CIED procedures that utilized an antibacterial envelope had a high rate of CIED implantation success (>99%). Although the follow-up to date is short, there was also a low rate of infection (<0.50%) in this population at high risk for CIED infection.

TO DEFIBRILLATE or cardiovert, passage of sufficient electrical current through the heart must occur. 1-3 However, the optimal currents for the termination of various arrhythmias have not previously been defined. In traditional clinical practice, the operator selects an energy arbitrarily; the American Heart Association at present recommends an initial shock energy of 200 J to terminate ventricular fibrillation.4 However, the actual current flow is determined not only by the selected energy but also by the transthoracic impedance. If the transthoracic impedance is high, low 1038energy may generate inadequate current to achieve defibrillation. For example, we previously found that defibrillation was achieved by only 20% of 100 J shocks given to patients with very high ( > 97 Q) transthoracic impedance, as opposed to a 70% success rate of 100 J shocks given to patients with low or average impedance.5 Although this problem could be overcome by selecting higher shock energies, excessive energy and current may cause morphologic and functional damage.6-9 Thus, low energies and current, when appropriate, are preferable. In view of these considerations, a reasonable first approach would be to base energy selection on transthoracic impedance: a relatively low energy, 100 J, should achieve defibrillation or cardioversion in most patients with low impedance, whereas higher energies, 200 J or more, are needed for high-impedance patients. We therefore devised an impedance-based energy

Although transient increases in heart rate typically occur, bradycardia has infrequently been noted in association with partial seizures. Five patients with temporal lobe epilepsy are described in whom sinus bradyarrhythmias and syncope were prominent manifestations of seizure activity. Partial improvement occurred in one of two patients in whom a permanent pacemaker was implanted before a diagnosis of epilepsy was established. Treatment with phenytoin or carbamazepine resulted in nearly complete resolution of symptoms in all five patients. Because pacemaker implantation does not prevent recurrent symptoms, but anticonvulsant therapy does, this experience underscores the importance of considering the diagnosis of partial epilepsy in selected patients with sinus bradyarrhythmias and syncope.

The purpose of this study was to determine the effect of the antiarrhythmic drugs lidocaine and bretylium on the minimal energy requirement for transthoracic defibrillation--the defibrillation threshold. Closed chest dogs were anesthetized with chloralose or pentobarbital; lidocaine was administered at varying rates for 2 hours and defibrillation threshold periodically redetermined. Similar protocols were followed for bretylium. Serum lidocaine levels from therapeutic to toxic ranges were obtained, and up to a 60% (p less than 0.05) increase in defibrillation threshold in the pentobarbital-anesthetized dogs was demonstrated. In chloralose-anesthetized dogs the lidocaine effect was modest, with only a 10 to 20% rise in defibrillation threshold (p = NS) despite similar increases in serum lidocaine levels. Thus, lidocaine increases the minimal energy requirements for transthoracic defibrillation, but this effect is in part anesthesia-related, indicating a lidocaine-pentobarbital interaction. When phentolamine was administered to chloralose-anesthetized dogs receiving lidocaine, defibrillation threshold rose 13% (p less than 0.05); this suggests that alpha-adrenergic receptor blockade is at least in part the mechanism of the pentobarbital-lidocaine interaction on defibrillation threshold. Bretylium with either anesthetic had no significant effect on defibrillation threshold.

Thirty-one patients with nonischemic dilated cardiomyopathy either idiopathic or due to regurgitant valvular disease were studied in the cardiac electrophysiology lab. The indications for study were sustained ventricular tachycardia (VT) in 16, ventricular fibrillation (VF) in 11, and syncope of unknown etiology in 4. Sustained VT was reproducibly induced in 17 patients, including 12 with a history of sustained VT, 2 with VF and 3 with syncope. Of 15 patients undergoing serial antiarrhythmic drug studies, sustained VT was rendered noninducible or nonsustained in 13. Three had recurrent arrhythmic events while on therapy predicted to be effective. One of 2 patients discharged on a regimen predicted to be ineffective had a recurrence of sustained VT that resulted in cardiac arrest. Of 14 patients in whom sustained VT could not be reproducibly induced, 2 subsequently had spontaneous occurrences of sustained VT, and 2 experienced aborted sudden death. These results suggest the following: (1) the induction of sustained VT in the setting of nonischemic dilated cardiomyopathy is dependent on the clinical presentation; (2) antiarrhythmic drugs frequently render sustained VT noninducible or nonsustained; (3) antiarrhythmic drug suppression of inducible sustained VT predicts long-term prevention of spontaneous recurrences; and (4) noninducibility of sustained VT in the baseline state does not predict freedom from subsequent episodes of VT or sudden death.

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The purpose of this study was to test the hypothesis that orthostatic stress shortens the right ventricular effective refractory period by reflex activation of beta-adrenergic receptors. Twelve patients undergoing electrophysiologic testing for standard clinical indications were studied. After a full electrophysiologic study, patients underwent graded lower body negative pressure before and after administration of either propranolol (0.2 mg/kg intravenously) in Group I or atropine (0.035 mg/kg intravenously) in Group II. Before the addition of drugs, lower body negative pressure produced decreases in systolic blood pressure and significant increases in sinus rate. The effective refractory period shortened from 214 +/- 8 (mean +/- SEM) to 206 +/- 7 ms at -40 cm H2O and to 197 +/- 4 ms at -60 cm H2O lower body negative pressure. After propranolol, Group I patients had no change in right ventricular effective refractory period despite similar changes in sinus rate and systolic blood pressure. In group II patients, atropine did not alter effective refractory period responses to lower body negative pressure. Thus, reflex adjustments to orthostatic stress result in shortening of right ventricular effective refractory period mediated by way of beta-adrenergic mechanisms. These findings constitute the first evidence that sympathetic influences mobilized by the body can directly modulate ventricular electrophysiologic changes.