The differential diagnosis on the electrocardiogram between ventricular tachycardia and preexcited tachycardia

The 12-lead surface electrocardiogram is a simple and useful tool for the differential diagnosis of regular wide QRS complex tachycardia. However, criteria do not as yet exist to discriminate between ventricular tachycardia and supraventricular tachycardia with anterograde conduction over an accessory pathway (preexcited tachycardia). Therefore, we designed a new stepwise approach with three criteria for the electrocardiographic differential diagnosis between ventricular tachycardia and preexcited tachycardia and prospectively studied 267 regular tachycardias with electrophysiologically proven mechanism and a wide QRS complex (≥ 0.12 s): 149 consecutive ventricular tachycardias and 118 consecutive preexcited regular tachycardias. Underlying heart disease was old myocardial infarction in 133 of 149 (89%) ventricular tachycardias. The patients presenting with preexcited tachycardia had no additional structural heart disease. Atrial fibrillation with preexcited QRS complex was not included. The criteria favoring ventricular tachycardia were: (1) presence of predominantly negative QRS complexes in the precordial leads V₄ to V₆, (2) presence of a QR complex in one or more of the precordial leads V₂ to V₆, and (3) AV relation different from 1:1 (more QRS complexes than P waves). The final sensitivity and specificity of these three consecutive steps to diagnose ventricular tachycardia were 0.75 and 1.00, respectively. This new stepwise approach is sensitive and highly specific for the differential diagnosis between ventricular tachycardia in coronary artery disease and preexcited regular tachycardia.     

Termination of re-entrant ventricular tachycardia by subthreshold stimulus applied to the zone of slow conduction

A 52-year-old female patient developed recurrent sustained ventriculartachycardia during the first week after left ventricular aneurysmectomy.The patient had no history of ventricular tachycardia preoperatively.As her tachycardias proved to be resistant to several antiarrhythmicdrugs, catheter ablation was considered. To define the siteof origin of ventricular tachycardia, endocardial catheter mappingand pace-mapping were performed. In addition, the response tosingle premature stimuli applied during ventricular tachycardiawas assessed. At a site in the basal portion of the antero-septalarea of the left ventricle, early presystolic endocardial activityduring ventricular tachycardia was found. Continuous pacingas well as premature stimulation from that site showed a markeddelay between the stimulus artefacts and the induced QRS complexes.The stimulus-induced QRS complexes were identical to QRS complexesof spontaneous and induced ventricular tachycardia. At veryshort critical coupling intervals of single premature stimulithat did not capture the ventricles (non-propagated stimuli),ventricular tachycardia was reproducibly terminated. These findings are explained by assuming that the catheter waslocated within the zone of slow conduction of the re-entrantcircuit, possibly in its proximal portion.     

Incidence and determinants of multiple morphologically distinct sustained ventricular tachycardias

The incidence and determinants of multiple morphologically distinct ventricular tachycardias were examined prospectively in 71 consecutive patients with at least one documented spontaneous episode of sustained monomorphic ventricular tachycardia. Mean frontal and horizontal QRS axes were determined from the 12 lead electrocardiograms (ECGs) of 190 spontaneous and 352 induced tachycardias. Two or more morphologically distinct spontaneous tachycardias were observed in 19 (43%) of 44 patients who had at least two documented spontaneous episodes. In 43 (61%) of the 71 patients, multiple morphologically distinct tachycardias were induced by programmed ventricular stimulation. Overall, 57 (80%) of the 71 patients had at least two morphologically distinct tachycardias. Predictors of multiple tachycardia configurations were selected by multivariate analysis from clinical and angiographic variables and were similar for both spontaneous and induced ventricular tachycardia: presence of multiple previous myocardial infarctions (p = 0.032 spontaneous, p = 0.005 induced) and number of different antiarrhythmic drug treatments during which ventricular tachycardia was documented (p = 0.0089 spontaneous, p less than 0.0001 induced). These data demonstrate that a large majority of patients with sustained monomorphic ventricular tachycardia exhibit more than one distinct QRS configuration when adequate ECG documentation of multiple episodes is obtained during different antiarrhythmic drug treatments. In individual patients, caution should be used in attributing clinical significance to a single unique QRS configuration.     

