Myocardial calcium overload was observed in a patient with giant cell myocarditis. The myocardial calcium content estimated by atomic absorption spectrophotometry amounted to 120 mEq/kg dry weight, and the von Kossa stain disclosed multiple foci with patchy calcifications of myocardial fibres. Cytochemical examination of the ultrastructural calcium localisation using the phosphate-pyroantimonate method showed considerable variation in the subcellular calcium distribution. In normal myocytes calcium precipitates were confined to the inner leaflet of the sarcolemma, T-tubules, intercalated disks, and sporadically to mitochondria. In contrast, extensive calcification of mitochondria and loss of sarcolemmal calcium was evident in necrotic myocytes. A number of grossly normal myocytes also showed an increase of calcium precipitates in slightly swollen mitochondria.These findings suggest that myocardial calcium overload in this case started in viable myocytes and was not merely a secondary phenomenon occurring after cell death.
ABSTRACT. Severe adenoviral infections such as the necrotizing adenovirus bronchiolitis occur sporadically in infants. Ascertaining the etiologic role of adenovirus in cases of lung disease can pose a diagnostic problem. We present two cases of severe bronchiolitis in previously healthy children in which adenovirus could be shown to be the causing agent. Both children received immunosuppressive therapy with steroids and Cyclosporin for 3 mo and a course of intravenous Ribavirin for 10 d. The results were conflicting: despite therapy Patient 1 died due to respiratory failure, Patient 2 improved notably. Conclusions: Adenovirus can cause severe bronchiolitis in previously healthy children. Diagnosis may be difficult to achieve. The role of antiviral therapy in the treatment of adenoviral infections remains to be cleared. □Adenovirus, bronchiolitis
This retrospective study was performed to determine the influence of multi-organ dysfunction and the type of preoperative hemodynamic support on mortality after heart transplantation. All patients undergoing heart transplantation during a 6 year period were divided into 3 groups: group A patients (n = 110) had stable hemodynamics on oral medication, group B recipients (n = 41) received continuous i.v. catecholamine application, and in group C (n = 21) mechanical hemodynamic support was necessary. In groups B and C elevated serum creatinine and transaminase levels-reflecting renal and hepatic dysfunction-were detected more often and the survival rate was worse during the first six months (A: 85%, B: 71%, C: 52%, p < 0.01). In group C the prognosis of patients with multi-organ dysfunction was significantly worse compared to patients with normal renal and hepatic function (38% vs. 75%; p < 0.01). In recipients surviving for six months, there was no difference in long-term prognosis between the groups studied. It is concluded that heart transplantation in patients with multi-organ dysfunction on invasive hemodynamic support bears a significantly increased risk in the early postoperative period. In view of the current donor shortage the condition of other organs should be improved before transplantation as far as possible, even using long-term mechanical support.
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