Angiotensin-Converting Enzyme Tissue Activity in the Diffuse In-Stent Restenotic Plaque
2000; Lippincott Williams & Wilkins; Volume: 101; Issue: 2 Linguagem: Inglês
10.1161/01.cir.101.2.e33
ISSN1524-4539
AutoresFlavio Ribichini, Francesco Pugno, Valeria Ferrero, Gianni Bussolati, Germano Melissano, Roberto Chiesa, Carlo Di Mario, Antonio Colombo,
Tópico(s)Atrial Fibrillation Management and Outcomes
ResumoHomeCirculationVol. 101, No. 2Angiotensin-Converting Enzyme Tissue Activity in the Diffuse In-Stent Restenotic Plaque Free AccessOtherPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessOtherPDF/EPUBAngiotensin-Converting Enzyme Tissue Activity in the Diffuse In-Stent Restenotic Plaque Flavio Ribichini, Francesco Pugno, Valeria Ferrero, Gianni Bussolati, Germano Melissano, Roberto Chiesa, Carlo Di Mario and Antonio Colombo Flavio RibichiniFlavio Ribichini From the Cardiac Catheterization Laboratory and Division of Cardiology (F.R., V.F.) and the Laboratory of Human Pathology (F.P.), Ospedale Santa Croce, Cuneo; the Department of Biomedical Science, Università di Torino (G.B.); and the Department of Vascular Surgery, Ospedale San Raffaele (G.M., R.C.) and Cardiac Catheterization Laboratory, Centro Cuore Columbus–Ospedale San Raffaele (C.D.M., A.C.), Milano, Italy. , Francesco PugnoFrancesco Pugno From the Cardiac Catheterization Laboratory and Division of Cardiology (F.R., V.F.) and the Laboratory of Human Pathology (F.P.), Ospedale Santa Croce, Cuneo; the Department of Biomedical Science, Università di Torino (G.B.); and the Department of Vascular Surgery, Ospedale San Raffaele (G.M., R.C.) and Cardiac Catheterization Laboratory, Centro Cuore Columbus–Ospedale San Raffaele (C.D.M., A.C.), Milano, Italy. , Valeria FerreroValeria Ferrero From the Cardiac Catheterization Laboratory and Division of Cardiology (F.R., V.F.) and the Laboratory of Human Pathology (F.P.), Ospedale Santa Croce, Cuneo; the Department of Biomedical Science, Università di Torino (G.B.); and the Department of Vascular Surgery, Ospedale San Raffaele (G.M., R.C.) and Cardiac Catheterization Laboratory, Centro Cuore Columbus–Ospedale San Raffaele (C.D.M., A.C.), Milano, Italy. , Gianni BussolatiGianni Bussolati From the Cardiac Catheterization Laboratory and Division of Cardiology (F.R., V.F.) and the Laboratory of Human Pathology (F.P.), Ospedale Santa Croce, Cuneo; the Department of Biomedical Science, Università di Torino (G.B.); and the Department of Vascular Surgery, Ospedale San Raffaele (G.M., R.C.) and Cardiac Catheterization Laboratory, Centro Cuore Columbus–Ospedale San Raffaele (C.D.M., A.C.), Milano, Italy. , Germano MelissanoGermano Melissano From the Cardiac Catheterization Laboratory and Division of Cardiology (F.R., V.F.) and the Laboratory of Human Pathology (F.P.), Ospedale Santa Croce, Cuneo; the Department of Biomedical Science, Università di Torino (G.B.); and the Department of Vascular Surgery, Ospedale San Raffaele (G.M., R.C.) and Cardiac Catheterization Laboratory, Centro Cuore Columbus–Ospedale San Raffaele (C.D.M., A.C.), Milano, Italy. , Roberto ChiesaRoberto Chiesa From the Cardiac Catheterization Laboratory and Division of Cardiology (F.R., V.F.) and the Laboratory of Human Pathology (F.P.), Ospedale Santa Croce, Cuneo; the Department of Biomedical Science, Università di Torino (G.B.); and the Department of Vascular Surgery, Ospedale San Raffaele (G.M., R.C.) and Cardiac Catheterization Laboratory, Centro Cuore Columbus–Ospedale San Raffaele (C.D.M., A.C.), Milano, Italy. , Carlo Di MarioCarlo Di Mario From the Cardiac Catheterization Laboratory and Division of Cardiology (F.R., V.F.) and the Laboratory of Human Pathology (F.P.), Ospedale Santa Croce, Cuneo; the Department of Biomedical Science, Università di Torino (G.B.); and the Department of Vascular Surgery, Ospedale San Raffaele (G.M., R.C.) and Cardiac Catheterization Laboratory, Centro Cuore Columbus–Ospedale San Raffaele (C.D.M., A.C.), Milano, Italy. and Antonio ColomboAntonio Colombo From the Cardiac Catheterization Laboratory and Division of Cardiology (F.R., V.F.) and the Laboratory of Human Pathology (F.P.), Ospedale Santa Croce, Cuneo; the Department of Biomedical Science, Università di Torino (G.B.); and the Department of Vascular Surgery, Ospedale San Raffaele (G.M., R.C.) and Cardiac Catheterization Laboratory, Centro Cuore Columbus–Ospedale San Raffaele (C.D.M., A.C.), Milano, Italy. Originally published18 Jan 2000https://doi.org/10.1161/01.CIR.101.2.e33Circulation. 