Athérosclérose - Plaque Physiopathologie, Evaluation
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1 Athérosclérose - Plaque Physiopathologie, Evaluation Dr Philippe GAROT Institut Cardiovasculaire Paris Sud MASSY-QUINCY
2 Mécanisme cellulaire Constitution de la plaque d athérome
3 Monocytes Platelets IEL Endothelial cells Smooth muscle cells
4 LDL Monocytes Adhesion Activation Macrophages LDL LDL-ox Foam cells
5
6 Davies et al. Circulation 1996
7 REMODELAGE ARTERIEL «GLAGOV Asymptomatique Stade clinique
8 Le remodelage vasculaire
9 Rupture de plaque
10 Davies et al. Circulation 1996
11 Thrombus * Extruded atherosclerotic material
12
13
14 La rupture de plaque Aspect qualitatif Plaque vulnérable Plaque stable
15 Sévérité et vulnérabilit rabilité % 35 Nombre d'idm (suivi moyen : 4 ans) <25% % % >75% Sévérité initiale Nobuyoshi et al. J Am Coll Cardiol 1991
16 Plaque stable / plaque instable Plaques rompues Plaques non rompues Tissu fibreux Calcifications Lipides Gertz et al. Am J Cardiol 1990
17 B D Cicatrisation Progression A C E Rupture Thrombus mural Embolies F Evolution après s rupture Occlusion totale
18 La rupture de plaque Aspect qualitatif : production de matrice extracellulaire Cellules musculaires lisses Collagène Elastine LUMIERE Zone fibreuse Zone lipidique
19 La rupture de plaque Aspect qualitatif: dégradation de la matrice extracellulaire Dégradation Métalloprotéases Macrophages
20 La rupture de plaque Régulation de l activitl activité protéolytique olytique dans la plaque Collagénase Stroméolysine olysine Gélatinase etc Métalloprotéinases TIMP1 TIMP2 etc Inhibiteurs des métalloprotéinases
21 Inflammation et rupture Falk et al. Int Cardiovasc Med 1994
22 Figure 4. Top, Representative examples of plaque composition in the darapladib- and placebo-treated groups. Serruys P W et al. Circulation 2008;118: Copyright American Heart Association
23 The results of the 3-dimensional reconstruction of a right coronary artery are given in A. The lumen is in red, and the media-bounded area is represented in gray. Gijsen F J H et al. Am J Physiol Heart Circ Physiol 2008;295:H1608-H by American Physiological Society
24 Figure 4 Metalloproteinase activity analysis (MMP-2 and MMP-9) of hot (black bars) plaques, cold (light grey bars) plaques, and the reference region (dark grey bars) of the aorta of atherosclerotic rabbits (n=11). Krams R et al. Eur Heart J 2005;26: The European Society of Cardiology All rights reserved. For Permissions, please journals.permissions@oxfordjournals.org
25 Inflammation et Syndrome coronaire aigu
26
27 Simvastatin reduces the PMA-stimulated release of MMP-9 at gelatin zymography and EIA. Confluent HUVECs were treated with simvastatin (SIM) in the presence or absence of mevalonate, GGpp, or Fpp (12 h before PMA stimulation) or only with NS-398 (30 min before PMA stimulation). Massaro M et al. Cardiovasc Res 2010;86: Published on behalf of the European Society of Cardiology. All rights reserved. The Author For permissions please journals.permissions@oxfordjournals.org.
28 La rupture de plaque Aspect qualitatif: dégradation de la matrice extracellulaire Dégradation Métalloprotéases phorbol myristate acetate PMA Macrophages Statines
29 La rupture de plaque: thrombose
30
31
32
33
34 Régression de la plaque?
35 From: Effect of Intensive Compared With Moderate Lipid-Lowering Therapy on Progression of Coronary Atherosclerosis: A Randomized Controlled Trial JAMA. 2004;291(9): doi: /jama B, Patient randomized to80 mg of atorvastatin. There is substantial reduction in atheroma area (from13.0 to 7.4 mm2). A lesser increase in lumen area is noted (from7.7 to 9.8 mm2).
36 Régression de plaque Remodelage vasculaire
37 Cas particulier des bifurcations?
38 Flow patterns and spatial distribution of Atherosclerotic lesions in humans Low wall shear stress = Pro-atherogenic High wall shear stress = Anti-atherogenic Asakura, Circulation Research 1990; 66:1045-
39 Low WSS Atheroma in the bifurcation Virmani, Chatzizisis
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