We describe the case of a 42-year-old woman developing cardiogenic shock with cardiac tamponade due to an acute myo-pericarditis caused by Parvovirus B19 (PVB19), successfully treated with intravenous (iv) immunoglobulin administration

Alberto Margonato

Carlo Ballarotto

Gabriele Fragasso

Luca Alberti

Marco Loffi

Roberto Spoladore

Case Reports in Cardiology

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We describe the case of a 42-year-old woman developing cardiogenic shock with cardiac tamponade due to an acute myo-pericarditis caused by Parvovirus B19 (PVB19), successfully treated with intravenous (iv) immunoglobulin administration.</jats:p

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Hindawi Publishing CorporationCase Reports in CardiologyVolume 2012, Article ID 180871, 2 pagesdoi:10.1155/2012/180871Case ReportAcute Heart Failure Caused by Parvovirus B-19 MyocarditisTreated with Human ImmunoglobulinLuca Alberti,1 Marco Loffi,2 Gabriele Fragasso,1 Roberto Spoladore,2Carlo Ballarotto,2 and Alberto Margonato1, 21 Heart Failure Unit, Ospedale San Raﬀaele, Via Olgettina 60, 20132 Milano, Italy2 Coronary Care Unit, Ospedale San Raﬀaele, Via Olgettina 60, 20132 Milano, ItalyCorrespondence should be addressed to Roberto Spoladore, spoladore.roberto@hsr.itReceived 4 April 2012; Accepted 26 June 2012Academic Editors: M. Barros and K.-R. ChiouCopyright © 2012 Luca Alberti et al. This is an open access article distributed under the Creative Commons Attribution License,which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.We describe the case of a 42-year-old woman developing cardiogenic shock with cardiac tamponade due to an acute myo-pericarditis caused by Parvovirus B19 (PVB19), successfully treated with intravenous (iv) immunoglobulin administration.1. Case ReportA 42-year-old healthy woman went to the emergency depart-ment after a malaise episode with fever, abdominal pain, andvomiting for few days. Past medical history was silent with nocardiovascular risk factors. Physical examination revealed ablood pressure (BP) of 70/50mmHg, heart rate was 90 bpm,temperature 37.5◦C, Sat O2 98%.Cardiopulmonary examination was normal, withoutany additional sounds, murmurs, or pericardial rub andany pulmonary crackles. There was also neither jugularturgor nor peripheral oedemas. The ECG performed inthe emergency department showed sinus tachycardia withdiﬀuse low voltages.Laboratory investigations revealed high levels of whiteblood cell (WBC) count 18200/mm3, C-reactive protein(CRP) 2.93mg/dL, haemoglobin 10.8, INR 1.3, and anti-thrombin III 57%. The first set of cardiac enzymes waselevated CKMB 7,3 and Troponin-T1.13. Haemogas analysisshowed metabolic acidosis pattern with severe hypoxia (pH7.31, pCO2 42, pO2 33, HCO3− 21, BE 5). At chest X-ray nei-ther, signs of pleural eﬀusion nor lung consolidations werepresent. Transthoracic echocardiography showed a moderatepericardial eﬀusion, left ventricular hypokinesis with ejec-tion fraction of 35%. Abdominal ultrasound scan revealed nofree fluid or biliary tract dilatation. There was a rapid wors-ening of clinical conditions complicated by cardiac arrest,which was successfully treated by cardiopulmonary resusci-tation procedures. Dopamine at 10 µg/Kg/min was started.A chest computerized tomography scan (CT) excluded pul-monary thromboembolism and an abdominal CT excludedsources of haemorrhage. Another hypotensive episodewith bradycardia occurred, epinephrine 0,25 µg/kg/min wasintroduced and dopamine was reduced to 4,5 µg/Kg/min.The patient was then transferred to our post cardiac surgeryintensive care unit. On physical examination performed atadmission, her BP was 90/60, despite inotropic support withepinephrine and dopamine; the heart rate was 130 bpm andon ECG tracing several run of atrial fibrillation with elevatedventricular response were registered. Central venous pressure(CVP) was 20mmHg. Haemogas analysis showed metabolicacidosis pattern. A laboratory investigation revealed thefollowing data: WBC 23700/µL; CRP 37.7mg/dL; glucose302mg/dL; N-terminal-pro brain natriuretic peptide (NT-proBNP) 12650 pg/mL: troponin-T 0.082. Transthoracic andtransesophageal