© 1996 American Heart Association, Inc.
Articles |
Molecular Mechanisms of Coronary Collateral Vessel Growth
the Max-Planck-Institute for Physiological and Clinical Research, Department of Experimental Cardiology, Bad Nauheim, Germany.
Correspondence to Prof Dr Wolfgang Schaper, Max-Planck-Institute for Physiological and Clinical Research, Department of Experimental Cardiology, Benekestrasse 2, D-61231 Bad Nauheim, Germany.
Key Words: angiogenesis • collateral arteries • heart
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Introduction |
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Growth of coronary collaterals can change markedly the natural history of coronary artery disease: Stenoses and occlusions of the coronary arteries, even of the left main coronary artery, can be survived without infarction provided that the stenosing process has not progressed too fast, since the process of collateral development by growth needs time (a few weeks).1 2 3
However, in most cases, thrombus formation proceeds faster than vascular growth and infarcts develop. In many cases, collaterals, although they cannot prevent infarction in the majority of cases, may limit the damage and infarcts are smaller than expected from the size of the region at risk.4
Understanding collateral growth may mean to be potentially and eventually able to stimulate it by the injection of drugs, by the injection of growth factors, or by somatic gene therapy in patients at risk of infarction.
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Collaterals Develop by Mitotic Growth |
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In the past we have shown that collaterals grow by DNA synthesis and mitosis of endothelial and smooth muscle cells.3 These cells are quiescent in normal adult arteries, with their population kinetics close to zero. Under abnormal conditions a rapid conversion to G1 can occur and the cell cycle can be completed in
22 hours.3 With rapidly progressing stenosis in dogs (3 days from the onset of stenosis to complete occlusion), the labeling index of the endothelium of the midzone segment reached 7.5% and was followed by a wave of smooth muscle cell mitosis of only slightly lesser magnitude.
Since controlled and regulated growth does not proceed without the presence and action
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M. Ziche, A. Parenti, F. Ledda, P. Dell'Era, H. J. Granger, C. A. Maggi, and M. Presta Nitric Oxide Promotes Proliferation and Plasminogen Activator Production by Coronary Venular Endothelium Through Endogenous bFGF Circ. Res., June 19, 1997; 80(6): 845 - 852. [Abstract] [Full Text]
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M. S. Pepper Manipulating Angiogenesis: From Basic Science to the Bedside Arterioscler Thromb Vasc Biol, April 1, 1997; 17(4): 605 - 619. [Abstract] [Full Text]
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B. Su, S. Mitra, H. Gregg, S. Flavahan, M. A. Chotani, K. R. Clark, P. J. Goldschmidt-Clermont, and N. A. Flavahan Redox Regulation of Vascular Smooth Muscle Cell Differentiation Circ. Res., July 6, 2001; 89(1): 39 - 46. [Abstract] [Full Text] [PDF]
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C. L. Buus, F. Pourageaud, G. E. Fazzi, G. Janssen, M. J. Mulvany, and J. G.R. De Mey Smooth Muscle Cell Changes During Flow-Related Remodeling of Rat Mesenteric Resistance Arteries Circ. Res., July 20, 2001; 89(2): 180 - 186. [Abstract] [Full Text] [PDF]
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H. Matsuo, S. Watanabe, T. Kadosaki, T. Yamaki, S. Tanaka, S. Miyata, T. Segawa, Y. Matsuno, M. Tomita, and H. Fujiwara Validation of Collateral Fractional Flow Reserve by Myocardial Perfusion Imaging Circulation, March 5, 2002; 105(9): 1060 - 1065. [Abstract] [Full Text] [PDF]
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