Parvovirus causing cardiac hypertrophy

HongDiem Nguyen, Mary Jo Rice, Peter Stenzel, Robert W. McDonald

Research output: Contribution to journalArticle

Abstract

Screening and therapy for causes of immune fetal hydrops have decreased it's incidence, making nonimmune fetal hydrops and its causes more important. From 1/80 to 6/95, 105 cases of fetal hydrops were identified (23 weeks to term). In 79 (75%), the cause was identified. There were 16 cases of immune fetal hydrops, 7 (44%) died; 15 cases had atrial tachycardia, 2 (13%) died; 7 had structural heart disease, 6 (86%) died; 5 had renal/urolgoic disease, 3 (60%) died; 4 had cytomegalovirus, 2 (50%) died; 4 had chromosomal abnormalities (1 also had significant structural heart disease), 0 died; 3 had metabolic disease, 2 (67%) died; 3 had hepatitis, 2 (67%) died; 3 had syndromes, 3 (100%) died; 2 had cystic adenomatoid malformation, 1 died; 2 had twin-twin transfusion, 1 twin died; 2 had diaphragmatic hernia, 2 died. There was one case each of fetal-maternal transfusion [alive (A)]; sacrococcygial teratoma [died (D)]; osteogenesis imperfecta (A); pulmonary arteriosclerosis (D); cystic fibrosis (A); erythrophagacytic lymphohistiocytosis (D); streptococcal sepsis (D). Three cases had unknown viral infection, 1 died. There were 26 of unknown etiology, 12 (46%) died. Three cases were found to have nuclear inclusions consistent with parvovirus at autopsy. Only 1 had been tested for parvovirus. In 2 there was significant cardiac hypertrophy both echocardiographically and at autopsy. Conclusions: 1) Fetal hydrops due to structural heart disease has a high mortality (86%) whereas mortality due to supraventricular tachycardia is low (13%); 2) Parvovirus induced anemia can lead to heart failure but parvovirus also appears to directly effect cardiac cells and their function; 3) Cardiac hypertrophy on echocardiogram may indicate the presence of parvovirus infection; 4) Parvovirus was tested for in <10% of the fetal hydrops cases.

Original languageEnglish (US)
JournalJournal of Investigative Medicine
Volume44
Issue number1
StatePublished - 1996

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Hydrops Fetalis
Parvovirus
Cardiomegaly
Heart Diseases
Autopsy
Intrauterine Blood Transfusion
Fetofetal Transfusion
Parvoviridae Infections
Intranuclear Inclusion Bodies
Osteogenesis Imperfecta
Supraventricular Tachycardia
Mortality
Arteriosclerosis
Metabolic Diseases
Teratoma
Virus Diseases
Cytomegalovirus
Screening
Tachycardia
Cystic Fibrosis

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Nguyen, H., Rice, M. J., Stenzel, P., & McDonald, R. W. (1996). Parvovirus causing cardiac hypertrophy. Journal of Investigative Medicine, 44(1).

Parvovirus causing cardiac hypertrophy. / Nguyen, HongDiem; Rice, Mary Jo; Stenzel, Peter; McDonald, Robert W.

In: Journal of Investigative Medicine, Vol. 44, No. 1, 1996.

Research output: Contribution to journalArticle

Nguyen, H, Rice, MJ, Stenzel, P & McDonald, RW 1996, 'Parvovirus causing cardiac hypertrophy', Journal of Investigative Medicine, vol. 44, no. 1.
Nguyen, HongDiem ; Rice, Mary Jo ; Stenzel, Peter ; McDonald, Robert W. / Parvovirus causing cardiac hypertrophy. In: Journal of Investigative Medicine. 1996 ; Vol. 44, No. 1.
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abstract = "Screening and therapy for causes of immune fetal hydrops have decreased it's incidence, making nonimmune fetal hydrops and its causes more important. From 1/80 to 6/95, 105 cases of fetal hydrops were identified (23 weeks to term). In 79 (75{\%}), the cause was identified. There were 16 cases of immune fetal hydrops, 7 (44{\%}) died; 15 cases had atrial tachycardia, 2 (13{\%}) died; 7 had structural heart disease, 6 (86{\%}) died; 5 had renal/urolgoic disease, 3 (60{\%}) died; 4 had cytomegalovirus, 2 (50{\%}) died; 4 had chromosomal abnormalities (1 also had significant structural heart disease), 0 died; 3 had metabolic disease, 2 (67{\%}) died; 3 had hepatitis, 2 (67{\%}) died; 3 had syndromes, 3 (100{\%}) died; 2 had cystic adenomatoid malformation, 1 died; 2 had twin-twin transfusion, 1 twin died; 2 had diaphragmatic hernia, 2 died. There was one case each of fetal-maternal transfusion [alive (A)]; sacrococcygial teratoma [died (D)]; osteogenesis imperfecta (A); pulmonary arteriosclerosis (D); cystic fibrosis (A); erythrophagacytic lymphohistiocytosis (D); streptococcal sepsis (D). Three cases had unknown viral infection, 1 died. There were 26 of unknown etiology, 12 (46{\%}) died. Three cases were found to have nuclear inclusions consistent with parvovirus at autopsy. Only 1 had been tested for parvovirus. In 2 there was significant cardiac hypertrophy both echocardiographically and at autopsy. Conclusions: 1) Fetal hydrops due to structural heart disease has a high mortality (86{\%}) whereas mortality due to supraventricular tachycardia is low (13{\%}); 2) Parvovirus induced anemia can lead to heart failure but parvovirus also appears to directly effect cardiac cells and their function; 3) Cardiac hypertrophy on echocardiogram may indicate the presence of parvovirus infection; 4) Parvovirus was tested for in <10{\%} of the fetal hydrops cases.",
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