Parvovirus B19–Associated Active Myocarditis With Biventricular Thrombi Results of Endomyocardial Biopsy Investigations and Cardiac Magnetic Resonance Imaging
2007; Lippincott Williams & Wilkins; Volume: 115; Issue: 13 Linguagem: Inglês
10.1161/circulationaha.106.667360
ISSN1524-4539
AutoresMichel Noutsias, Uwe Kuehl, Dirk Laßner, Ulrich Groß, Matthias Pauschinger, Heinz‐Peter Schultheiß, Matthias Gutberlet,
Tópico(s)Eosinophilic Disorders and Syndromes
ResumoHomeCirculationVol. 115, No. 13Parvovirus B19–Associated Active Myocarditis With Biventricular Thrombi Results of Endomyocardial Biopsy Investigations and Cardiac Magnetic Resonance Imaging Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBParvovirus B19–Associated Active Myocarditis With Biventricular Thrombi Results of Endomyocardial Biopsy Investigations and Cardiac Magnetic Resonance Imaging Michel Noutsias, MD, Uwe Kuehl, PhD, Dirk Lassner, PhD, Ulrich Gross, MD, Matthias Pauschinger, MD, Heinz-Peter Schultheiss, MD and Matthias Gutberlet, MD Michel NoutsiasMichel Noutsias From the Department of Cardiology and Pneumonology, Charité–Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany (M.N., U.K., M.P., H.-P.S.), Institute Cardiac Diagnostics and Therapy, Berlin, Germany (D.L., U.G.), and Department of Diagnostic and Interventional Radiology and Nuclear Medicine, Charité–Universitätsmedizin Berlin, Campus Virchow, Germany (M.G.). , Uwe KuehlUwe Kuehl From the Department of Cardiology and Pneumonology, Charité–Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany (M.N., U.K., M.P., H.-P.S.), Institute Cardiac Diagnostics and Therapy, Berlin, Germany (D.L., U.G.), and Department of Diagnostic and Interventional Radiology and Nuclear Medicine, Charité–Universitätsmedizin Berlin, Campus Virchow, Germany (M.G.). , Dirk LassnerDirk Lassner From the Department of Cardiology and Pneumonology, Charité–Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany (M.N., U.K., M.P., H.-P.S.), Institute Cardiac Diagnostics and Therapy, Berlin, Germany (D.L., U.G.), and Department of Diagnostic and Interventional Radiology and Nuclear Medicine, Charité–Universitätsmedizin Berlin, Campus Virchow, Germany (M.G.). , Ulrich GrossUlrich Gross From the Department of Cardiology and Pneumonology, Charité–Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany (M.N., U.K., M.P., H.-P.S.), Institute Cardiac Diagnostics and Therapy, Berlin, Germany (D.L., U.G.), and Department of Diagnostic and Interventional Radiology and Nuclear Medicine, Charité–Universitätsmedizin Berlin, Campus Virchow, Germany (M.G.). , Matthias PauschingerMatthias Pauschinger From the Department of Cardiology and Pneumonology, Charité–Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany (M.N., U.K., M.P., H.-P.S.), Institute Cardiac Diagnostics and Therapy, Berlin, Germany (D.L., U.G.), and Department of Diagnostic and Interventional Radiology and Nuclear Medicine, Charité–Universitätsmedizin Berlin, Campus Virchow, Germany (M.G.). , Heinz-Peter SchultheissHeinz-Peter Schultheiss From the Department of Cardiology and Pneumonology, Charité–Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany (M.N., U.K., M.P., H.-P.S.), Institute Cardiac Diagnostics and Therapy, Berlin, Germany (D.L., U.G.), and Department of Diagnostic and Interventional Radiology and Nuclear Medicine, Charité–Universitätsmedizin Berlin, Campus Virchow, Germany (M.G.). and Matthias GutberletMatthias Gutberlet From the Department of Cardiology and Pneumonology, Charité–Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany (M.N., U.K., M.P., H.-P.S.), Institute Cardiac Diagnostics and Therapy, Berlin, Germany (D.L., U.G.), and Department of Diagnostic and Interventional Radiology and Nuclear Medicine, Charité–Universitätsmedizin Berlin, Campus Virchow, Germany (M.G.). Originally published3 Apr 2007https://doi.org/10.1161/CIRCULATIONAHA.106.667360Circulation. 