2000;101:e33–e35We present the 6-month anatomic, histological, and immunohistochemical (IHC) images of a diffuse and aggressive type of in-stent restenosis of a popliteal artery of a patient homozygous for the D (deletion) allele of the ACE gene (Figures 1, 2, and 3).A detailed description of the histological changes of the arterial wall with time after coronary stenting in humans was published recently.1 These findings have confirmed that the ultrasound-detected "neointima" observed >1 month after implantation is composed primarily of smooth muscle cells (SMCs) and a proteoglycan-rich matrix. In the first weeks after stenting, the metallic struts associate with inflammatory cells, local thrombus formation, and "dedifferentiated" α-actin–negative spindle-shaped cells. Later, multinucleated giant cells and α-actin–positive spindle-shaped cells are observed in a more differentiated fibrocellular lesion.12 ACE increases up to 100-fold during the transformation of monocytes to macrophages, and most of the dedifferentiated SMCs (α-actin–negative cells) stain for ACE.3 However, ACE activity is thought to be limited only to the first 2 months of the reparative process that follows postballoon injury.Our samples reproduce the histological findings reported in 2 previous studies,12 but in contrast to the results of Ohishi et al3 obtained from postballoon restenotic samples, IHC staining for ACE was seen even 6 months after stent implantation. In fact, the spindle-shaped cells observed in the most external part of the restenotic plaque (close to the wire) stained for ACE in our sample (Figure 3A).The data presented suggest that the transition of the stent-induced inflammatory process, rich in ACE-positive cells, into a fibrocellular lesion composed of differentiated SMCs is not a time-determined sequence. Rather, it might be an ongoing process, evolving from peripheral areas (close to the wire) to central areas and ultimately leading to progressive lumen occlusion in patients with enhanced ACE activity. This is consistent with clinical studies that advocate a role of ACE in restenosis of coronary stents.4The editor of Images in Cardiovascular Medicine is Hugh A. McAllister, Jr, MD, Chief, Department of Pathology, St Luke's Episcopal Hospital and Texas Heart Institute, and Clinical Professor of Pathology, University of Texas Medical School and Baylor College of Medicine.Circulation encourages readers to submit cardiovascular images to Dr Hugh A. McAllister, Jr, St Luke's Episcopal Hospital and Texas Heart Institute, 6720 Bertner Ave, MC1-267, Houston, TX 77030.Download figureDownload PowerPoint Figure 1. Macroscopic view of a section of artery showing diffuse tissue growth within stent wires.Download figureDownload PowerPoint Figure 2. Hematoxylin-eosin microscopy of the arterial wall after removal of the metallic struts of the stent. Right, Muscularis of media of arterial wall. Around wire is a "wire cuffing" composed of inflammatory and spindle-shaped cells. Left, Core of restenotic plaque shows spindle-shaped cells and neovessels.Download figureDownload PowerPoint Figure 3. Amplification of wire cuffing tissue. IHC for ACE (Biomedicals Ag) and for α-actin (Dako) shows that (A) spindle-shaped cells in contact with metallic wires stain for ACE, and (B) spindle-shaped cells of plaque core, but not those close to stent wires, stain intensively for α-actin.FootnotesCorrespondence to Flavio Ribichini, MD, Laboratorio