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(Circulation. 2002;106:804.)
© 2002 American Heart Association, Inc.
Clinical Investigation and Reports |
From the Department of Hemodynamics, Cardiovascular Hospital and Claude Bernard University, Lyon (G.R., G.F., I.G., X.A.-F., R.R., A.T.); Department of Cardiology, Centre Hospitalier dAnnecy, Annecy (E.V., E.D.); Department of Cardiology, Centre Hospitalier de Roanne, Roanne (G.C.); and Department of Cardiology, Centre Hospitalier de Valence, Valence (J.F.H.), France.
Correspondence to Gilles Rioufol, MD, PhD, Department of Hemodynamics, Cardiovascular Hospital, B.P Lyon-Monchat, 69394 Lyon Cedex 03, France. E-mail gilles.rioufol{at}univ-lyon1.fr
Background To test the hypothesis of general atherosclerotic plaque destabilization during acute coronary syndrome (ACS), the present study sought to analyze the 3 coronary arteries by systematic intravascular ultrasound scan (IVUS).
Methods and Results Seventy-two arteries were explored in 24 patients referred for percutaneous coronary intervention after a first ACS with troponin I elevation. Fifty plaque ruptures (mean, 2.08 per patient; range, 0 to 6) were diagnosed by the association of a ruptured capsule with intraplaque cavity. Plaque rupture on the culprit lesion was found in 9 patients (37.5%). At least 1 plaque rupture was found somewhere other than on the culprit lesion in 19 patients (79%). These lesions were in a different artery than the culprit artery in 70.8% and were in both other arteries in 12.5% of these 24 patients. Complete IVUS examination of all 3 coronary axes in patients who had experienced a first ACS revealed that multiple atherosclerotic plaque ruptures were detected by IVUS; these multiple ruptures were present simultaneously with the culprit lesion; they were frequent and located (in three quarters of cases) on the 3 principal coronary trunks; and the multiple plaque ruptures in locations other than on the culprit lesion were less severe, nonstenosing, and less calcified.
Conclusion Although one single lesion is clinically active at the time of ACS, the syndrome seems nevertheless associated with overall coronary instability.
Key Words: ultrasonics atherosclerosis plaque coronary disease
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E. Zouridakis, P. Avanzas, R. Arroyo-Espliguero, S. Fredericks, and J. C. Kaski Markers of Inflammation and Rapid Coronary Artery Disease Progression in Patients With Stable Angina Pectoris Circulation, September 28, 2004; 110(13): 1747 - 1753. [Abstract] [Full Text] [PDF] |
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S. Okazaki, T. Yokoyama, K. Miyauchi, K. Shimada, T. Kurata, H. Sato, and H. Daida Early Statin Treatment in Patients With Acute Coronary Syndrome: Demonstration of the Beneficial Effect on Atherosclerotic Lesions by Serial Volumetric Intravascular Ultrasound Analysis During Half a Year After Coronary Event: The ESTABLISH Study Circulation, August 31, 2004; 110(9): 1061 - 1068. [Abstract] [Full Text] [PDF] |
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M.-K. Hong, G. S. Mintz, C. W. Lee, Y.-H. Kim, S.-W. Lee, J.-M. Song, K.-H. Han, D.-H. Kang, J.-K. Song, J.-J. Kim, et al. Comparison of Coronary Plaque Rupture Between Stable Angina and Acute Myocardial Infarction: A Three-Vessel Intravascular Ultrasound Study in 235 Patients Circulation, August 24, 2004; 110(8): 928 - 933. [Abstract] [Full Text] [PDF] |
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P Avanzas, R Arroyo-Espliguero, J Cosin-Sales, G Aldama, C Pizzi, J Quiles, and J C Kaski Markers of inflammation and multiple complex stenoses (pancoronary plaque vulnerability) in patients with non-ST segment elevation acute coronary syndromes Heart, August 1, 2004; 90(8): 847 - 852. [Abstract] [Full Text] [PDF] |
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A. Lombardo, L. M. Biasucci, G. A. Lanza, S. Coli, P. Silvestri, D. Cianflone, G. Liuzzo, F. Burzotta, F. Crea, and A. Maseri Inflammation as a Possible Link Between Coronary and Carotid Plaque Instability Circulation, June 29, 2004; 109(25): 3158 - 3163. [Abstract] [Full Text] [PDF] |
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F. C. Luft Cardiac Angiotensin Is Upregulated in the Hearts of Unstable Angina Patients Circ. Res., June 25, 2004; 94(12): 1530 - 1532. [Full Text] [PDF] |
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G. G. Neri Serneri, M. Boddi, P. A. Modesti, M. Coppo, I. Cecioni, T. Toscano, M. L. Papa, M. Bandinelli, G. F. Lisi, and M. Chiavarelli Cardiac Angiotensin II Participates in Coronary Microvessel Inflammation of Unstable Angina and Strengthens the Immunomediated Component Circ. Res., June 25, 2004; 94(12): 1630 - 1637. [Abstract] [Full Text] [PDF] |
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J. A. Schaar, E. Regar, F. Mastik, E. P. McFadden, F. Saia, C. Disco, C. L. de Korte, P. J. de Feyter, A. F.W. van der Steen, and P. W. Serruys Incidence of High-Strain Patterns in Human Coronary Arteries: Assessment With Three-Dimensional Intravascular Palpography and Correlation With Clinical Presentation Circulation, June 8, 2004; 109(22): 2716 - 2719. [Abstract] [Full Text] [PDF] |
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J. A Schaar, J. E Muller, E. Falk, R. Virmani, V. Fuster, P. W Serruys, A. Colombo, C. Stefanadis, S Ward Casscells, P. R Moreno, et al. Terminology for high-risk and vulnerable coronary artery plaques Eur. Heart J., June 2, 2004; 25(12): 1077 - 1082. [Abstract] [Full Text] [PDF] |
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