2007;115:e378–e380A previously healthy 39-year-old man was admitted to our department with biventricular cardiac decompensation (New York Heart Association class IV) and acute onset of angina pectoris after a flulike disease 1 week earlier. The ECG on admission displayed ST elevations in II, III, and aVF. Troponin T on admission was increased (2.20 mg/L, normal value<0.03 mg/L), with increased creatine phosphokinase (503 U/L; normal value<171 U/L) and creatine phosphokinase myocardial band (45 U/L; normal value=10 U/L). N-terminal pro-brain natriuretic peptide was highly elevated (15,848 pg/mL; normal value<125 pg/mL). Coronary artery disease was excluded by coronary angiography. Multiple nonsustained ventricular tachycardias were recorded by Holter monitoring and telemetry.Endomyocardial biopsies obtained from the right ventricular septum demonstrated active myocarditis by histological investigations according to the Dallas criteria (Figure 1A). By immunohistological staining of endomyocardial biopsies1 and quantification using digital image analysis, highly increased focal lymphocytic (CD3+: 267.4/mm2, CD11a/LFA-1+: 498.9/mm2; Figure 1B) and macrophage infiltrates (CD11b/Mac-1+: 481.6/mm2), sarcolemmal human leukocyte antigen class I expression (area fraction of human leukocyte antigen class I=35.6%; Figure 1C), and focal abundance of CD54/ICAM-1 (area fraction=4.7%) and CD106/VCAM-1 (area fraction: 0.22%) were detected. Nested polymerase chain reaction for cardiotropic viruses2 confirmed parvovirus B19 genomes in endomyocardial biopsies, with a parvovirus B19 virus load at 458 viral copies per microgram of nucleic acid as determined by real-time polymerase chain reaction. Cardiac magnetic resonance imaging (MRI) showed a severely depressed left ventricular ejection fraction (17%; Movie I). Left ventricular end diastolic volume (204 mL/m2) and left ventricular end systolic volume (169 mL/m2) were increased (normal values: left ventricular end diastolic volume=53 to 112 mL/m2, left ventricular end systolic volume=15 to 45 mL/m2). Moreover, apical thrombi were detected in both the left and right ventricles (Figure 2A). Hypo-/akinetic regions in the apical, inferoseptal, and inferolateral segments were colocalized with late gadolinium–diethylene triamine pentaacetic acid enhancement (LE)3 (Figure 2A). Increased edema ratio (2.2; scanner-dependent normal value<2.0) was detected in T2-weighted images (Figure 2C), localized at the inferoseptal and lateral wall. Global relative enhancement calculated from the spin echo images4 was highly elevated (7.4; normal value<4.0), consistent with florid myocarditis (Figure 2E). Download figureDownload PowerPointFigure 1. Histological and immunohistological findings of endomyocardial biopsies. A, Histology (hematoxylin and eosin staining) of the endomyocardial biopsy demonstrated active myocarditis with focal lymphocytic infiltration and myocytolysis (arrows; ×400). B, Immunohistological staining of CD11a/LFA-1+ lymphocytes with focal infiltration pattern (×200). C, Sarcolemmal human leukocyte antigen class I expression by virtually all cardiomyocytes (arrows) in the area of focal infiltration (×200).Download figureDownload PowerPointFigure 2. Cardiac magnetic resonance imaging (MRI). A, MRI in the acute phase, showing late enhancement in the apical, inferoseptal, and inferolateral segments (red arrows) and thrombi in the right and left ventricles (yellow arrows). B, Follow-up MRI with persisting late enhancement in the apical, inferoseptal, and inferolateral segments (red arrows), without any ventricular thrombi. C, T2-weighted short-axis image in the acute phase with elevated edema ratio (2.2), localized at the inferoseptal and lateral wall (arrows). D, T2-weighted image at follow-up assessment showing marginally elevated edema ratio (2.0) with edema localized at the lateral wall (arrow). E, At the initial