Narrow QRS Tachycardia with Ventriculoatrial Dissociation Mediated by a Left Fasciculoventricular Fiber

A 30-year-old man presented with narrow QRS tachycardia. The intracardiac electrocardiogram showed an atrial-HIS (AH) interval of 75 msec and a HIS-ventricular (HV) interval of 44 msec during baseline. Atrial incremental pacing revealed HV shortening, with apparent incomplete right bundle branch block (RBBB) morphology without QRS complex axis deviation. The induced tachycardia exhibited several QRS morphologies: a narrow QRS, complete RBBB and complete left bundle branch block (LBBB) morphology. Spontaneous conversion of the QRS pattern from wide to narrow was observed. The cycle length of the tachycardia was significantly shortened (from 316 to 272 ms) from LBBB morphology to narrow QRS complex. The atrial activation was dissociated from the ventricular activation during all tachycardias. Each QRS complex during tachycardia was preceded by a HIS deflection and HV interval was 35 ms, which was shorter than that of sinus rhythm. HIS deflection was earlier than right bundle potential during all kinds of tachycardia. This tachycardia is most likely mediated by a left fasciculoventricular fiber which connects the HIS bundle below the atrioventricular node to the myocardial tissue of the left ventricle. The HIS-Purkinje system is used as an antegrade conduction limb and the fasciculoventricular fiber as a retrograde limb in the tachycardia circuit.     

Ventricular tachycardia with QRS configuration similar to that in sinus rhythm and a myocardial origin: differential diagnosis with bundle branch reentry.

INTRODUCTION: Tachycardia with a QRS configuration which resembles that in sinus rhythm is usually thought to be supraventricular. Ventricular tachycardia, with a similar QRS configuration to that in sinus rhythm on the 12-lead ECG, can occur. The mechanisms of this form of ventricular tachycardia have not been previously reported. METHODS AND RESULTS: The mechanism of ventricular tachycardia was defined during electrophysiological study in five patients. During sinus rhythm, all patients had a wide QRS complex (>0.12 s) on the 12-lead ECG. The morphology remained grossly unchanged during spontaneous, symptomatic tachycardia. Four of the five patients had coronary artery disease and left ventricular dysfunction. The remaining patient had idiopathic dilated cardiomyopathy. The relationship between the His bundle, deflection, the right bundle branch and the QRS complex was evaluated during tachycardia. Atrial and ventricular pacing, and ventricular activation mapping were performed during tachycardia to define the tachycardia mechanism. The tachycardia induced at electrophysiological testing, which was similar to the clinical tachycardia, was proven to be ventricular tachycardia in each patient. The morphology of ventricular tachycardia was right bundle branch block in two patients and left bundle branch block in three patients. The median tachycardia cycle length was 300 ms (range: 260-480 ms). His bundle activation occurred in a 1:1 relationship with ventricular activation during tachycardia in all patients at least intermittently. The tachycardias were thought initially to be bundle branch reentry tachycardia. With further intervention and continued observation, it became clear that His bundle activation was passive and was not required for the tachycardia to sustain. During tachycardia, His bundle activation appeared to precede the local ventricular activation. Instead, the His bundle was activated slowly from the previous ventricular beat causing a long ventricular-His (VH) interval. This was shown by: (1) activation patterns, (2) response to pacing, (3) intermittent VH dissociation, and (4) termination of ventricular tachycardia. CONCLUSION: A unique form of ventricular tachycardia is described. The QRS complex morphology on the 12-lead ECG during tachycardia was grossly similar to that during sinus rhythm. The His bundle activation was passive and occurred with a long activation time from the ventricle to the His bundle. Although it mimics usual bundle branch reentry, this form of ventricular tachycardia appears to be due to a different mechanism in which the His bundle is not obligatory for the continuation of the reentrant phenomenon.     

