. The frequency, and consequently the morbidity and mortality, of arterial thrombosis alone has not been subject to accurate assessment for the very reason that thrombi intimately contribute to plaque formation and the progression of atherosclerosis. In contrast to deep vein thrombosis, which is often acute and frequently produces overt manifestations, arterial thrombosis may be chronic, extending over many years while plaques grow silently. Indeed, the question should be raised as to the desirability of considering thromboatherosclerosis as a distinct entity. Collected data indicate a definite contribution to plaque growth by thrombi, but many fundamental gaps remain to be filled before proper attention can be given to environmental risk factors and to therapeutic and prophylactic approaches. Among the several outstanding questions to be addressed are the following: What is the relative contribution of thrombosis to plaque growth? When in the life of the individual and of the plaque does the process begin? Are there subsets of the population in which thrombosis is, in fact, the dominant factor? Another aspect of thromboatherogenesis that requires detailed consideration is the complex relationship between dietary and plasma lipids and thrombosis. Plasma lipids may affect thrombus formation and thrombolysis by several mechanisms that concern platelet reactivity and blood coagulation. Fat in thromboatherosclerotic plaques may be derived from entrapped plasma lipids as well as from lipids of thrombotic cellular elements. It is of particular relevance to this issue that fibromuscular and fatty plaques can form from experimental thrombi produced in normolipemic states. Of special importance are recent observations relating arterial injury, the thrombotic process, and atherogenesis. For many years, investigators explored the idea that thrombosis initiates atherosclerosis, but found this possibility to be negligible in comparison to the effect of thrombi on plaque growth. However, it is now apparent that platelets and other components that share in the formation of thrombi might contribute to atherogenesis through initial injury to the arterial wall. Various factors involved in arterial damage including immunologic and hemodynamic injury must also take into account the associated effects of thrombotic components. More recently, it has been demonstrated by sophisticated in vitro investigations that, in addition to being injurious to endothelium, platelets may release a mitogenic factor that stimulates proliferation of vascular smooth muscle, a feature of most plaques. These relationships involving platelet injury and the response of the arterial wall are further related through plasma lipids which may also initiate injury, and through a special class of lipids, the prostaglandins, that are concerned with platelet reactivity and interactions between platelets and the arterial intima. The proceedings of this workshop brings together in a single document for the scientific community research relevant to the fields of thrombosis and atherogenesis. Recommendations have been developed for future research that will be helpful to individual investigators as well as to agencies that support research in these areas. It is hoped that this document will provide evidence to the Congress that basic research has yielded and continues to yield knowledge that will improve the health of the nation by attacking atherosclerosis early rather than in its terminal stages. Finally, it is a goal of this publication to provide a basis for stimulating widened interest in these closely allied fields. Clearly, there is ample opportunity for fertile collaboration among lipidologists, thrombologists, atherologists, and flow engineers, to name only a few of the relevant disciplines.

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This concept has not previously been given substantial recognition as a factor in atherogenesis, in part because of the paradoxical nature of the process: recent thrombi that have formed on established atherosclerotic lesions are readily identified; but once formed, the thrombi may undergo organization and conversion by the arterial wall into plaque tissue no longer recognizable as thrombotic in origin. The frequency, and consequently the morbidity and mortality, of arterial thrombosis alone has not been subject to accurate assessment for the very reason that thrombi intimately contribute to plaque formation and the progression of atherosclerosis. In contrast to deep vein thrombosis, which is often acute and frequently produces overt manifestations, arterial thrombosis may be chronic, extending over many years while plaques grow silently. Indeed, the question should be raised as to the desirability of considering thromboatherosclerosis as a distinct entity. Collected data indicate a definite contribution to plaque growth by thrombi, but many fundamental gaps remain to be filled before proper attention can be given to environmental risk factors and to therapeutic and prophylactic approaches. Among the several outstanding questions to be addressed are the following: What is the relative contribution of thrombosis to plaque growth? When in the life of the individual and of the plaque does the process begin? Are there subsets of the population in which thrombosis is, in fact, the dominant factor? Another aspect of thromboatherogenesis that requires detailed consideration is the complex relationship between dietary and plasma lipids and thrombosis. Plasma lipids may affect thrombus formation and thrombolysis by several mechanisms that concern platelet reactivity and blood coagulation. Fat in thromboatherosclerotic plaques may be derived from entrapped plasma lipids as well as from lipids of thrombotic cellular elements. It is of particular relevance to this issue that fibromuscular and fatty plaques can form from experimental thrombi produced in normolipemic states. Of special importance are recent observations relating arterial injury, the thrombotic process, and atherogenesis. For many years, investigators explored the idea that thrombosis initiates atherosclerosis, but found this possibility to be negligible in comparison to the effect of thrombi on plaque growth. However, it is now apparent that platelets and other components that share in the formation of thrombi might contribute to atherogenesis through initial injury to the arterial wall. Various factors involved in arterial damage including immunologic and hemodynamic injury must also take into account the associated effects of thrombotic components. More recently, it has been demonstrated by sophisticated in vitro investigations that, in addition to being injurious to endothelium, platelets may release a mitogenic factor that stimulates proliferation of vascular smooth muscle, a feature of most plaques. These relationships involving platelet injury and the response of the arterial wall are further related through plasma lipids which may also initiate injury, and through a special class of lipids, the prostaglandins, that are concerned with platelet reactivity and interactions between platelets and the arterial intima. The proceedings of this workshop brings together in a single document for the scientific community research relevant to the fields of thrombosis and atherogenesis. Recommendations have been developed for future research that will be helpful to individual investigators as well as to agencies that support research in these areas. It is hoped that this document will provide evidence to the Congress that basic research has yielded and continues to yield knowledge that will improve the health of the nation by attacking atherosclerosis early rather than in its terminal stages. Finally, it is a goal of this publication to provide a basis for stimulating widened interest in these closely allied fields. Clearly, there is ample opportunity for fertile collaboration among lipidologists, thrombologists, atherologists, and flow engineers, to name only a few of the relevant disciplines."@en ;
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