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Postpericardiotomy syndrome: no evidence for a viral etiology

Published online by Cambridge University Press:  01 July 2011

Steven A. Webber*
Affiliation:
Division of Cardiology, Vancouver, BC, Canada
Nigel J. Wilson
Affiliation:
Division of Cardiology, Vancouver, BC, Canada
Anne K. Junker
Affiliation:
Infectious and Immunological Diseases, Department of Pediatrics, Vancouver, BC, Canada
Sean K. Byrne
Affiliation:
BC Centre for Disease Control, Vancouver, BC, Canada
Angela Perry
Affiliation:
BC Centre for Disease Control, Vancouver, BC, Canada
Eva E. Thomas
Affiliation:
Department of Pathology and Laboratory Medicine, University of British Columbia and BC Children‘s Hospital, Vancouver, BC, Canada
Laura Book
Affiliation:
Department of Pathology and Laboratory Medicine, University of British Columbia and BC Children‘s Hospital, Vancouver, BC, Canada
Marion Tipple
Affiliation:
Division of Cardiology, Vancouver, BC, Canada
Michael W H Patterson
Affiliation:
Division of Cardiology, Vancouver, BC, Canada
George G.S. Sandor
Affiliation:
Division of Cardiology, Vancouver, BC, Canada
*
Correspondence to: Dr S Webber, Division of Cardiology, Children's Hospital of Pittsburgh, 3705 5th Avenue at DeSoto Street, Pittsburgh, PA 15213. Tel: (412) 692-5541; Fax: (412) 692 6991; E-mail: webbers@heart.chp.edu

Abstract

Background: Postpericardiotomy syndrome has been considered a disorder induced by viral infection. This conclusion is based on serologic criterions, but these may be unreliable following either cardiopulmonary bypass or transfusion therapy. Previous studies have not verified the proposed etiology either by isolation of viruses, or by detection of their genome. We sought, therefore, to clarify the role, if any, of viruses in this syndrome. Methods and Results: We studied prospectively 149 children aged from 6 months to 16 years who were undergoing open heart surgery. Blood samples were collected from all prior to operation, and again 7 to 10 days post-operatively, and 47 were sampled at the time of development of symptoms of pericardial involvement. Serums were analyzed for the presence of IgM and IgG antibodies to cytomegalovirus, herpes simplex virus, and Epstein-Barr virus. The polymerase chain reaction was used for amplification when assessing the genome of the enteroviruses. Cultures for viruses were established on samples of stool, urine, and throat swabs collected 7 days post-operatively, and at the time of postpericardial symptoms. Pericardial fluid obtained from 5 patients with the syndrome was cultured for viruses, and tested for enterovirus genome. On the basis of clinical and echocardiographic findings, 34 children were determined to have definite evidence of the syndrome, 13 were considered to have possible evidence, and the results from these patients were compared to those from patients with no pericardial symptoms, the latter being matched for age and transfusion status. We isolated viruses from one or more sites in five patients with definite evidence (16%), from one (9%) of those with possible evidence, and from seven (19%) of the controls. All serums and pericardial samples were negative for enterovirus genome. IgM antibodies were found in only 5 patients, three with symptoms of pericardial involvement and two without. Rates of seroconversion to IgG for the viruses were lower in the patients with symptoms of pericardial involvement compared to controls, but were strongly influenced by transfusion status. Conclusion: Our study has provided no evidence to support a viral etiology for the postpericardiotomy syndrome.

Type
Original Articles
Copyright
Copyright © Cambridge University Press 2001

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