Arteriosclerosis New Insights into Pathogenetic Mechanisms and Prevention

A vast literature has been concerned with arteriosclerosis and yet, many aspects of pathogenesis and of the mechanism of development of the arteriosclerotic vascular lesion remain only poorly understood. In recent years, our knowledge of the earliest stages of arteriosclerosis have greatly improved....

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Bibliographic Details
Other Authors: Just, H. (Editor), Hort, W. (Editor), Zeiher, A.M. (Editor)
Format: eBook
Language:English
Published: Heidelberg Steinkopff 1994, 1994
Edition:1st ed. 1994
Subjects:
Online Access:
Collection: Springer Book Archives -2004 - Collection details see MPG.ReNa
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100 1 |a Just, H.  |e [editor] 
245 0 0 |a Arteriosclerosis  |h Elektronische Ressource  |b New Insights into Pathogenetic Mechanisms and Prevention  |c edited by H. Just, W. Hort, A.M. Zeiher 
250 |a 1st ed. 1994 
260 |a Heidelberg  |b Steinkopff  |c 1994, 1994 
300 |a X, 202 p  |b online resource 
505 0 |a Arteriosclerosis: Its morphology in the past and today -- Changes in components and structure of atherosclerotic lesions developing from childhood to middle age in coronary arteries -- Lipid and cellular constituents of unstable human aortic plaques -- Immunological control mechanisms in plaque formation -- Proliferation versus atrophy - the ambivalent role of smooth muscle cells in human atherosclerosis -- Extracellular matrix degrading metalloproteinases in the pathogenesis of arteriosclerosis -- Vascular renin-angiotensin-system, endothelial function and atherosclerosis? -- Endothelial dysfunction in atherosclerosis -- New determinants of the uptake of atherogenic plasma proteins by arteries -- Hyperlipidemic endothelial injury and angiogenesis -- Assessment of endothelial modulation of coronary vasomotor tone: Insights into a fundamental functional disturbance in vascular biology of atherosclerosis -- In vitro assessment of luminal dimensions of coronary arteries by intravascular ultrasound with and without application of echogenic contrast dye -- Therapeutic approaches to the control of coronary atherosclerosis -- Role of calcium in arteriosclerosis - Experimental evaluation of antiarteriosclerotic potencies of Ca antagonists -- Role of calcium antagonists in progression of arteriosclerosis. Evidence from animal experiments and clinical experience. -- I: Preventive effects of calcium antagonists in animal experiments -- Lipid-lowering therapy - Implications for the prevention of atherosclerosis 
653 |a Cardiology 
653 |a Human Physiology 
653 |a Human physiology 
700 1 |a Hort, W.  |e [editor] 
700 1 |a Zeiher, A.M.  |e [editor] 
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520 |a A vast literature has been concerned with arteriosclerosis and yet, many aspects of pathogenesis and of the mechanism of development of the arteriosclerotic vascular lesion remain only poorly understood. In recent years, our knowledge of the earliest stages of arteriosclerosis have greatly improved. By now, we have learned to relate morphologic changes to disturbances in function. It has been of particular impor­ tance that components of the arterial wall could be analyzed in regard to dysfunction, for example, in the endothelium or the vascular smooth muscle. The interaction of the different morphological components of the vascular wall could thus be much bet­ ter understood. Likewise, the interaction between the arterial wall and the flowing blood could be much better described, including the intimate relationship between platelets and the endothelium, the coagulation system and the endothelium, the granulocytes and the endothelial cell layer, as well as processes of migration of blood cells into the subendothelial space. The recognition of functional and morphological disturbance has attained clinical significance not only because the arteriosclerotic diseases have quantitatively reached the dimensions of an epidemic, that is, of a magnitude never been witnessed. It is also because of the development of new drugs that interfere with the atherogenic process and thereby prevent the development of the disease or halt its progression. It is also becoming increasingly possible to inhibit the occurrence of complications in existing arteriosclerotic lesions in manifest disease, i. e