Non-contact mapping to guide catheter ablation of untolerated ventricular tachycardia.

AIMS: The role of a novel non-contact mapping system (ESI 3000, Endocardial Solutions) to guide radiofrequency catheter ablation of untolerated ventricular tachycardia was investigated in 17 patients; 11 with prior myocardial infarction, three with arrhythmogenic right ventricular dysplasia, and three with idiopathic dilated cardiomyopathy. METHODS: Twenty-seven monomorphic ventricular tachycardias were induced (mean cycle 320+/-60 ms, range 230-450 ms), mapped for 15-20 s, and terminated by overdrive pacing or DC shock. Off-line analysis of isopotential activation mapping was performed to identify the diastolic pathway and/or the exit point of the ventricular tachycardia reentry circuit. Radiofrequency current was applied to create a line of block across the diastolic pathway or around the exit point. RESULTS: All 27 ventricular tachycardias were mapped with the non-contact system. The endocardial exit point (-7+/-15 ms before QRS onset) was defined in 21/21 postinfarction ventricular tachycardias, in 3/3 arrhythmogenic right ventricular dysplasia and in 1/3 idiopathic dilated cardiomyopathy ventricular tachycardias, respectively. The diastolic pathway (earliest endocardial diastolic activity: -65+/-49 ms before QRS onset) was identified in 17/21 postinfarction ventricular tachycardias, in 1/3 arrhythmogenic right ventricular dysplasia and in 1/3 idiopathic dilated cardiomyopathy ventricular tachycardias, respectively. Catheter ablation was performed in 25/27 ventricular tachycardias (93%) in 15/17 patients (88%): 16/25 ventricular tachycardias (64%) were successfully ablated in 10/17 patients (59%). Catheter ablation was not performed in two patients or proved unsuccessful in five patients. At a follow-up of 15+/-5 months, there was no recurrence of documented ventricular tachycardia in all 10 patients with successful catheter ablation; in two of them a previously non-documented ventricular tachycardia occurred. A high recurrence of ventricular tachycardia was observed in patients with a failed procedure (5/7: 71%). No major complication or death occurred. CONCLUSIONS: Non-contact mapping can be effectively used to map and guide radiofrequency catheter ablation of untolerated ventricular tachycardias. Given the favourable acute and clinical long-term results, this approach proves to be more effective in patients with postinfarction ventricular tachycardias, in comparison to patients with arrhythmogenic right ventricular dysplasia and idiopathic dilated cardiomyopathy.     

Electrophysiologic Characteristics of Wide QRS Complexes during Pharmacologic Termination of Sustained Supraventricular Tachycardias with Verapamil and Adenosine: Observations from Electrophysiologic Study

Background: In this study we evaluate wide QRS complexes observed during pharmacologic termination of supraventricular tachycardias. Methods: Patients with supraventricular tachycardia, undergoing electrophysiologic study were enrolled. 12 mg of adenosine or 10 mg of verapamil were administered during tachycardia, under continuous monitoring of intaracardiac and surface electrocardiograms. Electrocardiographic features of ventricular ectopy were noted. Results: Seventy‐four patients were enrolled. 48 patients were randomized to adenosine and 26 to verapamil. Five different appearance patterns of ventricular ectopy were observed during termination of tachycardias. All wide QRS complexes were of ventricular origin and all of them were observed during the termination of tachycardia. Adenosine more frequently resulted in appearance of ventricular beats (15.4% vs 41.7%, P = 0.003), and this was more frequently observed in patients with atrioventricular nodal reentrant tachycardia. Patients with ventricular beats were younger than those without, in both, verapamil (47.5 ± 15.6 vs 65.0 ± 8.8 years, P = 0.04) and adenosine (40.9 ± 13.8 vs 49.7 ± 16.8, P = 0.03) groups. Left bundle branch block (LBBB)/superior axis morphology was most frequent morphology in adenosine group (55%). Two of 4 patients in verapamil group displayed LBBB/inferior axis QRS morphology and another 2 patients displayed LBBB/superior axis morphology. Conclusions: Noncatheter induced, five different appearance patterns and four distinct morphologies of ventricular origin were observed. Most of them do not directly terminate tachycardia, but are associated with its termination and are not observed in ongoing tachycardia.     

