Pleomorphic Ventricular Tachycardia: Demonstration of Conduction Reversal Within the Reentry Circuit

A case is presented of a patient with incessant venfricular tacbycardia of left bundle branch block morphology. Endocardial mapping revealed the site of earliest activation during tachycardia to be the proximal right ventricular septum. Pacing at this site elicited the clinical tachycardia, whereas pacing at the proximal left ventricular septum induced a right bundle branch block morphology identical to that of a previously recorded spontaneous ventricuiar tachycardia. Electrophysiological evidence is given that both types of tachycardia originate from a single reentry circuit located in the proximal ventricular septum in which the reentrant wavefront may travel either orthodromically (during spontaneous tachycardia and right ventricular pacing) or antidromically (during left ventricular pacing).     

Ostial PV Isolation:

Pulmonary vein (PV) isolation by elimination of spike potentials has been reported to cure drug refractory atrial fibrillation. Because of the heterogenous morphology of the PVs, sequential electroanatomic reconstruction of the PVs was performed in 39 patients (group A), who underwent subsequent PV isolation by interruption of all conductive myocardial fibers by distinct RF current applications using a "lasso" approach. In group B (157 patients), only biplane two-dimensional fluoroscopy was performed to guide the diagnostic and the ablation catheters. After reprocedures (in 7% of patients in group A and 22% of group B), which depicted a recurrence of a spike potential inside or at the ostium of  >1 previously isolated PV in all restudied patients, stable sinus rhythm was documented in 69% of patients in group A and 60% of patients in group B. Reasons for the relapse of the previously eliminated spike potentials include a temporary ablation effect and a too distal interruption of the conducting myocardial fiber. Detailed knowledge of the individual three-dimensional morphology enhanced the clinical success rate of PV isolation but is time-consuming using CARTO   (8.0 ± 1.7 vs 5.0 ± 1.6, P < 0.001)   . Further technical improvement to fuse the individual three-dimensional anatomy and the electrophysiological markers to a composed "electroanatomic" map may overcome this limitation in the future. (PACE 2003; 26[Pt. II]:1624–1630)     

Clinical Recurrences After Successful Accessory Pathway Ablation:

Dormant Accessory Pathways. Introduction : Recurrence of clinical symptoms after radiofrequency catheter ablation of an accessory atrioventricular pathway (AP) may be due to the late manifestation of an additional AP that was not detected during the initial ablation session. It was the purpose of this study to elucidate the phenomenon of these "dormant" APs.
Methods and Results : Of 1280 consecutive patients who underwent radiofrequency catheter ablation of an AP, 54 patients (4.2 %) developed clinical symptoms postablation, necessitating a repeat ablation session. Recurrence of conduction over the AP targeted al the initial ablation session was found in 45 patients, whereas in the other 9 patients (0.7%) the manifestation of a previously unnoticed AP had caused symptom recurrence. Retrospective analysis of the data from these patients' ablation sessions revealed that the late manifesting AP was ablated at a site clearly different from that of the initially targeted AP, and that the manifestation of conduction over a previously "dormant" AP occurred significantly later than the recovery of a presumably ablated AP. Seven (78%) of the 9 "dormant" APs were concealed, and none exhibited decremental conduction properties.
Conclusion : The incidence of clinical recurrences mediated by the late manifestation of conduction over a previously "dormant" AP is low. The lack of an anatomic vicinity of these predominantly concealed APs with the initially targeted AP and the lack of evidence for their presence during the initial ablation session suggest intermittent conduction as the most likely explanation for their late manifestation.     

