Negative participation of the left posterior fascicle in the reentry circuit of verapamil-sensitive idiopathic left ventricular tachycardia

Left posterior fascicle and idiopathic Left VT. The left posterior fascicle may be a bystander of the circuit of verapamil-sensitive idiopathic left ventricular tachycardia. During ventricular tachycardia (VT), 3 sequences of potentials were seen at the left posterior septum: diastolic Purkinje potentials propagating from base to apex and presystolic left posterior fascicular potentials and systolic left ventricular (LV) myocardial potentials propagating in the reverse direction. Selective capture of the left posterior fascicle by the sinus beat did not affect the VT cycle length. Entrainment pacing revealed that the retrograde limb of the circuit was not the left posterior fascicle, but the LV myocardium.     

Diastolic potentials observed in idiopathic left ventricular tachycardia

Radiofrequency catheter ablation (RF-CA) has demonstrated a high success rate in eliminating idiopathic left ventricular tachycardia (ILVT), and the target site is determined by the score of pace mapping or the Purkinje potential (PP) preceding the onset of the ventricular activation, which is considered to indicate the exit site of the reentrant circuit. However, only a few reports have described the potential obtained from the slow conduction zone. RF-CA was successfully performed in 8 patients with ILVT. Careful mapping of the left ventricle during tachycardia was carried out to find the diastolic potential (DP). A DP was obtained in 4 patients (group 1), but not in 4 others (group 2). The local electrogram was recorded from the distal tip of the ablation catheter during the RF current application in order to investigate the pattern of termination of ILVT. A DP was recorded at the point where the catheter was slightly pulled back to a site proximal to the exit site of the reentrant circuit at the left interventricular basal septum. In group 1, conduction block between the DP and PP eliminated ILVT in 3 out of 4 cases, and 1 case showed conduction block between the DP and ventricular potential. In 2 out of 4 patients in group 2, the local electrogram showed conduction block between PP and the ventricular potential when VT terminated. The ablation site in group 1 was located relatively more basal than that in group 2 in anatomy. A DP was obtained in a half of the cases with ILVT and RF-CA at this site could eliminate ILVT. A DP was obtained at a site relatively basal to the exit of the reentrant circuit and it is considered that this is a useful marker in terms of the successful ablation of ILVT.     

Demonstration of diastolic and presystolic Purkinje potentials as critical potentials in a macroreentry circuit of verapamil-sensitive idiopathic left ventricular tachycardia

OBJECTIVES: The purpose of this study was to determine the relation of diastolic and presystolic potentials recorded during verapamil-sensitive idiopathic left ventricular tachycardia (ILVT) to reentry circuit. BACKGROUND: Successful ablation of verapamil-sensitive ILVT at the zone of slow conduction from which the diastolic potential is recorded has been reported. However, the relationship between the diastolic potential and the reentrant circuit remains a matter of debate. METHODS: Radiofrequency (RF) ablation was performed in 20 patients with verapamil-sensitive ILVT. After identifying the ventricular tachycardia (VT) exit site, we searched for the mid-diastolic potential (P1) during VT. Entrainment followed by RF current application was performed. If the mid-diastolic potential could not be detected, RF current was applied at the VT exit site showing the earliest ventricular activation with a single fused presystolic Purkinje potential (P2). RESULTS: In 15 of 20 patients, both P1 and P2 were recorded during VT from midseptal region. Entrainment pacing captured P1 orthodromically and reset the VT. The interval from stimulus to P1 was prolonged as the pacing rate was increased. Radiofrequency ablation was successfully performed at this site in all 15 patients. After successful ablation, P1 appeared after the QRS complex during sinus rhythm with the identical sequence to that during VT. In the remaining five patients, the diastolic potential could not be detected, and a single fused P2 was recorded only at the VT exit site. Successful ablation was performed at this site in all five patients. CONCLUSIONS: This study demonstrates that P1 and P2 are critical potentials in a circuit of verapamil-sensitive ILVT and suggests the presence of a macroreentry circuit involving the normal Purkinje system and the abnormal Purkinje tissue with decremental property and verapamil-sensitivity.     

