This is a report of a case of bidirectional tachycardia in a 6-year-old girl with no evidence of any structural abnormality of the heart. The patient had never received digitalis. The arrhythmia appeared to be precipitated by effort and emotional stress, and could be induced by increasing the heart rate by atrial pacing or isoprenaline administration. His bundle electrography showed that the arrhythmia was ventricular in origin. This emphasizes the importance of recording an effort electrocardiogram in all children with unexplained syncopal episodes, even when the resting electrocardiogram is normal.

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Summary Background:  Severe hypophosphataemia associated with refeeding syndrome requires treatment with intravenous phosphate to prevent potentially life‐threatening complications. However, evidence for replacement regimens is limited and current regimens are complex and replace phosphate inadequately. Aim:  To assess the effectiveness and safety of 50 mmol intravenous phosphate infusion, given as a ‘Phosphates Polyfusor’, for the treatment of severe hypophosphataemia in refeeding syndrome. Methods:  Patients with refeeding syndrome and normal renal function received a Phosphates Polyfusor infusion for the treatment of severe hypophosphataemia (< 0.50 mmol/L). The outcome measures were serial serum phosphate, creatinine and calcium concentrations for 4 days following phosphate infusion and adverse events. Results:  Over 2 years, 30 patients were treated. Following treatment, 37% of cases had a normal serum phosphate concentration and 73% had a serum phosphate concentration of > 0.5 mmol/L within 24 h. Ten patients required more than one Phosphates Polyfusor infusion. Within 72 h, 93% of cases had achieved a serum phosphate concentration of ≥ 0.50 mmol/L. No patient developed renal failure. Three episodes of transient mild hyperphosphataemia were recorded. Four patients developed mild hypocalcaemia. Conclusions:  This is the largest published series of the use of intravenous phosphate for the treatment of severe hypophosphataemia (< 0.50 mmol/L), and is the most effective regimen described. All patients had refeeding syndrome and were managed on general wards.

Background-In acute myocardial infarction patients who do not reperfuse their infarct arteries shortly after thrombolytic treatment have a high morbidity and mortality. Management of this high risk group remains problematic, especially in centres without access to interventional cardiology. Additional thrombolytic treatment may result in reperfusion and improved left ventricular function. Methods-Failure of reperfusion was assessed non-invasively as less than 25% reduction of ST elevation in the electrocardiographic lead with maximum ST shift on a pretreatment electrocardiogram. 37 patients with acute myocardial infarction who showed electrocardiographic evidence of failed reperfusion 30 minutes after 1.5 MU streptokinase over 60 minutes were randomly allocated to receive either alteplase (tissue type plasminogen activator (rt-PA) 100 mg over three hours) (19 patients) or placebo (18 patients). 43 patients with electrocardiographic evidence of reperfusion after streptokinase acted as controls. Outcome was assessed from the Selvester Q wave score of a predischarge electrocardiogram and a nuclear gated scan for left ventricular ejection fraction 4-6 weeks after discharge. Results-Among patients in whom ST segment elevation was not reduced after streptokinase, alteplase treatment resulted in a significantly smaller electrocardiographic infarct size (14% (8%) v 20% (90%), P = 0.03) and improved left ventricular ejection fraction (44 (10%) v 34% (16%), P = 0-04) compared with placebo. This benefit was confined to patients who failed fibrinogenolysis after streptokinase (fibrinogen > 1 gIl). In patients in whom ST segment elevation was reduced after streptokinase, infarct size and left ventricular ejection fraction were not significantly different from those in patients treated with additional alteplase. Conclusion-Patients without electrocardiographic evidence of reperfusion after streptokinase may benefit from further thrombolysis with alteplase. (Br Heart 7 1995;74:348-353)

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