Human parvovirus B19 infection is occasionally associated with acute lymphocytic myocarditis (ALM). Three infants with B19 virus-associated ALM were followed up clinically, histologically, and immunovirologically. Each infant had B19 virus DNA in the blood or B19 virus-specific IgM antibodies. Two infants with postnatal infection recovered after immunosuppressive therapy. The third infant with possible prenatal infection developed chronic persistent myocarditis associated with persistent B19 virus DNA in the blood. All 3 infants had increased levels of interferon-gamma, tumor necrosis factor-alpha, and interleukins -6 and -8. Four newborns with congenital B19 virus infection and 4 infants and children who had postnatally acquired B19 virus infection without myocarditis all had normal levels of these cytokines. These observations suggest that B19 virus infection in infancy causes ALM in some infants and children.

We have evaluated 46 patients with Turner syndrome by clinical examination, M-mode and two-dimensional echocardiography, dynamic exercise testing and 24 h Holter monitoring. Twelve patients (26.1%) had mitral valve prolapse and 7 patients (15.2%) had isolated non stenotic bicuspid aortic valve. Aortic root dilation was present in 2 patients (4.3%). Our data indicate that incidence of mitral valve prolapse is significantly higher in Turner syndrome than in the general population (P less than 0.025).

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