经食管心房调搏在特发性室速诊断中的应用

目的探讨经食管心房调搏在特发性室性心动过速(室速)中的应用价值。方法回顾分析30例特发性室速患者的经食管心房调搏资料。结果经食管心房调搏基础刺激诱发心动过速6例(20%),静脉滴注异丙肾上腺素激发后刺激诱发12例(40%),心动过速时通过食管心电图证实QRS波群与P波非1∶1关系,且心室率>心房率而确诊为室速26例(86.67%)。心动过速自行终止5例(16.67%),药物或其它方法终止19例,经食管心房调搏超速刺激法终止6例(20%)。结论经食管心房调搏对诱发和确诊室速有较大的帮助,经食管心房调搏终止室速成功率不高。     

Taquicardia de QRS largos – importância eletrocardiográfica no diagnóstico diferencial

Correct diagnosis in wide QRS complex tachycardia remains a challenge. Differential diagnosis between ventricular and supraventricular tachycardia has important therapeutic and prognostic implications, and although data from clinical history and physical examination may suggest a particular origin, it is the 12‐lead surface electrocardiogram that usually enables this differentiation.Since 1978, various electrocardiographic criteria have been proposed for the differential diagnosis of wide complex tachycardias, particularly the presence of atrioventricular dissociation, and the axis, duration and morphology of QRS complexes. Despite the wide variety of criteria, diagnosis is still often difficult, and errors can have serious consequences. To reduce such errors, several differential diagnosis algorithms have been proposed since 1991. However, in a small percentage of wide QRS tachycardias the diagnosis remains uncertain and in these the wisest decision is to treat them as ventricular tachycardias.The authors’ objective was to review the main electrocardiographic criteria and differential diagnosis algorithms of wide QRS tachycardia.     

AV reentrant and idiopathic ventricular double tachycardias: complicated interactions between two tachycardias

An electrophysiological study was performed in a 61 year old man with Wolff- Parkinson-White (WPW) syndrome. At baseline, neither ventricular nor supraventricular tachycardias could be induced. During isoprenaline infusion, ventricular tachycardia originating from the right ventricular outflow tract (RVOT) with a cycle length of 280 ms was induced and subsequently atrioventricular reentrant tachycardia (AVRT) with a cycle length of 300 ms using an accessory pathway in the left free wall appeared. During these tachycardias, AVRT was entrained by ventricular tachycardia. The earliest ventricular activation site during the ventricular tachycardia was determined to be the RVOT site and a radiofrequency current at 30 W successfully ablated the ventricular tachycardia at this site. The left free wall accessory pathway was also successfully ablated during right ventricular pacing. The coexistence of WPW syndrome and cathecolamine sensitive ventricular tachycardia originating from the RVOT has rarely been reported. Furthermore, the tachycardias were triggered by previous tachycardias.     

