Elsevier

Human Pathology

Volume 34, Issue 1, January 2003, Pages 92-95
Human Pathology

Case Studies
Fatal parvovirus B19–associated myocarditis clinically mimicking ischemic heart disease: An endothelial cell–mediated disease,☆☆,

https://doi.org/10.1053/hupa.2003.48Get rights and content

Abstract

We report the case of a 34-year-old female patient who died 4 days after hospital admission of acute heart failure clinically mimicking ischemic heart disease. Microscopic examination of the heart showed severe myocarditis. Polymerase chain reaction (PCR), including quantitative real-time PCR, disclosed exclusively parvovirus B19 (PVB19), with a high viral load of 4.3×105 PVB19 viral genome equivalents per μg myocardial nucleic acid. Radioactive in situ hybridization detected viral genomes in endothelial cells (ECs) predominantly in the venular compartment and (to a lesser degree) in small arteries and arterioles of the heart, but not in cardiac myocytes or other tissue components. Concomitant with EC infection, marked expression of the adhesion molecule E-selectin was noted, accompanied by margination, adherence, penetration, and perivascular infiltration of T lymphocytes. We speculate that, due to the high viral load in cardiac ECs, PVB19 infection of endothelial cells was sufficient to induce impaired coronary microcirculation with secondary cardiac myocyte necrosis. HUM PATHOL 34:92-95. Copyright 2003, Elsevier Science (USA). All rights reserved.

Section snippets

Case report

A previously healthy, immunocompetent 34-year-old woman presented 4 days before her death with unexplained chest pain. One day later, on admission to the hospital, an electrocardiogram (ECG) showed ST segment elevation in lead aVL and depressed ST and T segments in leads II, III, aVF, and V4-6, findings suspicious of myocardial infarction. Coronary angiography disclosed no signs of coronary heart disease or thrombosis. Within 3 days, the patient's troponin I level increased from 4.4 μg/L to 70

Immunohistology

Immunostaining was performed with avidin-biotin complex using peroxidase and/or alkaline phosphatase for double labeling with antibodies against CD3, CD62E (E-selectin, clone 16G4), CD62P (P-selectin, clone C34), PVB19 (clone R92F6) (Novocastra, Newcastle, U.K.), CD20, C3, C1q, PGM1, and SM-actin (Dako, Hamburg, Germany). Control tissue was taken from hearts explanted from patients suffering from end-stage dilated cardiomyopathy.

Polymerase chain reaction and reverse transcription- polymerase chain reaction

DNA and RNA were extracted simultaneously from deparaffinized

Results

Light microscopy examination of the heart revealed active myocarditis with randomly distributed small foci of myocyte necrosis infiltrated by macrophages and surrounded by T lymphocytes, involving about 20% of the myocardium (Fig 1A).

. (A) Areas of myocardial necrosis infiltrated by PGM1-positive macrophages (brown). Interstitial inflammation is dominated by CD3-positive T lymphocytes (red) (original magnification ×200). (B) Marked dilatation of intramyocardial SM-actin–positive small veins and

Discussion

Three target cells for PVB19 infection have been identified: erythroid precursor cells, fetal cardiac myocytes, and ECs, providing that they express the blood-group P-antigen, which serves as the cellular receptor for PVB19.9 In our patient, ISH revealed the presence of PVB19 genomes exclusively in ECs of the microcirculatory periphery and not in cardiac myocytes or other tissue components. Immunohistochemical staining with monoclonal antibodies to detect VP1 and VP2-PVB19 viral capsid proteins

Acknowledgements

The authors thank A. Mall for her skillful technical assistance with the immunohistochemical staining procedures.

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Cited by (0)

B. D. Bültmann and K. Klingel contributed equally to this study and thus share first authorship.

☆☆

Supported in part by grants from the Federal Ministry of Education and Research (Fö 01KS9602) and the Interdisciplinary Center of Clinical Research Tübingen (IZKF) awarded to K.K.

Address correspondence and reprint requests to Burkhard D. Bültmann, MD, Institute of Pathology, University of Tübingen, Liebermeisterstrasse 8, D-72076 Tübingen, Germany.

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