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Unlabelled: Perioperative malignant ventricular tachyarrhythmias pose an imminent clinical danger by potentially precipitating myocardial ischemia and severely compromising hemodynamics. Thus, immediate and effective therapy is required, which is not always provided by currently recommended IV drug regimens, indicating a need for more effective drugs. We examined antiarrhythmic effects of the new benzofurane compound E 047/1 on spontaneous ventricular tachyarrhythmia in a conscious dog model. One day after experimental myocardial infarction, 40 dogs exhibiting tachyarrhythmia randomly received (bolus plus 1-h infusion) E 047/1 6 mg/kg plus 6 mg x kg(-1) x h(-1), lidocaine 1 mg/kg plus 4.8 mg x kg(-1) x h(-1), flecainide 1 mg/kg plus 0.05 mg x kg(-1) x h(-1), amiodarone 10 mg/kg plus 1.8 mg x kg(-1) x h(-1), or bretylium 10 mg/kg plus 20 mg x kg(-1) x h(-1). Electrocardiogram was evaluated for number of premature ventricular contractions (PVC), normally conducted beats originating from the sinoatrial node, and episodes of ventricular tachycardia. Immediately after the bolus, E 047/1 reduced PVCs by 46% and increased sinoatrial beats from 4 to 61 bpm. The ratio of PVCs to total beats decreased from 98% to 58%. Amiodarone and flecainide exhibited antiarrhythmic effects with delayed onset. Lidocaine did not suppress PVCs significantly, and bretylium was proarrhythmic. The antiarrhythmic E 047/1 has desirable features, suppressing ischemia-induced ventricular tachyarrhythmia quickly and efficiently, and may be a useful addition to current therapeutic regimens., Implications: Life-threatening arrhythmias of the heart after myocardial infarction or ischemia may be treated quickly and efficiently by the new drug E 047/1.

Background: Although desflurane (DES) and sevoflurane (SEV) have desirable features for use in patients with coronary artery disease, their effects on ventricular dysrhythmias following infarction are less known. We therefore examined the effects of DES and SEV upon spontaneous postinfarction ventricular dysrhythmias in dogs, and compared those effects to the well-established antidysrhythmic effects of halothane (HAL) in this model., Methods: After institutional approval, the left anterior descending coronary artery was ligated in 16 adult mongrel dogs during isoflurane anesthesia. All dogs developed acute myocardial infarction and severe ventricular tachydysrhythmias. Twenty-two hours after infarction, dogs were anesthetized at 1.5 MAC with desflurane (10.8%) followed by sevoflurane (3.5%) in the treatment group (n = 10), or halothane (1.3%) in the other group (n = 6). Anesthetic gases were allowed to equilibrate for at least 20 min at each end-tidal concentration. At this time, the ECG was recorded for 9 min and evaluated for the number of ventricular ectopic and sinoatrial beats and summed duration of ventricular tachycardia., Results: DES and SEV reduced the average rate of total ventricular ectopic beats by 40 +/- 4% and 42 +/- 4%, respectively. HAL decreased total ventricular ectopic rate by 59 +/- 6% and 62 +/- 5% after durations of anesthesia comparable to DES and SEV, respectively. Decreases in dysrhythmia in the presence of DES and SEV were significantly smaller than those produced by HAL after a comparable total duration of anesthesia., Conclusion: DES and SEV inhibit spontaneous postinfarction ventricular dysrhythmias, although attenuation of dysrhythmias was smaller than the inhibition during comparable doses of HAL.

Background and Objectives: Sympathetic neural activity contributes to the genesis of ventricular ectopic activity, particularly in the setting of myocardial ischemia and infarction, so thoracic epidural anesthesia should diminish ventricular ectopy by blocking sympathetic innervation of the heart. However, the possible antidysrhythmic effect of epidural anesthesia has been studied only in the presence of general anesthesia. We therefore examined changes in spontaneous postinfarction ventricular dysrhythmia during thoracic epidural anesthesia in awake dogs., Methods: A survivable myocardial infarction was created by two-stage ligation of the left anterior descending coronary artery. The following day, multifocal idioventricular tachycardia was the predominant cardiac rhythm. Lidocaine was administered either by thoracic epidural catheter to achieve block of at least the first five thoracic segments or intravenously as a control for direct effects, without concurrent general anesthesia or sedation. Electrocardiographic recordings were analyzed for the number of ventricular ectopic and sinoatrial depolarizations., Results: Epidural and intravenous administration both produced plasma lidocaine concentrations of about 2 mg/mL. There was no change in rhythm following intravenous lidocaine. During epidural anesthesia, total ectopic beats per minute decreased from 167 +/- 8 to 135 +/- 14 (mean +/- SE, P < .05), and the dysrhythmic ratio (ventricular beats/total beats) decreased from 0.93 +/- 0.03 to 0.81 +/- 0.08 (P < .05). However, ventricular tachydysrhythmia remained the predominant rhythm., Conclusions: Epidural block modestly reduces spontaneous ventricular dysrhythmia in a perioperative setting in dogs following a large myocardial infarction. These findings do not support the choice of thoracic epidural anesthesia for the purpose of preventing or decreasing severe ventricular dysrhythmia.