echocardiographies were performed withevidence of biventricular failure (EF < 20%, TAPSE 10);2 cm pericardial eﬀusion with initial signs of tamponade(complete right atrium and partial right ventricle collapse);moderate mitral regurgitation: mild tricuspidalic regur-gitation. Epinephrine was increased to 0.3 µg/kg/min. Apericardiocentesis was performed, but drainage of 150mL ofsierous, citrine liquid resulted only in partial improvementin global systolic function (EF 25%, BP 70/40mmHg,2 Case Reports in CardiologyCVP 8mmHg, wedge pressure 15mmHg, PAPs 30mmHg).Dopamine was stopped and the patient was transferred toCardiac Cath Lab where coronarography showed normalcoronary vessels. Subsequently, an endomyocardial biopsywas performed showing, by the PCR analysis, positivityfor Parvovirus B19 genome at high title (1200UL/mL).The histological and immunohistochemistry analysis ofmyocardial tissue revealed focal myocytes vacuolization,mild fibrosis, and moderate lymphocytes infiltrate bothT (CD3+), and B (CD20+), rare plasma-cells (CD138+)and macrophage monocytes (CD68+). The histologicalpattern was reliable with myocarditis. Intra-aortic balloonpump (IABP) was placed with modest improvement inmean arterial blood pressure (88mmHg). According to theendomyocardial biopsy results, i.v. high doses pentaglobulintreatment was started. Some hours after IABP placement andimmunoglobulins administration, transthoracic echocardio-graphy showed improvement in biventricular contractilefunction (cardiac index 2.4mL/min·m2). Another pericar-diocentesis was performed and 180mL of sierohaematic liq-uid was drained. The following day, epinephrine was reducedto 0.16 µg/kg/min and norepinephrine 0.05 µg/kg/min wasintroduced. Myocardial systolic function gradually improved(EF 55–60%, cardiac index 3.5mL/min·m2). Epinephrineand norepinephrine dosage was gradually reduced and thenstopped. IABP was then removed. Clinical conditions werestable so the patient was extubated and transferred tocoronary intensive care unit. On clinical examination atadmission, her BP was 135/85mmHg with sinus tachycardia(135 bpm).Laboratory investigations showed an increase of WBCcount of 44000/mm3 (94% neutrophils), haemoglobin 9.2,platelet count of 85000/mm3, CK-MB 7575 (MB 66),troponin-T 0.155, LDH 549, NT-proBNP 24000. Completeautoantibodies screening (ANA, aDNA, SSA, SSB, SM, RNP,Scl70, Jo-1) was performed but revealed no evidence of anyautoimmune disorders; a screening for common pathogensinvolved in myocarditis was performed too. There were notantibodies anticoxsackie or echo virus. Polymerase chainreaction (PCR) was made on plasma samples looking forthe genome of: EBV, CMV, HSV 1, HSV 2, HHV 6,adenovirus, enterovirus, echovirus with negative results. Ahigh title (>1 : 40) of IgM antiparvovirus B19 was found.Haemocultures and pericardial fluid cultures did not showany growth. In the following days, there was reduction of car-diac and inflammatory enzymes. Echocardiography showednormal systolic left and right ventricular function, moderatetricuspid regurgitation, PAPs of 35mmHg, no pericardialfluid. Rate control therapy was started with bisoprolol1.25mg qd. Normalization of cardiac and inflammatoryenzymes was observed, the patient gradually recovered andshe was discharged from our hospital.2. DiscussionThis case illustrates PVB19-induced myopericarditis leadingto severe cardiac dysfunction. Parvovirus B19 infection couldlead to direct myocardial injury, and could trigger a severeautoimmune reaction of the myocardium [1]. Myocarditisis an inflammatory disease with a variable natural history,ranging from spontaneous recovery, subclinical course withevolution to dilated cardiomyopathy (DCM) or early deathfrom multisystem failure [2, 3]. The progression to DCMcan result from both direct viral-mediated damage orsecondary autoimmune-mediated myocardial injury [4].This secondary autoimmunity is induced by molecularmimicry, inducing cross-reaction between antiviral anti-bodies with autoantigen-binding properties, a phenomenondemonstrated also in parvovirus B19 myocardial infections[5, 6]. In a previous study by Dennert et al., I was shownhow immunoglobulin therapy in