A Case with Occurrence of Antidromic Tachycardia After Ablation of Idiopathic Left Fascicular Tachycardia: Mechanism of Left Upper Septal Ventricular Tachycardia

A 36‐year‐old male presented with verapamil‐sensitive narrow QRS tachycardia. The patient underwent the catheter ablation of common idiopathic left fascicular ventricular tachycardia (ILVT) 2 years ago. During narrow QRS tachycardia, the diastolic and presystolic potentials (P1 and P2) were recorded at the left septum. Activation sequences of P1 and P2 were opposite from those in common ILVT. Entrainment of P1 at the upper septum exhibited concealed fusion and S‐QRS equal to P1‐QRS. Radiofrequency current to P1 suppressed VT. Idiopathic left upper septal VT might be the antidromic macroreentry of the common form of ILVT.     

Effects of verapamil and lidocaine on two components of the re-entry circuit of verapamil-senstitive idiopathic left ventricular tachycardia

OBJECTIVES: We characterized pharmacologically the slow conduction zone of verapamil-sensitive idiopathic left ventricular tachycardia (ILVT) with regard to the late diastolic potential (LDP). BACKGROUND: We showed that the slow conduction zone of ILVT could be divided into two components by LDP; that is, the distal component with a tachycardia-dependent conduction delay property and the proximal one without it. METHODS: Electrophysiologic studies were performed in eight consecutive patients. The LDP was recorded during left ventricular (LV) mapping during ILVT. Entrainment was performed from the right ventricular outflow tract while recording LDP. The effects of lidocaine (1 mg/kg body weight) and verapamil (0.5 or 1.0 mg) were examined during entrainment. RESULTS: The LDPs preceding the Purkinje potential (PP) were serially recorded from the upper third to the middle of the LV septum along the narrow longitudinal line. The ventricular tachycardia (VT) cycle length increased after lidocaine (p < 0.05), and further after verapamil (p < 0.05). The increments in the VT cycle length after administration of the drugs strongly correlated with those in LDP-PP (r > 0.9 for both drugs). The interval from the ventricular potential to LDP was unchanged after administration of the drugs. In one patient, verapamil terminated VT by local conduction block between LDP and PP. The LDP-PP measured during entrainment increased after lidocaine, and further after verapamil, whereas the interval from the stimulus to LDP remained unchanged. CONCLUSIONS: The component distal to LDP is mainly calcium channel-dependent and partly depressed sodium channel-dependent. The proximal component is considered to be sodium channel-dependent (normal).     

左室特发性室性心动过速折返路径标测和消融点的选择

报道 1 0例 (男 8、女 2 )左室特发性室性心动过速 (简称室速 )折返路径标测结果和选择折返路径的不同部位为消融点的消融效果。电生理检查常规插入右室心尖与冠状静脉窦电极 ,并经左、右股动脉分别插入大头电极和2 8 2mm间距冠状静脉窦 1 0极标测电极至左室 ,后者贴靠在室间隔表面。窦性心律时各电极对可依次记录到His束电位 (HP)、左束支电位 (LBP)和左后分支的蒲氏纤维电位 (PP) ,室速时仍可同时记录到上述各电位 ,但顺序相反 ,PP领先 ,HP最后 ;而各部位的V波激动顺序在窦性心律和室速时是相同的 ,都是远端电极 (PP以远 )的V波最早 ,近端电极 (HP)的V波最晚。大头电极置于PP电极对附近。结果 :1 0例中 9例能记录到折返路径各电位心内电图 ,折返路径记录成功率为 90 % ( 9/1 0 )。第 1例大头电极位于PP电极对略上方处放电 ,消融成功 ,但导致完全性左束支阻滞。第 2 ,3例开始在PP电极对略下方处放电 ,但凡未记录到PP的点 ,虽然V波最早 ,都是放电无效点。最后消融成功的点 ,都记录到最领先的PP。第 4例以后 ,都必须记录到最领先的PP后才放电 ,除 1例 2次放电成功外 ,都是 1次放电成功。 1 0例随访至今 3～ 1 8个月 ,未服任何抗心律失常药均无室速发作。结论 :左室标测法不仅对研究左室特发性室速的折返     