室性心动过速合并室上性心动过速的射频消融

目的报道7例室性心动过速（VT）合并室上性心动过速（sVT）的射频消融。方法7例患者男6例,女1例,平均年龄（21±9）岁。阵发性心动过速病史（3．7±2．0）年。术中心房和心室刺激诱发VT和SVT,并进行消融。结果7例患者心房或心室刺激能反复诱发和终止VT合并SVT。法洛四联症矫治术后右心室VT合并三尖瓣环峡部依赖性心房扑动（AFL）1例,其余6例均为维拉帕米敏感性左心室特发性室速（ILVT）,分别合并AFL1例,左后间隔旁路参与的顺向型房室折返性心动过速（AVRT）1例,冠状静脉窦口慢旁路参与的顺向型AVRT1例,慢慢型房室结折返性心动过速（AVNRT）1例,左侧游离壁旁路参与的顺向型AVRT2例。7例患者的两种心动过速均成功消融,所有患者消融术后随访2年,无一例VT或SVT复发。结论VT合并SVT并不少见,消融术中应放置必需的心腔内电极导管,完成详细电生理检查,避免漏诊。一次消融应根除两种疾病。     

An unusual form of bundle branch reentrant tachycardia

INTRODUCTION: We report the case of a 36-year-old patient with a longstanding history of paroxysmal tachycardia. METHODS AND RESULTS: During the electrophysiological study, the H-V interval was prolonged in sinus rhythm, and a second potential (H') with distal to proximal activation pattern was recorded in the region of the proximal His-Purkinje system. Two wide QRS complex tachycardias were induced, both with V-A dissociation. One application of radiofrequency energy at the site with earliest and largest H' potential during sinus rhythm cured both tachycardias. The right and left bundle branch block morphology tachycardias were diagnosed as clockwise and counterclockwise bundle branch reentrant tachycardia. The H' potential represented the retrograde right bundle potential during sinus rhythm and bundle branch block reentrant tachycardia.     

Idiopathic Left Ventricular Tachycardia with Left and Right Bundle Branch Block Configurations

Fascicular Tachycardia. Introduction : Idiopathic left ventricular tachycardia typically has a right bundle branch block configuration. The purpose of this case report is to demonstrate that idiopathic ventricular tachycardia arising in or near the left posterior fascicle also may have a left bundle branch block configuration.
Methods and Results : A 27-year-old woman underwent an electrophysiologic procedure because of recurrent, verapamil-responsive, wide QRS complex tachycardia. Two types of ventricular tachycardia (cycle lengths 330 to 340 msec) were reproducibly inducible, one with a right bundle branch block configuration and left-axis deviation that had been documented clinically, and the other with a left bundle branch block configuration and axis of zero. A Purkinje potential recorded at the junction of the left ventricular mid-septum and inferior wall preceded the ventricular complex by 40 msec in both tachycardias. A single application of ra-diofrequency energy at this site successfully ablated both ventricular tachycardias.
Conclusion : The findings of this case report demonstrate that idiopathic ventricular tachycardia arising in or near the left posterior fascicle may have a left bundle branch block configuration     

无人区心电轴在宽QRS波心动过速中的鉴别诊断价值

目的探讨无人区心电轴在宽QRS波心动过速(WCT)中的鉴别诊断价值。方法收集并测量北京大学人民医院2000年1月至2005年10月经心内电生理检查明确诊断的WCT患者窦性心律及心动过速时心电图中Ⅰ、Ⅲ标准导联QRS波振幅的代数和,计算QRS波额面平均心电轴,观察无人区心电轴出现的心律失常类型及规律。结果137例[其中特发性室性心动过速(IVT)65例,室上性心动过速(室上速,SVT)72例]明确诊断的WCT患者中,18例出现无人区心电轴,其中室性心动过速(室速)16例(占室速24.6%,占总病例11.7%),均为左心室特发性室速;宽QRS波室上速2例(占宽QRS波室上速2.8%,占总病例1.5%),均为心房颤动(房颤)伴左侧旁路前传。结论无人区心电轴可以作为鉴别室速与宽QRS波室上速的一项可靠指标。     

Regular Wide QRS Complex Tachycardia During Atrial Fibrillation in a Patient with Preexcitation Syndrome: A Case Report

AV Conduction in WPW. We report an unusual case of a relatively regular wide QRS complex tachycardia alternating with periods of an irregular narrow QRS complex tachycardia during atrial fibrillation in a patient with Wolff-Parkinson-White syndrome. Both tachycardias resulted from atrial fibrillation, the wide QRS complex tachycardia being due to 2:1 AV conduction of a type I atrial fibrillation across a posteroseptal accessory AV connection.     