acute phase, the global relative enhancement was significantly elevated (7.4), with a focal enhancement (red arrow) at the lateral wall (E). F, At follow-up assessment, global relative enhancement had decreased to a normal value (1.9; F).Cardiac recompensation was initiated with heart failure medication (diuretics, ramipril, carvedilol, eplerenone, and digitalis). In light of the known potential of acute myocarditis, which was confirmed in this case by histology, immunohistology, and cardiac MRI, for spontaneous improvement, we opted for an observational strategy and did not implant an implantable cardioverter defibrillator for primary prevention of sudden cardiac death. The patient was set on anticoagulation with heparin and then with phenprocoumon (international normalized ratio=2.0 to 3.0). The patient was discharged at a recompensated status (New York Heart Association class II).The patient was reevaluated 8 weeks after discharge in our outpatient clinic. The N-terminal pro-brain natriuretic peptide had decreased substantially from 15 848 to 1435 pg/mL. Cardiac MRI showed an improved left ventricular ejection fraction to 38% (Movie II), left ventricular end diastolic volume had decreased to 117 mL/m2, and left ventricular end systolic volume had decreased to 73 mL/m2. The late enhancement areas had not changed substantially (Figure 2B). However, the edema ratio had decreased to a marginally elevated 2.0 (Figure 2D), and global relative enhancement had decreased substantially to normal values (1.9, Figure 2F). Furthermore, no left or right ventricular thrombi were detectable. Holter monitoring did not record any ventricular tachycardias at follow-up.Endomyocardial biopsies and MRI investigations are suitable to identify acute myocarditis as a potentially reversible cause of a recent-onset left ventricular dysfunction and, therefore, may be helpful in deciding whether to use implantable cardioverter defibrillator implantation for primary sudden cardiac death prevention in patients with recently diagnosed nonischemic cardiomyopathy.5 Cardiac MRI is potentially useful for monitoring the natural course of cardiac inflammation noninvasively. In this respect, late enhancement may be superposed by cardiac injury processes, whereas edema ratio and, especially, global relative enhancement may reflect more specifically and sensitively the dynamics of the inflammatory process after the onset of acute myocarditis, as recently elucidated in patients with clinically suspected chronic myocarditis.6The online-only Data Supplement, consisting of Movies I and II, is available with this article at http://circ.ahajournals.org/cgi/content/full/115/13/e378/DC1.AcknowledgmentsThese investigations have been supported by the Deutsche Forschungsgemeinschaft through the Sonderforschungsbereich Trans-Regio 19 (TPZ1 to UK and HPS).DisclosuresNone.FootnotesCorrespondence to Michel Noutsias, MD, Medizinische Klinik II, Department of Cardiology and Pneumonoly, Charité–Universitätsmedizin Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, D-12200 Berlin, Germany. E-mail [email protected]References1 Noutsias M, Seeberg B, Schultheiss HP, Kuhl U. Expression of cell adhesion molecules in dilated cardiomyopathy: evidence for endothelial activation in inflammatory cardiomyopathy. Circulation. 1999; 99: 2124–2131.CrossrefMedlineGoogle Scholar2 Kuhl U, Pauschinger M, Bock T, Klingel K, Schwimmbeck CP, Seeberg B, Krautwurm L, Poller W, Schultheiss HP, Kandolf R. Parvovirus B19 infection mimicking acute myocardial infarction. Circulation. 2003; 108: 945–950.LinkGoogle Scholar3 Mahrholdt H, Goedecke C, Wagner A, Meinhardt G, Athanasiadis A, Vogelsberg H, Fritz P, Klingel K, Kandolf R, Sechtem U. Cardiovascular magnetic resonance assessment of human myocarditis: a comparison to histology and molecular pathology. Circulation. 