Catheter Ablation of Recurrent Scar-Related Ventricular Tachycardia Using Electroanatomical Mapping and Irrigated Ablation Technology: Results of the Prospective Multicenter Euro-VT-Study

Catheter Ablation of Ventricular Tachycardia.   Introduction: Ventricular tachycardia (VT) late after myocardial infarction is an important contributor to morbidity and mortality. This prospective multicenter study assessed the efficacy and safety of electroanatomical mapping in combination with open-saline irrigated ablation technology for ablation of chronic recurrent mappable and unmappable VT in remote myocardial infarction.
Methods and Results: In 8 European institutions, 63 patients (89% males) were enrolled in the study. All patients had remote myocardial infarction and presented with a median number of 17 (range 1–380) VTs in the preceding 6 months. Incessant VT was present in 14 patients (22%). Left ventricular ejection fraction measured 30 ± 13%. A mean of 3 VTs were targeted per patient and 22% of all patients had only unmappable VT. The mean follow-up period was 12 ± 3 months. A total of 164 VTs were targeted during catheter ablation. Ablation was acutely successful in 51 patients (81%). One patient (1.5%) experienced a major complication with degeneration of VT into ventricular fibrillation necessitating cardiopulmonary resuscitation maneuvers. However, no death occurred acutely or within the first 30 days after catheter ablation. During the follow-up, 19 of the initially successful ablated patients (37%) and 31 of all ablated patients (49%) developed some type of VT recurrence.
Conclusions: The results of this multicenter study demonstrate the high acute success rate and a low complication rate of irrigated tip catheter ablation of all clinical relevant VTs in remote myocardial infarction. However, during the follow-up a relevant number of recurrences occurred. (J Cardiovasc Electrophysiol, Vol. 21, pp. 47–53, January 2010)     

Influence of Internal Current and Pacing Current on Pacemaker Longevity

The effects of lower pulse amplitude on battery current and pacemaker longevity were studied comparing the new, small-sized VVI pacemaker, Minix 8341, with the former model, Pasys 8329. Battery current was telemetrically measured at 0.8. 1.6, 2.5, and 5.0 V pulse amplitude and 0.05, 0.25, 0.5, and 1.0 msec pulse duration. Internal current was assumed to be equal to the battery current at 0.8 V and 0.05 msec. Pacing current was calculated subtracting internal current from battery current. The Minix pacemaker had a significantly lower battery current because of a lower internal current (Minix: 4.1 ±0.1 μA; Pasys: 16.1 ± 0.1 μA); pacing current of both units was similar. At 0.5 msec pulse duration, the programming from 5.0-2.5 V puise amplitude resulted in a greater relative reduction of battery current in the newer pacemaker (51% vs 25%). Projected longevity of each pacemaker was 7.9 years at 5.0 V and 0.5 msec. The programming from 5.0–2.5 V extended the projected longevity by 2.3 years (Pasys) and by 7.1 years (Minix). The longevity was negligibly longer after programming to 1.6 V. Conclusion: Extension of pacemaker longevity can be achieved with the programming to 2.5 V or less if the connected pacemakers need a low internal current for their circuitry.     

Benefits of Smaller Electrode Surface Area (4 mm2) on Steroid-Eluting Leads

The purpose was to test whether a reduction of pacemaker electrode surface area below 8 mm2 improves leads that elute steroid from the electrode tip to the surrounding myocardium. A standard-sized 8 mm2 lead with 1 mg dexamethasone was implanted in 12 patients and a lead with 4 mm2 electrode surface area and 0.5 mg dexamethasone in ten patients. Pacing threshold, impedance, and sensing threshold were measured at implantation and after 1, 4, and 12 weeks. Pacing thresholds were similar for both groups and were always less than or equal to 0.8 V at 0.5 msec pulse duration in all patients. Impedance was significantly higher (P less than 0.05) for the 4 mm2 lead (implantation: 726 +/- 119 ohms; 1 week: 596 +/- 71 ohms; 4 weeks: 624 +/- 68 ohms; 12 weeks: 643 +/- 56 ohms) than for the 8 mm2 lead (implantation: 422 +/- 43 ohms; 1 week: 402 +/- 48 ohms; 4 weeks: 439 +/- 57 ohms; 12 weeks: 449 +/- 61 ohms). R wave amplitudes did not differ between both groups; no sensing failure occurred at 5 mV sensitivity. Compared to the 8 mm2 lead the reduction of surface area to 4 mm2 did not influence pacing threshold, but resulted in a higher pacing impedance. The amount of pacing energy was lower in the smaller-sized electrode. For clinical impact, low pacing threshold and high impedance leads are the condition to implant pulse generators with smaller battery capacity.     