Structure of the reentrant circuit of idiopathic left ventricular tachycardia: new insights into the role of the Purkinje network

In idiopathic left ventricular tachycardia (ILVT), the reentrant circuit is considered to involve the Purkinje system, and the Purkinje potential (P-potential) appears to be a marker for successful ablation. However, the characteristics of the reentrant circuit in ILVT have not yet been defined. In 2 cases of ILVT, we performed detailed mapping along the left ventricular septum during VT and sinus rhythm. ILVTs were successfully ablated at the posteroapical area of the left ventricular septum where the high frequency P-potential was recorded and this portion was considered to be the exit site of the reentrant circuit. A small P-potential was also recorded at the portion proximal to the exit site, and it preceded the P-potential at the exit site. However, the local ventricular electrogram at the exit site preceded that at the proximal site during VT. Moreover, the small P-potential was orthodromically entrained by ventricular pacing from the proximal site. These findings suggest that the reentry circuit of ILVT appeared to have considerable size.     

特发性左心室心动过速致心律失常基质的电解剖差异

目的 探索特发性左心室心动过速（ILVT）和房室折返性心动过速（AVRT）患者左心室传导系统和缓慢传导区电解剖变异情况.方法 选取2009年5月至2011年12月20例成功消融的ILVT患者（ILVT组）,年龄20～51（37±7）岁,男16例;26例AVRT患者（对照组）,年龄25～51（38±8）岁,男20例,窦性心律下分别建立左心室三维电解剖标测,标记左心室传导系统、缓慢传导区及其交汇区,分析变异情况.ILVT组患者依据消融关键区和拖带刺激进行消融.结果 根据浦肯野电位分布将传导系统变异分为3个亚型：两分支、三分支和扇形分布于左心室间隔,两组间各分支长度差异无统计学意义（P＞0.05）.缓慢传导区在ILVT中亦存在变异：17例位于后下间隔,1例位于下间隔近心尖处,2例于中、后间隔处.浦肯野电位和舒张期电位间存在面积约（1.5±0.4） cm2的交汇区,该处拖带和消融均取得成功.6例AVRT患者于后下间隔处记录到缓慢传导区,长度[12.0～28.7 （20.4±4.7） mm对11.8～ 20.3（16.1±3.3） mm,t=2.1,P=0.048]、面积[1.6～ 3.5（2.5±0.5） cm2对1.4～2.1 （1.8±0.3） cm2,t=3.0,P=0.006]显著小于ILVT组.结论 左心室传导系统和缓慢传导区存在多种变异,使ILVT折返机制更为复杂.     

Identification and catheter ablation of a zone of slow conduction in the reentrant circuit of ventricular tachycardia in humans

Three patients who had incessant ventricular tachycardia and in whom a zone of slow conduction was identified are presented. Each patient's tachycardia was refractory to multiple antiarrhythmic drugs and was being treated with amiodarone at the time of the electrophysiologic study. The ventricular tachycardia cycle length was 500 to 580 ms. In Patients 1 and 2, a single site at the posterolateral wall or low septum in the left ventricle was identified at which overdrive pacing during ventricular tachycardia resulted in ventricular capture with a stimulus to QRS interval of 280 to 400 ms and with little or no change in the configuration of the QRS complexes during pacing as compared with during ventricular tachycardia. In Patient 3, the same phenomenon was observed at two areas in the left ventricle: at the inferior wall, overdrive pacing during ventricular tachycardia resulted in a stimulus to QRS interval of 440 to 470 ms, whereas at the posterolateral wall, the stimulus to QRS interval was 320 to 360 ms. Transcatheter shocks of 100 to 240 J delivered at the pacing sites have been successful in preventing recurrences of ventricular tachycardia over a follow-up period of 10 to 11 months. These observations may be explained by the pacing site being located within a reentrant circuit in a zone of slow conduction bounded by inexcitable tissue between the pacing site and the exit site of the reentrant circuit. In Patient 3, the variable stimulus to QRS intervals are explained by variable proximity of the pacing sites within the slow conduction zone to the exit site of the reentrant circuit.(ABSTRACT TRUNCATED AT 250 WORDS)     

