Human parvovirus B19 infection in infancy associated with acute and chronic lymphocytic myocarditis and high cytokine levels: report of 3 cases and review.

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.

Exertional chest pain in child due to gastroesophageal reflux with a family history of rumination.

A child affected by exertional chest pain secondary to gastroesophageal reflux (GER) disease is reported. Family history revealed the presence of rumination in two members. In our patient, heart diseases as well as other causes of chest pain were excluded. An ultrasound examination of the gastro-esophageal junction, performed in the first 15 minute of the post-prandial period, showed a pathological number of GER episodes. The patient was treated with cisapride (0.2 mg/kg t.i.d. per os). At follow-up, after three months, he was symptom-free. We repeated an ultrasound examination, which resulted normal. Ours is the first paediatric case characterized by exertional chest pain secondary to GER disease.

Altered cardiac repolarization during exercise in congenital aortic stenosis.

The incidence of sudden death in children with congenital aortic stenosis (CAS) varies between 4 and 20%. In several syndromes sudden death is associated with a long QT interval in the electrocardiogram (ECG). The aim of the study was to evaluate the cardiac repolarization in CAS during stress. We included 40 children and young persons, 20 with CAS and 20 healthy controls. All underwent echocardiographic study and treadmill stress test. The QT and relative RR intervals were measured in leads II and V6 at rest and during exercise at preselected heart rates. Mean values of QT were compared by analysis of variance, Student's t-test, and linear regression method. No statistically significant differences in the resting ECG were found between the two groups, whereas during exercise the mean QT of the CAS group was significantly longer than in the controls (p < 0.05), except at a heart rate of 140 +/- 5. Our study demonstrates that patients with CAS have transiently altered cardiac repolarization when there are sudden variations in heart rate. Such a defect could predispose patients with CAS to fatal arrhythmias and sudden death.

Lack of adverse cardiac effects of combined treatment with theophylline and albuterol in asthmatic children.

Our study was designed to assess potential cardiovascular adverse effects in clinically stable asthmatic children due either to oral sustained-release theophylline or theophylline in combination with an inhaled beta-2 adrenergic agonist. Twenty-five asthmatic children were evaluated while receiving no drugs, theophylline alone, and theophylline with an inhaled beta-2 adrenergic agonist. In each phase all patients underwent 24- to 48-hour Holter monitoring and a maximal treadmill exercise test. The results show that neither theophylline alone nor combined therapy was associated with any relevant cardiovascular adverse effect, including ectopic cardiac activity. A nonsignificant increase in mean heart rate was observed between each period of study. The data suggest that the use of theophylline either alone or in combination with a beta-2 adrenergic agonist in clinically stable asthmatic children is not associated with any serious cardiovascular effect.

Mitral valve prolapse in Turner syndrome.

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).

[Cardiac arrhythmias and mitral valve prolapse in childhood. Therapeutic considerations]. / Aritmie cardiache e prolasso della mitrale nell'infanzia. Considerazioni terapeutiche.

Our report concerns 18 cases of mitral valve prolapse, all documented by M-mode and D2-mode echocardiographic study. Of these patients three presented severe cardiac arrhythmias and therefore therapeutic treatment was necessary. One of them presented repeated episodes of paroxysmal supraventricular tachycardia and premature supraventricular and ventricular contractions. In another the arrhythmia consisted of numerous ventricular premature contractions. The third presented a sinus tachycardia which necessitated pharmacological treatment. In this study we have examined several forms of arrhythmias associated with mitral valve prolapse and discussed the antiarrhythmic therapy with quinidine, verapamil, amiodarone and propranolol. Since most people with mitral valve prolapse are young, arrhythmia suppression therapy might subject them to a course of treatment for possibly several decades. Therefore, the physician must weigh the risk of antiarrhythmic therapy against the risk of morbidity without therapy in each individual patient.

Ventricular thrombosis during permanent endocardial pacing in a pediatric patient with hemorrheological disorders.

Thrombosis in the right atrium or ventricle is a rare complication of permanent endocardial pacing in adults. To the best of our knowledge, this complication has not been previously reported at all in the pediatric age group. We report on a case of a 7-year-old boy who had large left ventricular thrombi that occurred during permanent endocardial electrical stimulation. Subsequent pulmonary emboli complicated congestive heart failure in this patient. As a diagnostic approach, echocardiography and pulmonary perfusion scintigraphy were used. We comment on possible causes of this serious complication and suggest hemorrheological and platelet activation studies in patients with permanent endocardial pacing.

Non-Ebstein concomitant dysplasia of tricuspid and mitral valves in newborns.

This paper describes 2 cases of tricuspid valvular dysplasia (TVD) associated with aortic stenosis and mitral incompetence in newborns. Mitral regurgitation was due to dysplasia, which resembles its tricuspid counterpart and should be termed 'mitral valve dysplasia'. This association of tricuspid and mitral valve dysplasia has been reported only once before. The concomitance of mitral and tricuspid incompetence is noteworthy, since mitral regurgitation can produce left heart failure and mask tricuspid valve disease.

The in vitro inhibitory effect on thrombin by 2,3-diphosphoglycerate.

Thrombin incubated with 2,3-diphosphoglycerate (150 nmol 2,3-DPG/1 NIH thrombin unit) lost up to 70% of its clotting activity, whereas the esterase activity remained unchanged. No fibrinopeptide release by thrombin was observed in the presence of 2,3-DPG. The fibrin polymerization was normal. By chromatography on Amberlite IRC-50, alpha-thrombin was eluted at pH 8.0. In presence of 2,3-DPG, alpha-thrombin was not eluted. Likely, 2,3-DPG can interfere with thrombin.

The effect of 2,3-diphosphoglycerate on oxygen consumption burst in thrombin-stimulated platelets.

2,3-Diphosphoglycerate (2,3-DPG) modifies platelet function; it diminishes aggregation and the release reaction. The hypothesis that this occurs through a modification of the intracellular level of cyclic AMP or through an alteration in the synthesis of prostaglandins has been proposed. Since the release reaction occurs simultaneously with a burst in the consumption of oxygen, the authors have studied the effect of 2,3-DPG on oxygen consumption after the addition of thrombin with or without the addition of substances which modify platelet metabolism (aspirin, theophylline, glucagon, etc.). It was observed that 2,3-DPG diminishes oxygen consumption induced by thrombin. This mechanism alters the platelet membrane function.