(Circulation. 1996;94:3090-3097.)
© 1996 American Heart Association, Inc.
Articles |
the Cardiac Unit, Massachusetts General Hospital, Harvard Medical School, Boston, and the Cardiovascular Institute (R.M., S.K.S., Y.N., V.F., J.T.F.), Mount Sinai School of Medicine, New York, NY.
Correspondence to Pedro R. Moreno, MD, Department of Medicine, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115. E-mail prmoreno@bics.bwh.harvard.edu.
Background Macrophage expression of tissue factor may be responsible for coronary thrombogenicity in patients with plaque rupture. In patients without plaque rupture, smooth muscle cells may be the thrombogenic substrate. This study was designed to identify the cellular correlations of tissue factor in patients with unstable angina.
Methods and Results Tissue from 50 coronary specimens (1560 pieces) from patients with unstable angina and 15 specimens from patients with stable angina were analyzed. Total and segmental areas (in square millimeters) were identified with trichrome staining. Macrophages, smooth muscle cells, and tissue factor were identified by immunostaining. Tissue factor content was larger in unstable angina (42±3%) than in stable angina (18±4%) (P=.0001). Macrophage content was also larger in unstable angina (16±2%) than in stable angina (5±2%) (P=.002). The percentage of tissue factor located in cellular areas was larger in coronary samples from patients with unstable angina (67±8%) than in samples from patients with stable angina (40±5%) (P=.00007). Multiple linear stepwise regression analysis showed that coronary tissue factor content correlated significantly (r=.83, P<.0001) with macrophage and smooth muscle cell areas only in tissue from patients with unstable angina, with a strong relationship between tissue factor content and macrophages in the atheromatous gruel (r=.98, P<.0001).
Conclusions Tissue factor content is increased in unstable angina and correlates with areas of macrophages and smooth muscle cells, suggesting a cell-mediated thrombogenicity in patients with acute coronary syndromes.
Key Words: atherosclerosis coronary disease thrombosis leukocytes
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V. Fuster, J. J. Badimon, and J. H Chesebro Atherothrombosis: mechanisms and clinical therapeutic approaches Vascular Medicine, August 1, 1998; 3(3): 231 - 239. [Abstract] [PDF] |
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S. Jander, M. Sitzer, R. Schumann, M. Schroeter, M. Siebler, H. Steinmetz, and G. Stoll Inflammation in High-Grade Carotid Stenosis : A Possible Role for Macrophages and T Cells in Plaque Destabilization Stroke, August 1, 1998; 29(8): 1625 - 1630. [Abstract] [Full Text] [PDF] |
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P. Theroux and V. Fuster Acute Coronary Syndromes : Unstable Angina and Non–Q-Wave Myocardial Infarction Circulation, March 31, 1998; 97(12): 1195 - 1206. [Full Text] [PDF] |
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S. S. Patel, R. Thiagarajan, J. T. Willerson, and E. T. H. Yeh Inhibition of {alpha}4 Integrin and ICAM-1 Markedly Attenuate Macrophage Homing to Atherosclerotic Plaques in ApoE-Deficient Mice Circulation, January 13, 1998; 97(1): 75 - 81. [Abstract] [Full Text] [PDF] |
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A. D. Schecter, B. J. Rollins, Y. J. Zhang, I. F. Charo, J. T. Fallon, M. Rossikhina, P. L. A. Giesen, Y. Nemerson, and M. B. Taubman Tissue Factor Is Induced by Monocyte Chemoattractant Protein-1 in Human Aortic Smooth Muscle and THP-1 Cells J. Biol. Chem., November 7, 1997; 272(45): 28568 - 28573. [Abstract] [Full Text] [PDF] |
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F. Mach, U. Schonbeck, J.-Y. Bonnefoy, J. S. Pober, and P. Libby Activation of Monocyte/Macrophage Functions Related to Acute Atheroma Complication by Ligation of CD40 : Induction of Collagenase, Stromelysin, and Tissue Factor Circulation, July 15, 1997; 96(2): 396 - 399. [Abstract] [Full Text] |
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P. R. Moreno, V. H. Bernardi, J. Lopez-Cuellar, J. B. Newell, C. McMellon, H. K. Gold, I. F. Palacios, V. Fuster, and J. T. Fallon Macrophage Infiltration Predicts Restenosis After Coronary Intervention in Patients With Unstable Angina Circulation, December 15, 1996; 94(12): 3098 - 3102. [Abstract] [Full Text] |
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A. a. Belaaouaj, A. Li, T.-C. Wun, H. G. Welgus, and S. D. Shapiro Matrix Metalloproteinases Cleave Tissue Factor Pathway Inhibitor. EFFECTS ON COAGULATION J. Biol. Chem., August 25, 2000; 275(35): 27123 - 27128. [Abstract] [Full Text] [PDF] |
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P. R. Moreno, R. A. Lodder, K. R. Purushothaman, W. E. Charash, W. N. O'Connor, and J. E. Muller Detection of Lipid Pool, Thin Fibrous Cap, and Inflammatory Cells in Human Aortic Atherosclerotic Plaques by Near-Infrared Spectroscopy Circulation, February 26, 2002; 105(8): 923 - 927. [Abstract] [Full Text] [PDF] |
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R. Baetta, M. Camera, C. Comparato, C. Altana, M. D. Ezekowitz, and E. Tremoli Fluvastatin Reduces Tissue Factor Expression and Macrophage Accumulation in Carotid Lesions of Cholesterol-Fed Rabbits in the Absence of Lipid Lowering Arterioscler Thromb Vasc Biol, April 1, 2002; 22(4): 692 - 698. [Abstract] [Full Text] [PDF] |
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