Identification of the slow conduction zone in a macroreentry circuit of verapamil-sensitive idiopathic left ventricular tachycardia using electroanatomic mapping

Identification of the Slow Conduction Zone in a Macroreentry. Background: Although idiopathic left ventricular tachycardia (ILVT) has been shown to possess a slow conduction zone (SCZ), the details of the electrophysiological and anatomic aspects are still not well understood. Objective: We hypothesized that the SCZ can be identified using a 3‐dimensional electroanatomic (EA) mapping system. Methods : Ten patients with ILVT were mapped using a 3‐dimensional electroanatomic (EA) mapping system. After a 3‐dimensional endocardial geometry of the left ventricular was created, the conduction system with left Purkinje potential (PP) and the SCZ with diastolic potential (DP) in LV were mapped during sinus rhythm (SR) and ventricular tachycardia (VT) and were tagged as special landmarks in the geometry. The electrophysiological and anatomic aspects of it were investigated. Results: EA mapping during SR and VT was successfully performed in 7 patients, during VT in 3 patients. The SCZ with DPs located at the inferoposterior septum was found in 7 patients during SR and all patients during VT. The length of the SCZ was 25.2 ± 2.3 mm with conduction velocity 0.08 ± 0.01 m/s. No differences in these parameters were found between patients during SR and VT (P > 0.05). An area with PP was found within the posterior septum. A crossover junction area with DP and PP was found in 7 patients during SR and VT. This area with DP and PP during SR coincided or were in proximity to such area during VT and radiofrequency ablation targeting the site within the area abolished VT in all patients. Conclusion: The ILVT substrate within the junction area of the SCZ and the posterior fascicular can be identified and can be used to guide the ablation of ILVT. (J Cardiovasc Electrophysiol, Vol. 23, pp. 840‐845, August 2012)     

电解剖标测消融左室特发性室性心动过速

目的报道三维电解剖标测指导下左室特发性室性心动过速(ILVT)的射频消融方法。方法4例经常规电生理标测消融失败的ILVT患者,应用三维电解剖(CARTO)标测指导确定消融部位。结果4例患者室性心动过速时CARTO标测的V波最早激动点在前中间隔,在此部位消融无效。以左后分支电位标测的最早激动点在左后间隔区域,在此部位消融终止所有ILVT,此成功部位距V波最早记录点1.0~2.0cm。随访1~7个月无复发。结论左后分支及其浦氏纤维是构成折返环的关键部位,也是射频消融的关键部位,并与折返的出口有一定距离。     

Mechanisms of Idiopathic Left Ventricular Tachycardia

Idiopathic Left Ventricular Tachycardia. Idiopathic left ventricular tachycardia (ILVT) differs from idiopathic right ventricular outflow tract (RVOT) tachycardia with respect to mechanism and pharmacologic sensitivity. ILVT can he categorized into three subgroups. The most prevalent form, verapamil-sensitive intrafascicular tachycardia, originates in the region of left posterior fascicle of the left bundle. This tachycardia is adenosine insensitive , demonstrates entrainment, and is thought to he due to reentry. The tachycardia is most often ablated in the region of the posteroinferior interventricular septum. A second type of ILVT is a form analogous to adenosine- sensitive RVOT tachycardia. This tachycardia appears to originate from deep within the interventricular septum and exits from the left side of the septum. This form of VT also responds to verapamil and is thought to he due to cAMP-mediated triggered activity. A third form of ILVT is propranolol sensitive. It is neither initiated or terminated by programmed stimulation, does not terminate with verapamil, and is transiently suppressed by adenosine, responses consistent with an automatic mechanism. Recognition of the heterogeneity of ILVT and its unique characteristics should facilitate appropriate diagnosis and therapy in this group of patients.     