di Emodinamica, Ospedale Santa Croce, Via Michele Copino 26, 12100 Cuneo, Italy. E-mail [email protected] References 1 Farb A, Sangiorgi G, Carter AJ, Walley VM, Edwards WD, Schwartz RS, Virmani R. Pathology of acute and chronic coronary stenting in humans. Circulation.1999; 99:44–52.CrossrefMedlineGoogle Scholar2 Komatsu R, Ueda M, Naruko T, Kojima A, Becker AE. Neointimal tissue response at sites of coronary stenting in humans. Circulation.1998; 98:224–233.CrossrefMedlineGoogle Scholar3 Ohishi M, Ueda M, Rakugi H, Okamura A, Naruko T, Becker AE, Hiwada K, Kamitani A, Kamide K, Higaki J, Ogihara Y. Upregulation of angiotensin-converting enzyme during the healing process after injury at the site of percutaneous transluminal coronary angioplasty in humans. Circulation.1997; 96:3328–3337.CrossrefMedlineGoogle Scholar4 Ribichini F, Steffenino G, Dellavalle A, Matullo G, Colajanni E, Camilla T, Vado A, Benetton G, Uslenghi E, Piazza A. Plasma activity and insertion/deletion polymorphism of angiotensin I–converting enzyme: a major risk factor and a marker of risk for coronary stent restenosis. Circulation.1998; 97:147–154.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By MAMAS M, FOLEY J, NAIR S, WIPER A, CLARKE B, EL-OMAR M, FRASER D, KHATTAR R, NEYSES L and FATH-ORDOUBADI F (2011) A Comparison of Drug-Eluting Stents versus Bare Metal Stents in Saphenous Vein Graft PCI Outcomes: A Meta-Analysis, Journal of Interventional Cardiology, 10.1111/j.1540-8183.2010.00620.x, 24:2, (172-180), Online publication date: 1-Apr-2011. Ribichini F, Pugno F, Ferrero V, Wijns W, Vacca G, Vassanelli C and Virmani R (2008) Long-term histological and immunohistochemical findings in human venous aorto-coronary bypass grafts, Clinical Science, 10.1042/CS20070243, 114:3, (211-220), Online publication date: 1-Feb-2008. Langeveld B, Roks A, Tio R, Voors A, Zijlstra F and van Gilst W (2005) Renin-Angiotensin System Intervention to Prevent In-Stent Restenosis, Journal of Cardiovascular Pharmacology, 10.1097/00005344-200501000-00015, 45:1, (88-98), Online publication date: 1-Jan-2005. Lazar H (2005) Role of Angiotensin-Converting Enzyme Inhibitors in the Coronary Artery Bypass Patient, The Annals of Thoracic Surgery, 10.1016/j.athoracsur.2004.05.046, 79:3, (1081-1089), Online publication date: 1-Mar-2005. Ribichini F, Ferrero V, Rognoni A, Vacca G and Vassanelli C (2005) Angiotensin Antagonism in Coronary Artery Disease, Drugs, 10.2165/00003495-200565080-00004, 65:8, (1073-1096), . Lazar H (2005) The use of angiotensin-converting enzyme inhibitors in patients undergoing coronary artery bypass graft surgery, Vascular Pharmacology, 10.1016/j.vph.2005.01.012, 42:3, (119-123), Online publication date: 1-Feb-2005. Ribichini F, Ferrero V, Piessens M, Heyndrickx G, de Bruyne B, Verbeke L, Matullo G, Büchi M, Piazza A, Guarrera S, Lüscher T and Wijns W (2005) Intracoronary β-irradiation prevents excessive in-stent neointimal proliferation in de novo lesions of patients with high plasma ACE levels. The BetAce randomized trial, Cardiovascular Revascularization Medicine, 10.1016/j.carrev.2005.02.005, 6:1, (7-13), Online publication date: 1-Jan-2005. Ribichini F, Vado A, Uslenghi E, Matullo G and Piazza A (2000) Relationship between plasma ACE activity and the proliferative healing process in coronary vessel injury after coronary stenting, Atherosclerosis, 10.1016/S0021-9150(00)00509-8, 152:1, (261-263), Online publication date: 1-Sep-2000. Lima C, Silva J, Viegas K, Oliveira T, Lima R, Souza L, Aragão D, Casarini D, Irigoyen M, Lacchini S and Aikawa M (2015) Increase in Vascular Injury of Sodium Overloaded Mice May be Related to Vascular Angiotensin Modulation, PLOS ONE, 10.1371/journal.pone.0128141, 10:6, (e0128141) January 18, 2000Vol 101, Issue 2 Advertisement Article InformationMetrics Copyright © 2000 by American Heart Associationhttps://doi.org/10.1161/01.CIR.101.2.e33 Originally publishedJanuary 18, 2000 PDF download Advertisement
Referência(s)