Arrhythmias in Hypertrophic Cardiomyopathy

Supraventricular and ventncular arrhythmias, particularly nonsustained ventricular tachycardia, and ventricular premature beats are a common finding in patients with hypertrophic cardiomyopathy. Several investigations have demonstrated that nonsustained ventricular tachycardia on Holter monitoring is associated with an increased risk of sudden cardiac death. It has been a long lasting controversial discussion whether suppression of these arrhythmias with drugs, such as amiodarone is capable to reduce the incidence of sudden cardiac death. While recent studies have indicated that nonsustained ventricular tachycardia in asymptomatic patients without additional risk factors, such as a positive family history of sudden cardiac death or syncope should not be treated prophylactically with amiodarone. Symptomatic patients with sustained ventricular tachycardias and/or syncope related to ventricular arrhythmias should undergo ICD implantation. The implantation of an ICD in asymptomatic patients should be limited to those who have several risk factors for sudden cardiac death. It is questionable whether other risk stratifiers, such as programmed electrical stimulation may be helpful to identify asymptomatic patients who are at risk to die suddenly. Moreover, whether the demonstration of electrocardiogram fractionation during electrophysiological study is superior to the induction of sustained ventricular arrhythmias for risk stratification, needs further investigation.     

Percutaneous Catheter Ablation at the Mitral Annulus in Canines Using a Bipolar Epicardial-Endocardial Electrode Configuration

For potential application in ablating left free-wall accessory AV pathways with direct current shocks, a new epicardial-endocardial electrode configuration, designed to focus the current field across the mitral annulus, was tested in dogs. A catheter electrode in (he coronary sinus (epicardial electrode) was used as the cathode, and a catheter electrode in the left ventricle (endocardial electrode) placed beneath the mitral valve, high against the mitral annulus and directly across from the epicardial electrode formed the anode. Two shocks, each of 30, 40, or 50 joules (J) were delivered in nine, three, and four dogs, respectively. The first shock was applied to the anterior or lateral wail and the second shock to the posterior wall, except in one dog which received one anterior and one lateral shock. Two dogs receiving 50] shocks died acutely, one due to rupture of the coronary sinus and cardiac tamponade and the other had unexplained electromechanical dissociation. The remaining 14 dogs tolerated the two shocks well and were sacrificed 3–5 days later for pathological examination of the heart. Shocks in the anterior and lateral regions produced atrial necrosis (height 1.5–11 mm, width 1.5–12 mm and depth 1–3 mm) in 10 of 14 dogs and ventricular necrosis (height 4–27 mm, width 4–33 mm, and depth 5–14 mm) in all 14 dogs. Ideal lesions with atrial necrosis extending down to the annulus and ventricular necrosis extending to the epicardial aspect of the ventricular crest occurred in five dogs in which the endocardial electrode was positioned high against the annulus. In the other nine dogs, the endocardial electrode was located 6–18 mm below the annulus, as estimated by the center of ventricular necrosis. In these dogs, the ventricular lesions did not extend to the epicardial aspect of the crest and, in four dogs, no atrial necrosis was found. Shocks delivered to the posterior wall produced no atrial or ventricular necrosis except in one dog receiving a 50 J shock. It is concluded that, using the epicardial-endocardial electrode configuration with the LV catheter positioned high against the annulus, shocks of less than 50 J in dogs safely produce atrial and ventricular necrosis adjacent to the mitral annulus in the anterior and lateral regions but not in the posterior regions. Similar lesions in man may be capable of interrupting left anterior and lateral accessory AV pathways.