Verapamil-Sensitive Left Anterior Fascicular Ventricular Tachycardia: Results of Radiofrequency Ablation in Six Patients

Verapamil-Sensitive Left Anterior Fascicular VT. Introduction: Verapamil-sensitive left ventricular tachycardia (VT) with a right bundle branch block (RBBB) configuration and left-axis deviation bas been demonstrated to arise from the left posterior fascicle, and can be cured by catheter ablation guided by Purkinje potentials. Verapamil-sensitive VT with an RBBB configuration and right-axis deviation is rare, and may originate in the left anterior fascicle. Methods and Results: Six patients (five men and one woman, mean age 54 ± 15 years) with a history of sustained VT with an RBBB configuration and right-axis deviation underwent electrophysiologic study and radiofrequency (RF) ablation. VT was slowed and terminated by intravenous administration of verapamil in all six patients. Left ventricular endocardial mapping during VT identified the earliest ventricular activation in the anterolateral wall of the left ventricle in all patients. RF current delivered to this site suppressed the VT in three patients (ablation at the VT exit). The fused Purkinje potential was recorded at that site, and preceded the QRS complex by 35, 30, and 20 msec, with pace mapping showing an optimal match between the paced rhythm and the clinical VT. In the remaining three patients, RF catheter ablation at the site of the earliest ventricular activation was unsuccessful. In these three patients, Purkinje potential was recorded in the diastolic phase during VT at the mid-anterior left ventricular septum. The Purkinje potential preceded the QRS during VT by 66, 56, and 63 msec, and catheter ablation at these sites was successful (ablation at the zone of slow conduction). During 19 to 46 months of follow-up (mean 32 ± 9 months), one patient in the group of ablation at the VT exit bad sustained VT with a left bundle branch block configuration and an inferior axis, and one patient in the group of ablation at the zone of slow conduction experienced typical idiopathic VT with an RBBB configuration and left-axis deviation. Conclusion: Verapamil-sensitive VT with an RBBB configuration and right-axis deviation originates close to the anterior fascicle. RF catheter ablation can be performed successfully from the VT exit site or the zone of slow conduction where the Purkinje potential was recorded in the diastolic phase.     

Cure of Interfascicular Reentrant Ventricular Tachycardia by Ablation of the Anterior Fascicle of the Left Bundle Branch

Ablation of Interfascicular Reentrant Tachycardia. Introduction: Fascicular reentrant ventricular tachycardia (VT) using the anterior fascicle of the left bundle anterogradely is rare and may produce identical QRS morphology during sinus rhythm and VT. Catheter ablation of this type of VT has not been described in detail.
Methods and Results: In a postinfarct patient with dilated left ventricle and recurrent VT (showing a QRS configuration of right bundle branch, left posterior fascicular block), endocardial recordings from the His-Purkinje system showed that VT was due to interfascicular reentry. Induction of VT occurred after progressive retrograde conduction delay on increasing the prematurity of the extrastimulus. Anterograde conduction occurred exclusively over the left anterior fascicle, which caused identical QRS morphology during sinus rhythm and VT. During VT, the left posterior fascicle was used retrogradely. The usual target for bundle branch reentry ablation, the right bundle, did not participate in the reentrant circuit. While performing left ventricular endocardial mapping, VT was interrupted when positioning the catheter on the left anterior fascicle, and "reversed" nonsustained bundle branch reentry occurred with anterograde conduction over the posterior fascicle and retrograde conduction over the anterior fascicle. Ablation of conduction in the anterior fascicle led to cure of the VT.
Conclusion: Interfascicular reentrant VT with right bundle branch block, right-axis QRS configuration can be cured by catheter ablation of anterior fascicle conduction.     

