Nonsurgical Electrical Ablation of Tachycardias: Importance of Prior in Vitro Testing of Catheter Leads

Nonsurgical electrical ablation of tachycardia pathways or foci has been attempted or carried out using a variety of temporary pacing catheter leads. To determine the ability of such leads to withstand the high energies used in such procedures, 34 leads were suspended in saline, and subjected to repeated electrical shocks. Small (4 French) temporary pacing leads made by a variety of manufacturers tolerated multiple shocks up to 100 joules; above this level, failures became increasingly common, although usually the failure mode was benign with respect to patient care implications. Testing of 6, 7, and 8 French leads revealed considerable inter-and intra-manufacturer differences in the ability to withstand higher energy shocks, reflecting differences in materials and fabrication techniques. It is concluded that careful in vitro lead testing is required prior to using identical models in humans for arrhythmia ablation procedures.     

Morphogenesis and Regulation of Bergmann Glial Processes During Purkinje Cell Dendritic Spine Ensheathment and Synaptogenesis

星形胶质细胞在突触形成中发挥重要作用,但星形胶质细胞突起如何在发育过程中与突触结构相联系还不是很清楚。本文分析在小脑突触发生过程中Bergmann胶质细胞(BG)突起生长的类型。本文发现在这个过程中,BG突起向外生长与树突棘增多的包被作用相关。此外,双光子时间分辩显像显示BG突起是高度动态的,在棘包被过程中突起趋于稳定。虽然突触活力依赖于肌动蛋白的聚合作用,但细胞骨架调节器Rac1和RhoG的活动在胶质细胞突起的动力或密度上并未发挥作用,而是对于保持突起长度起关键性作用。本文扩展这个发现,探查突起形态和包被之间的关系,发现缩短的突起导致棘覆盖的减少。本文进一步发现在BG表达dn-Rac1和低水平突触包被的区域,显示突触数量的增加。这些分析提示BG突起如何生长并包围突触结构,阐明BG突起结构对突触包被适当发育的重要性,并提示包被在突触形成中的作用。     

Just How Stable Are Escape Rhythms after Atrioventricular Junction Ablation?

Background: Atrioventricular (AV) node ablation with implantation of a permanent pacemaker is an established mode of therapy in the treatment of atrial fibrillation. However, concern exists regarding subsequent dependency on an entirely paced rhythm and the possible sequela of unheralded pacemaker failure. Data regarding escape rhythm lability, an important feature of pacemaker dependency, are limited. Aims and Methods: The purpose of this study was twofold: (1) to determine the characteristics of escape rhythms at predefined serial time intervals following AV node ablation and pacemaker implantation, and (2) to identify risk factors predictive of unstable escape rhythms. Patients undergoing AV node ablation and pacemaker implantation were assessed for the presence or absence of an escape rhythm during pacemaker interrogation at five predetermined serial time points. Baseline demographics and comorbid conditions were evaluated as potential predictors of those with labile escape rhythms. Results : Seventy‐nine percent of the 96 patients studied had an underlying escape rhythm (≥30 beats per minute) immediately postablation. Although the percentage of patients with an escape rhythm increased at each follow‐up interval, the number of patients who consistently demonstrated an escape rhythm declined with each follow‐up, with 28% of patients lacking an escape rhythm at some time point, i.e., labile escape rhythm. There were no significant predictors of a labile escape rhythm. Conclusion: Among patients who have undergone AV node ablation and pacemaker implantation, 72% have a stable escape rhythm over time, but others are at risk for pacemaker dependency, as predicted by an underlying absent or labile escape rhythm. (PACE 2010; 939–944)     

Duplication of the Vertebro-Basilar System

During the examination of 75 fixed brains and 2086 vertebral angiograms we encountered two cases of fenestration of the vertebral artery and two cases of partial duplication of the basilar artery. In the first case, an 81 year old male, there was fenestration, of the basilar artery at the union of the two vertebral arteries. The fenestration was 9mm long with no associated vascular disease. The other partial duplication of the basilar artery was observed in the upper portion of the artery in a 54 year old male patient investigated angiographically for subarachniod haemorrhage. The fenestration of the third case was demonstrated in the intracranial part of the right vertebral artery of a 50 year old female patient during digital substraction angiography for subarachnoid haemorrhage. In the fourth case, the fenestration was found angiographically at the atlanto-axial level in the extracranial portion of the left vertebral artery in a 37 year old female patient with subarachnoid haemorrhage from an arteriovenous malformation in the left cerebral hemisphere. The embryonic, histological and radiological implications of the duplication are discussed.     

Antiarrhythmic Effects of VVI Pacing at Physiologic Rates: A Crossover Controlled Evaluation

Ventricular pacing can prevent bradycardia-dependent ventricular ectopic activity (VEA) and is helpful in some cases of drug-refractory venfricuiar tachycardia (VT). This study is a prospective evaluation of VVI pacing for the control of VEA not related to underlying bradycardia, drug side-effects, or prolonged QT interval syndromes. Twenty-nine patients undergoing serial electrophysioiogic-pharmacoiogic testing for VT control were studied. Eighteen of these patients (12 men; meon age = 60.1) both completed ihe protocol and had sufficient VEA for analysis. Coronary disease was present in 13 patients, cardiomyopathy in two patients, and one patient each had myocarditis, mitral valve prolapse, and no structural heart disease. Ambulatory (Holter) monitor recordings during VVI pacing were compared with control recordings made in the absence of pacing, VVI pacing rates were 10–15 bpm above the mean daily heart rate (mean = 92 bpm; range = 63–110). Hours from paced recordings were paired with hours from control (prior to analysis) according to time of day to reduce the effects of spontaneous variability in VEA frequency. Overall, VVI pacing reduced ventricular premature complexes (VPGs) 26% from 331 to 245/hour (p < 0.001). During pacing, couplets (pairs, successive VPGs) were reduced from 6.95 to 1.03/hour (p < 0.000001) and VT (≥3 successive VPCs) from 0.89 to 0.045 episodes/hour (p < 0.003). Of 13 patients with couplets, 11 had ≥50% reduction and five had ≥90% reduction. Baseline VT was eliminated in four out of nine patients during pacing. Pacing did not increase VEA significantly in any patient. In this group of patients, reduction of VEA by VVI pacing was significant and was comparable to pharmacologic interventions. Higher forms of VEA fcouplets and VT) appeared to respond better than single VPCs. Further studies may define patients with VEA who can benefit from pacing     

Amiodarone: Value of Programmed Electrical Stimulation and Holter Monitoring

The value of programmed electrical stimulation (PES) and Holter monitoring in the assessment of amiodarone efficacy was reviewed. Many physicians have been disturbed by the persistent inducibility of arrhythmias in patients treated with amiodarone, who nevertheless do very well during the follow-up period. Noninducibility was associated with a favorable prognosis among 366 VT patients. Eighty-eight (24%) were noninducible on amiodarone, and 10% of these had recurrences, vs 39% in patients who remained inducible. Further, increased difficulty of induction with PES or induction of a slower or better tolerated VT may indicate a favorable outlook, and add to the value of PES. Few papers rigorously employed Holter monitoring in the assessment of amiodarone. In general, suppression of previously frequent arrhythmias implies excellent protection for patients with benign arrhythmias and moderate protection with malignant arrhythmias. By Holter assessment in 186 VT patients, arrhythmias were suppressed in 114 (61%), and 18% of these had recurrences vs 50% in patients whose arrhythmias were not suppressed. Studies attempting to correlate the results of PES and Holter monitoring in the same patients are lacking and may prove useful.