Case StudiesFatal parvovirus B19–associated myocarditis clinically mimicking ischemic heart disease: An endothelial cell–mediated disease☆,☆☆,★
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).
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)
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B. D. Bültmann and K. Klingel contributed equally to this study and thus share first authorship.
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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.
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Address correspondence and reprint requests to Burkhard D. Bültmann, MD, Institute of Pathology, University of Tübingen, Liebermeisterstrasse 8, D-72076 Tübingen, Germany.