Functional role of the epicardium in postinfarction ventricular tachycardia. Observations derived from computerized epicardial activation mapping, entrainment, and epicardial laser photoablation

BACKGROUND. Conventionally, monomorphic sustained ventricular tachycardia in patients with remote myocardial infarction is believed to originate from the subendocardium. In a previous study, we demonstrated that electrical activation patterns during ventricular tachycardia occasionally suggest a subepicardial rather than subendocardial reentry. METHODS AND RESULTS. This study prospectively evaluated the functional role of the epicardium in postinfarction ventricular tachycardia with complex intraoperative techniques including computerized electrical activation mapping, entrainment, observation of changes in activation pattern during successful epicardial laser photoblation, and histological study. Five of 10 consecutive patients undergoing intraoperative computerized activation mapping had 10 ventricular tachycardia morphologies displaying epicardial diastolic activation These 10 "epicardial" ventricular tachycardias revealed the following global activation patterns: monoregional spread (two), figure-eight activation (five), and circular macroreentry (three). Entrainment of ventricular tachycardia using epicardial stimulation was successfully performed from an area of slow diastolic conduction in four tachycardia morphologies. During entrainment, global activation remained undisturbed with recordings showing a long stimulus to QRS interval, unchanged QRS morphology, and pacing capture of all components of the reentry circuit. Neodymium:yttrium aluminum garnet laser photocoagulation was delivered during ventricular tachycardia to epicardial sites of presumed reentry. Epicardial photoablation terminated five of five figure-eight tachycardias, two of three circular macroreentry tachycardias but not the monoregional tachycardias. Electrophysiological recordings during epicardial laser photocoagulation demonstrated progressive prolongation of ventricular tachycardia cycle length and apparent interruption of the presumed reentrant circuit. Histological evaluation of the reentrant region (three patients) showed a rim of surviving myocardium under the epicardial surface. CONCLUSIONS. This study suggests that 1) chronic postinfarction ventricular tachycardia may result from subepicardial macroreentry, 2) slow conduction within the reentry circuit can be localized by computerized mapping and epicardial entrainment, and 3) ventricular tachycardia interruption by laser photocoagulation results from conduction delay and block within critical elements of the reentrant pathway. Viable subepicardial muscle fibers may constitute the underlying pathology.     

Different Forms of Ventricular Tachycardia Involving the Left Anterior Fascicle in Nonischemic Cardiomyopathy: Critical Sites of the Reentrant Circuit in Low-Voltage Areas

Introduction: The purpose of this study was to examine the reentrant circuit of ventricular tachycardias (VTs) involving the left anterior fascicle (LAF) in nonischemic cardiomyopathy.
Methods and Results: Six patients with nonischemic cardiomyopathy presented with VTs involving the LAF. Potentials in the diastolic or presystolic phase of the VT were identified close to the LAF in 3 patients and in the mid or inferior left ventricular (LV) septum in 3 patients. Superimposed on a CARTO or NavX 3-dimensional voltage map, the diastolic and presystolic potentials were recorded within or at the border of a low-voltage zone in the LV septum in all cases. In 2 patients, both left bundle fascicles participated in the reentrant circuit including a possible interfascicular VT in one case. Ablation targeting the diastolic or presystolic potentials near the LAF or in the midinferior LV septum eliminated the VTs in all patients with the occurrence of a left posterior fascicular block and the delayed occurrence of a complete atrioventricular block in each one patient. During the follow-up of 23 ± 20 months after ablation, 4 patients were free of ventricular tachyarrhythmias. Due to detoriation of heart failure, one patient died after 12 months and one patient underwent heart transplantation after 40 months.
Conclusions: Slow conduction in diseased myocardium close to the LAF or in the middle and inferior aspects of the LV septum may represent the diastolic pathway of VT involving the LAF.     

Entrance Site of the Slow Conduction Zone of Verapamil-Sensitive Idiopathic Left Ventricular Tachycardia:

Entrance Site in ILVT. The entrance site of the slow conduction zone was identified by entrainment study in an 18 year-old woman with verapamil-sensitive idiopathic left ventricular tachycardia. Radiofrequency catheter ablation at this site eliminated the tachycardia. The entrance site was at a mid-septal location and was more than 2 cm away from the exit site. Electrophysiologic findings suggested macroreentry in the Purkinje system as the mechanism of idiopathic left ventricular tachycardia.     

