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Background: Electrocardiography is the fundamental investigation for decision making regarding thrombolytic treatment in acute myocardial infarction (MI). Increasing the accuracy of ECG analysis by input from consultant staff may assist in management decisions in patients with suspected MI., Aims: To evaluate a system whereby out of hours ECGs can be faxed to the consultant to aid in decision making regarding thrombolytic treatment., Methods: 112 patients with suspected MI were assessed on admission by the senior house officer (SHO) who faxed to a cardiology consultant the ECG trace and a predesigned form with information on: clinical assessment of the patient; interpretation of the ECG; and views regarding administration of thrombolytic treatment including choice of agent. The consultant reviewed the information and communicated his views to the SHO. Subsequent diagnosis was recorded in all patients and the forms were analysed in regard to areas of agreement and disagreement between the SHO and the consultant., Results: A diagnosis of MI was confirmed in 52 of the 112 patients (46.4%). The consultant agreed with the SHO's decision on thrombolysis in 98 patients (87.5%). The reason for disagreement in the remaining 14 patients (12.5%) was SHO misinterpretation of the ECG (10 patients) and clinical assessment (four patients). Eight patients were saved unnecessary thrombolytic treatment and four received it when they otherwise would not have. Additionally the choice of thrombolytic agent was changed in six patients from streptokinase to tissue plasminogen activator., Conclusion: The use of fax machine assists in decision making with regard to thrombolytic treatment and provides support to junior doctors in what can be a difficult, yet critical decision.

1. Opioid receptor antagonists such as naloxone have shown antiarrhythmic activity in animal models of coronary artery occlusion. Studies have indicated that these effects are stereospecific but both isomers of naloxone prolong action potential duration and refractoriness in guinea-pig and rabbit isolated ventricular myocardium (Class III effect). 2. This study was performed to identify whether this Class III effect of naloxone could be reproduced in human myocardium in vivo. Twenty patients with coronary artery disease received intravenous racemic naloxone (1-40 micrograms kg-1 min-1). Surface electrocardiographic parameters were measured and refractory periods were determined during fixed rate pacing by programmed stimulation. 3. The corrected QT interval during sinus rhythm (SR-QTc) was prolonged by 5(3)% (P = 0.06) at a dose of 20 micrograms kg-1 min-1 and by 9(10)% at 40 micrograms kg-1 min-1 (P = 0.03). These small changes were lost at higher paced heart rates. No significant effects on atrial, atrioventricular nodal or ventricular refractoriness were seen. 4. Plasma naloxone concentrations well into the micromolar range were achieved with both of the higher doses of naloxone administered. Plasma beta-endorphin concentrations invariably increased following naloxone infusion. There was no statistical relationship between peak plasma naloxone concentrations and the absolute or percent prolongation of SR-QTc. 5. It seems unlikely that racemic naloxone would have any clinical utility as an antiarrhythmic agent. Racemic naloxone may enhance cardiac adrenergic nerve activity and this receptor mediated effect may have prevented the demonstration of any nonreceptor mediated prolongation of cardiac refractoriness. Studies with the individual stereoisomers of naloxone would be of interest.

The provocation or worsening of arrhythmias by antiarrhythmic regimens was evaluated in patients with malignant ventricular arrhythmias undergoing electrophysiologic studies. In 314 patients with sustained or nonsustained ventricular tachycardia or ventricular fibrillation, 801 drug studies were performed using a standard protocol of programmed electrical stimulation. The criteria for proarrhythmia were: 1) initiation of sustained ventricular tachyarrhythmia in a patient in whom only nonsustained tachycardia was induced at baseline; 2) conversion of a sustained tachycardia that could be terminated by programmed electrical stimulation at baseline to one that required cardioversion for termination during drug therapy; 3) initiation of a sustained tachyarrhythmia by a less aggressive mode of stimulation than was required at baseline; and 4) development of spontaneous or incessant ventricular tachycardia. Proarrhythmia criterion 1 occurred during 20 (18%) of 118 studies and at least once in 15 (28%) of 54 patients. Criterion 2 was met during 39 (7%) of 578 studies and at least once in 29 (13%) of 220 patients. Criterion 3 was achieved during 135 (20%) of 687 studies in patients with sustained ventricular tachyarrhythmias at baseline. Criterion 4 occurred during 9 (1%) of 801 drug studies. In 40 patients in whom well tolerated ventricular tachycardia was initiated with fewer extrastimuli during drug study than at baseline, the drug was continued and the patients were followed up. The recurrence rate of tachycardia was the same in these patients as in 73 patients followed up on regimens on which the number of extrastimuli required for initiation was not reduced.(ABSTRACT TRUNCATED AT 250 WORDS)

When APCs are symptomatic or are a potential trigger for supraventricular tachycardia or atrial fibrillation, suppressive therapy with beta-blocking drugs or type I antiarrhythmic agents is indicated. If APCs are infrequent and produce no symptoms, attention to possible provocative factors--excess tobacco or caffeine, or drugs (eg, sympathomimetic amines, monoamine oxidase inhibitors, tricyclic antidepressants)--is all that is required.

The prognostic implications of changes in ventricular ectopic activity on serial 24 hour ambulatory electrocardiographic (Holter) recordings were prospectively evaluated in 107 patients with a history of sustained ventricular tachyarrhythmias treated with amiodarone for at least 30 days. Twenty-seven patients (25%) had insufficient ventricular ectopic activity (less than 10 ventricular premature complexes/h and no repetitive forms) on baseline Holter recordings for serial statistical analysis. In 53 (66%) of the remaining 80 patients, serial 24 hour Holter monitor recordings showed efficacy of treatment, defined as a 75% decrease in ventricular premature complexes, a 95% decrease in ventricular couplets and absence of ventricular tachycardia. During a mean follow-up period of 14.2 +/- 9.9 months, 34 (32%) of the 107 patients had recurrence of a sustained ventricular tachyarrhythmia. Holter recording correctly predicted nine recurrences and correctly identified 37 patients who did not experience a recurrence. Holter efficacy failed to predict recurrence of a sustained ventricular tachyarrhythmia in 16 patients, and 18 patients remained free of recurrence despite failure to achieve Holter efficacy. The positive predictive value of Holter monitoring efficacy was 33% and the negative predictive value was 70%; however, these differences were not statistically significant by chi-square analysis. Similar results were obtained using Holter recordings performed relatively early in therapy (6 weeks and 4 months). Of the 27 patients without significant ventricular ectopic activity on the baseline Holter recording, 9 had an arrhythmia recurrence despite continued infrequent ventricular premature complexes and no repetitive forms on subsequent recordings. The recurrence rate in this group (33%) was similar to the overall recurrence rate.(ABSTRACT TRUNCATED AT 250 WORDS)