2004; 109: 1250–1258.LinkGoogle Scholar4 Abdel-Aty H, Boye P, Zagrosek A, Wassmuth R, Kumar A, Messroghli D, Bock P, Dietz R, Friedrich MG, Schulz-Menger J. Diagnostic performance of cardiovascular magnetic resonance in patients with suspected acute myocarditis: comparison of different approaches. J Am Coll Cardiol. 2005; 45: 1815–1822.CrossrefMedlineGoogle Scholar5 Kadish A, Schaechter A, Subacius H, Thattassery E, Sanders W, Anderson KP, Dyer A, Goldberger J, Levine J. Patients with recently diagnosed nonischemic cardiomyopathy benefit from implantable cardioverter-defibrillators. J Am Coll Cardiol. 2006; 47: 2477–2482.CrossrefMedlineGoogle Scholar6 Gutberlet M, Spors B, Thoma T, Bertram H, Denecke T, Noutsias M, Schultheis HP, Kuhl U. Diagnostic accuracy of cardiac MRI in patients with clinically suspected chronic myocarditis–association with immunohistologically detected inflammation and viral persistence. Radiology. 2007 (in press).Google Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Hou Y, Han P, Wu X, Lin J, Zheng F, Lin L and Xu R (2020) Myocarditis presenting as typical acute myocardial infarction: A case report and review of the literature, World Journal of Clinical Cases, 10.12998/wjcc.v8.i2.415, 8:2, (415-424), Online publication date: 26-Jan-2020. Gutberlet M, Lücke C, Krieghoff C, Hildebrand L, Lurz P, Steiner J, Adam J, Eitel I, Thiele H, Grotthoff M and Lehmkuhl L (2013) MRT bei MyokarditisMRI for myocarditis, Der Radiologe, 10.1007/s00117-012-2385-1, 53:1, (30-37), Online publication date: 1-Jan-2013. Koepsell S, Anderson D and Radio S (2012) Parvovirus B19 is a bystander in adult myocarditis, Cardiovascular Pathology, 10.1016/j.carpath.2012.02.002, 21:6, (476-481), Online publication date: 1-Nov-2012. Noutsias M, Patil V and Maisch B (2012) Cellular immune mechanisms in myocarditisZelluläre Immunmechanismen bei Myokarditis, Herz, 10.1007/s00059-012-3700-3, 37:8, (830-835), Online publication date: 1-Dec-2012. Noutsias M, Schultheiss H and Kühl U (2010) Immunohistological diagnosis of inflammatory cardiomyopathy and diagnosis of cardiotropic viral infections Inflammatory Cardiomyopathy (DCMi), 10.1007/978-3-7643-8352-7_10, (201-225), . Gutberlet M (2010) Cardiac magnetic resonance imaging: A non-invasive approach for the detection of myocardial inflammation — Potentials and limitations Inflammatory Cardiomyopathy (DCMi), 10.1007/978-3-7643-8352-7_11, (227-235), . Gutberlet M and Thiele H (2010) Comment on: Jeserich M, Konstantinides S, Pavlik G, Bode C, Geibel A (2009) Non-invasive imaging in the diagnosis of acute viral myocarditis. Clin Res Cardiol 98:753–763, Clinical Research in Cardiology, 10.1007/s00392-010-0132-z, 99:4, (261-263), Online publication date: 1-Apr-2010. Noutsias M, Pankuweit S and Maisch B (2010) Biomarkers in Inflammatory and Noninflammatory CardiomyopathyBiomarker bei inflammatorischer und nichtinflammatorischer Kardiomyopathie, Herz, 10.1007/s00059-009-3318-2, 34:8, (614-623), Online publication date: 1-Dec-2009. Tavora F, Gonzalez-Cuyar L, Dalal J, O'Malley M, Zhao R, Peng H and Burke A (2008) Fatal parvoviral myocarditis: A case report and review of literature, Diagnostic Pathology, 10.1186/1746-1596-3-21, 3:1, Online publication date: 1-Dec-2008. Gutberlet M, Spors B, Thoma T, Bertram H, Denecke T, Felix R, Noutsias M, Schultheiss H and Kühl U (2008) Suspected Chronic Myocarditis at Cardiac MR: Diagnostic Accuracy and Association with Immunohistologically Detected Inflammation and Viral Persistence, Radiology, 10.1148/radiol.2461062179, 246:2, (401-409), Online publication date: 1-Feb-2008. April 3, 2007Vol 115, Issue 13 Advertisement Article InformationMetrics https://doi.org/10.1161/CIRCULATIONAHA.106.667360PMID: 17404165 Originally publishedApril 3, 2007 PDF download Advertisement SubjectsAcute Coronary SyndromesCardiomyopathyCatheter Ablation and Implantable Cardioverter-DefibrillatorComputerized Tomography (CT)Congenital Heart DiseaseImaging
Referência(s)