特发性左心室性心动过速射频导管消融后体表心电图的改变

目的 观察特发性左心室性心动过速患者射频导管消融后体表心电图的变化及其可能机制。方法 对35例行射频导管消融的特发性左后分支室性心动过速患者,比较术前术后12导联体表心电图,并作随访6个月时体表心电图的对比观察。结果全组35例患者的消融均取得成功。其中6例术后Ⅱ、Ⅲ、aVF导联新出现q波,R波电压较前增高;I、aVL导联的s波加深,QRs波群电压增加。并伴有QRS波群电轴改变,均未见ST段改变。出现心电图改变与未见心电图改变患者间消融中放电时间和消融靶点数无明显差异。在随访期间所有患者的体表心电图QRS波群和ST段末见动态改变。结论 特发性左心室性心动过速患者射频导管消融后体表心电图出现的左后分支不同程度阻滞的图形改变可能因术中左后分支的分支及浦肯野纤维损伤引起。     

Left bundle branch block-type ventricular tachycardia originating from the left ventricular septum in a patient with cardiac sarcoidosis

This case report describes a left bundle branch block (LBBB)-type ventricular tachycardia (VT) with a unique reentrant circuit in a patient with cardiac sarcoidosis. The VT morphology and pace mapping supported an exit site of the VT from the basal posterior right ventricle (RV) septum. Nonetheless, concealed entrainment was established by pacing from a septal left ventricular (LV) site recording a diastolic potential, opposite site to the RV site. A point ablation at that LV site could successfully terminate the VT, suggesting that a critical isthmus was located on the LV side of the interventricular septum despite the demonstration of an LBBB-type VT.     

Fascicular ventricular tachycardia: experience with radiofrequency ablation.

Fascicular ventricular tachycardia (VT), the commonest form of idiopathic left VT, occurs more frequently in young males without structural heart disease and usually presents as paroxysmal palpitations. It is subdivided into two more common subtypes, posterior and anterior. A macro-reentrant circuit involving a considerable and variable extent of the left interventricular septum is presumed to be the underlying arrhythmogenic mechanism. A slow conduction zone with particular sensitivity to verapamil participates in the circuit and it seems that diastolic potentials (DP) represent the electrical activity in or near this zone. The fascicles of the left bundle appear to constitute part of the retrograde pathway and Purkinje potentials (PP) are assumed to represent their activation. In the present retrospective study, the authors review twelve cases of fascicular VT (ten posterior and two anterior) evaluated in the electrophysiology laboratory. Although initial induction was obtained in all patients, reproducibility was poor as a consequence of frequent contact inhibition during endocardial mapping of the left ventricle and this meant that ablation was not possible in two cases. Two cases of associated atrioventricular nodal reentrant tachycardia (AVNRT) and a case of associated atrioventricular reentrant tachycardia by a right posterior accessory pathway were documented, which suggest a correlated anatomic substrate. After ablation of the slow nodal pathway in one of the AVNRTs, fascicular VT was no longer inducible. Ablation of the fascicular VT was attempted in nine patients, at the tachycardia exit site (characterized by an early ventricular electrogram fused with a Purkinje potential) in two patients with anterior fascicular VT and in five patients with the posterior subtype, and near the slow conduction pathway (site with simultaneous recording of DP and PP) in the other two patients. The initial success rate with a single procedure was 78%, two of the ablations at the tachycardia exit site failing, with no complications. If we include the success of a repeated case with three-dimensional mapping, the overall success rate was 80%. Ablation of fascicular tachycardia appears to be a good therapeutic option with a good success rate and without significant adverse events. The poor reproducibility as a consequence of contact inhibition during endocardial left ventricular mapping is the principal limiting factor. With the help of currently available mapping systems, we hope that this limitation will disappear, as it is now possible with some devices to acquire accurate information on suitable sites for subsequent radiofrequency application with little or no contact, facilitating the ablation procedure. Ablation at a site with simultaneous recording of DP and PP is considered by most authors to be more effective than that performed at the tachycardia exit site.