Prolongation Of Atrial Refractory Period Research Articles

P164 PERCUTANEOUS LEFT STELLATE GANGLION BLOCK IN REFRACTORY LEFT ATRIAL TACHYCARDIA

Abstract Percutaneous left stellate ganglion block (PLSGB) has been recently implemented for the acute treatment of refractory ventricular arrhythmias (VAs). The beneficial effect on supraventricular arrhythmias susceptibility and their ventricular response is well characterized in animal models, less so in humans. Available data suggest a significant prolongation of atrial refractory period, a reduction in inducibility and duration of atrial fibrillation and of all spontaneous intra– and postoperative atrial arrhythmias after thoracic and cardiac surgery. Here we describe a case of PLSGB for focal atrial tachycardia (AT). Case: we present a 68–year–old men with hypertension, obesity, OSAS and previous anterior myocardial infarction in the setting of a trivessel coronary disease, treated with PCI and complicated by apical aneurysm, with a LVEF of 38% and a moderate mitral and aortic regurgitation. He was on chronic antiarrhythmic therapy with bisoprolol 1.25 mg and ranolazine. He presented in the ED due to palpitations, pre–syncopal episodes, and worsening dyspnea. The ECG showed very frequent, self–limiting episodes of AT with a 1:1 atrioventricular (AV) conduction and a variable heart rate (HR) between 100 and 160 bpm, alternating with sinus rhythm at 45–50 bpm, sometimes conducted with aberrancy. Isolated and repetitive premature ventricular beats (PVB, maximum 8 beats) were also documented. Amiodarone, lidocaine, and intravenous unloading therapy were tried, without benefit. Coronary angiography was negative. PLSGB with an ultrasound–guided lateral approach (local bolus of lidocaine 100 mg+ropivacaine 20 mg) was performed, without complications, inducing palpebral ptosis. Over the next 15 hours we observed the disappearance of non–sustained VAs, the reduction of PVBs, and a progressive reduction of AT burden, of mean hourly HR (from 84 to 50 bpm, –40%) and of mean HR during AT (from 158 to 84 bpm, –47%, with AV 1:1 conduction). The patient subsequently underwent ablation of an extra systolic focus found near the ostium of the right inferior pulmonary vein, with no recurrences after 18 months. Conclusions This case highlights the potential efficacy of PLSGB in the acute treatment of supraventricular arrhythmias refractory to medical therapy. Prospective studies will help us to identify the extent, time of onset, and duration of its benefit depending on the type and mechanism of the underlying arrhythmia and the clinical characteristics of the patient.

Limitations to Activation of the Antitachycardia Burst Pacing Function of the Symbios 7008 Pacemaker in the Universal (DDD) Mode

The Symbios 7008 antitachycardia pacemaker was implanted in five patients for control of supraventricular tachycardia. Shortly after implantation in the first two patients, it was noted that the burst pacing sequence was not automatically activated by tachycardia when the pacemaker was in the DDD mode. Data from these two and the subsequent three patients were evaluated to explain this observation. The problem was primarily related to the operation of the device during the postventricular atrial refractory period. In all patients, the atrial electrogram encroached upon the programmed postventricular atrial refractory period because VA conduction during SVT was less than the lowest programmable interval (155 ms). Atrial events occurring during this interval will not trigger the tachycardia termination sequence. In all five patients, the size of the atrial electrogram decreased substantially (48 +/- 10%; mean +/- SD) during supraventricular tachycardia compared to sinus rhythm. In at least two of the five patients, decreased atrial size during supraventricular tachycardia may also have resulted in intermittent failure of atrial sensing during tachycardia, even at the most sensitive setting (0.6 mV). The latter may remain a problem even if the technical fault in SVT detection in the DDD mode were corrected. Two related problems were noted in the DDD mode: ventricular events during rapid SVT do not reset the low rate interval, resulting in random low rate pacing; and, automatic prolongation of atrial refractory period by two successive ventricular events without an intervening atrial sensed event compounds problems of atrial sensing. All of these problems were easily circumvented in all patients by noninvasive reprogramming to the DVI mode in which supraventricular tachycardia detection is based on ventricular sensing. These findings have implications for the future design of such devices.

Dose-dependent electrophysiologic effects of amiodarone in the immature canine heart

The electrophysiologic effects of incremental doses of intravenous amiodarone were studied in the intact neonatal canine heart and were compared with the responses observed in the adult. Seven neonatal puppies aged 5 to 14 days, and 6 adult dogs were studied. Assessment of sinus and atrioventricular (AV) nodal function and atrial and ventricular refractory periods was performed using standard His bundle recording techniques and programmed extrastimulation before and after doses of 2.5, 5 and 10 mg/kg of intravenous amiodarone. Amiodarone depressed sinus node cycle length, sinus node recovery time and AV nodal conduction in both groups. Atrial and ventricular refractory periods were also prolonged in a dose-dependent fashion in both the neonatal and adult dogs. Although similar responses to amiodarone were observed in both groups, the immature dogs were more sensitive to amiodarone in prolongation of atrial refractory periods and depression of sinus node recovery time. The neonatal group, however, demonstrated more resistance to amiodarone-induced depression of AV nodal conduction. Thus, intravenous amiodarone produces dose-dependent electrophysiologic changes in the neonate similar to those in the adult, although the significant differences in drug sensitivity may be clinically important.

Effects of prindolol on impulse formation and conduction in man

Electrophysiologic changes produced by intravenous administration of 0.6 mg Prindolol were studied in 16 subjects with normal impulse formation and conduction. The most important changes were: sinus bradycardia, prolongation of atrial refractory periods, depression of intranodal conduction and prolongation of A-V node refractory periods. Sinus node recovery time was unchanged, and sinoatrial conduction time was only slightly increased. Intraventricular conduction time and the refractory period of the His-Purkinje system and of the bundle branches were unchanged.