addition to conventionalheart failure therapy is able to improve cardiac function inpatients with chronic dilated cardiomyopathy (DCM) anda significant PVB19 viral load in the heart [7]. Based onthese evidences, we tried to perform the same treatmentmodality obtaining an early improvement in left ventricularperformance. The peculiarity of this case is the eﬀectivenessof immunoglobulin administration in the acute phase ofheart failure. According to this result, it is now time tointensify the diagnostic tools in order to get an earlyetiologic diagnosis of myocarditis and to perform dedicatedtreatment options that could promptly restore an acutecardiac impairment, blocking the possible evolution towardsend-stage forms of dilated cardiomyopathy.References[1] C. T. Bock, K. Klingel, and R. Kandolf, “Human parvovirusB19-associated myocarditis,” New England Journal of Medicine,vol. 362, no. 13, pp. 1248–1249, 2010.[2] H. T. Aretz, M. E. Billingham, W. D. Edwards et al., “Myo-carditis. A histopathologic definition and classification,” TheAmerican Journal of Cardiovascular Pathology, vol. 1, no. 1, pp.3–14, 1987.[3] E. B. Lieberman, G. M. Hutchins, A. Herskowitz, N. R. Rose,and K. L. Baughman, “Clinicopathologic description of myo-carditis,” Journal of the American College of Cardiology, vol. 18,no. 7, pp. 1617–1626, 1991.[4] M. Afanasyeva, D. Georgakopoulos, and N. R. Rose, “Autoim-mune myocarditis: cellular mediators of cardiac dysfunction,”Autoimmunity Reviews, vol. 3, no. 7-8, pp. 476–486, 2004.[5] C. Lunardi, E. Tinazzi, C. Bason, M. Dolcino, R. Corrocher, andA. Puccetti, “Human parvovirus B19 infection and autoimmu-nity,” Autoimmunity Reviews, vol. 8, no. 2, pp. 116–120, 2008.[6] U. Ku¨hl, M. Pauschinger, B. Seeberg et al., “Viral persistencein the myocardium is associated with progressive cardiacdysfunction,” Circulation, vol. 112, no. 13, pp. 1965–1970, 2005.[7] R. Dennert, S. Velthuis, S. Schalla et al., “Intravenous imm-unoglobulin therapy for patients with idiopathic cardiomyopa-thy and endomyocardial biopsy-proven high PVB19 viral load,”Antiviral Therapy, vol. 15, no. 2, pp. 193–201, 2010.Submit your manuscripts athttp://www.hindawi.comStem CellsInternationalHindawi Publishing Corporationhttp://www.hindawi.com Volume 2014Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014MEDIATORSINFLAMMATIONofHindawi Publishing Corporationhttp://www.hindawi.com Volume 2014Behavioural NeurologyEndocrinologyInternational Journal ofHindawi Publishing Corporationhttp://www.hindawi.com Volume 2014Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014Disease MarkersHindawi Publishing Corporationhttp://www.hindawi.com Volume 2014BioMed Research InternationalOncologyJournal ofHindawi Publishing Corporationhttp://www.hindawi.com Volume 2014Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014Oxidative Medicine and Cellular LongevityHindawi Publishing Corporationhttp://www.hindawi.com Volume 2014PPAR ResearchThe Scientific World JournalHindawi Publishing Corporation http://www.hindawi.com Volume 2014Immunology ResearchHindawi Publishing Corporationhttp://www.hindawi.com Volume 2014Journal ofObesityJournal ofHindawi Publishing Corporationhttp://www.hindawi.com Volume 2014Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014 Computational and  Mathematical Methods in MedicineOphthalmologyJournal ofHindawi Publishing Corporationhttp://www.hindawi.com Volume 2014Diabetes ResearchJournal ofHindawi Publishing Corporationhttp://www.hindawi.com Volume 2014Hindawi Publishing Corporationhttp://www.hindawi.com Volume 2014Research and TreatmentAIDSHindawi Publishing Corporationhttp://www.hindawi.com Volume 2014Gastroenterology Research and PracticeHindawi Publishing Corporationhttp://www.hindawi.com Volume 2014Parkinson’s DiseaseEvidence-Based Complementary and Alternative MedicineVolume 2014Hindawi Publishing Corporationhttp://www.hindawi.com

Acute Heart Failure Caused by Parvovirus B-19 Myocarditis Treated with Human Immunoglobulin

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Acute Heart Failure Caused by Parvovirus B-19 Myocarditis Treated with Human Immunoglobulin

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