Augmentation of QRS wave amplitudes in the precordial leads during narrow QRS tachycardia

INTRODUCTION: QRS morphology during narrow QRS supraventricular tachycardia in patients without ventricular preexcitation generally is considered the same as that seen during sinus rhythm. This study presents a new ECG observation that the QRS amplitude increased significantly in leads V2 through V5 during tachycardia. METHODS AND RESULTS: Using the same ECG machine and the same electrode patches applied to the same electrode positions, 12-lead ECGs during sinus rhythm and narrow QRS tachycardia were analyzed comparatively in 23 patients without ventricular preexcitation. Precordial QRS amplitudes were measured as the vertical distance from the peak of the R to the nadir of the S wave. The amplitudes also were measured during atrial rapid pacing and extrastimulation. Furthermore, ventricular excitation during sinus rhythm and tachycardia was studied using body surface mapping. Body surface distributions of QRS potentials and ventricular activation time (VAT) were displayed as maps. Gross area of QRS (AQRS, equivalent to the QRS amplitude) was compared during sinus rhythm versus tachycardia. During tachycardia, QRS amplitude significantly increased in leads V2 through V5, without any noticeable change in the transitional zone or QRS wave duration. Increase of QRS amplitude also was noted during atrial rapid pacing and extrastimulation. Gross AQRS values during tachycardia significantly increased in the left parasternal area, whereas QRS isopotential and VAT isochronal maps were similar during sinus rhythm and tachycardia, suggesting a minimal role of conduction delay in the increase of QRS amplitude. CONCLUSION: QRS wave amplitude significantly increased in leads V2 through V5 during narrow QRS tachycardia compared with QRS waves in sinus rhythm. Increase of QRS amplitude seemed unlikely due to a conduction delay within the ventricular myocardium.     

A transcardiac lead system for identification and termination of supraventricular and ventricular tachycardia

The value of a transcardiac lead system (coronary sinus to right ventricular apex) to record atrial and ventricular electrical activity and its pacing capabilities was assessed in 20 patients with a variety of tachycardias (atrial tachycardia in 3 patients, atrial flutter in 4, intranodal tachycardia in 6, circus movement tachycardia using an accessory pathway in 1 patient, and ventricular tachycardia in 9). The transcardiac lead invariably showed both atrial and ventricular electrical activity during sinus rhythm and tachycardias, allowing application of the same criteria as used when analyzing cardiac rhythm on the surface electrocardiogram. Atrial complexes had a mean amplitude of 4.2 mV during sinus rhythm and varied from 3.0 to 4.1 mV during the different types of tachycardia. Ventricular complexes had a mean amplitude of 9.8 mV during sinus rhythm, 13.8 mV during supraventricular tachycardia and 16.1 mV during ventricular tachycardia. The duration of the QRS complex on the transcardiac lead was equal to the duration of the QRS complex on the surface electrocardiogram during tachycardias with a small or wide QRS complex. By varying the intensity of current delivered through the transcardiac lead, only right ventricular pacing (mean current intensity 1.2 +/- 0.4 mA) or simultaneous atrioventricular pacing (mean current intensity 4.7 +/- 3.3 mA) could be achieved. Termination of all episodes of tachycardia was achieved with either ventricular pacing or simultaneous atrioventricular pacing. This transcardiac lead system allows clear identification of atrial and ventricular events, is suitable for tachycardia analysis using simple surface electrocardiographic algorithms and allows pacing termination of a variety of tachycardias.     

The therapeutic and diagnostic cardiac electrophysiological uses of adenosine

Summary Adenosine is a purine nucleoside with a rapid onset and brief duration of action after intravenous bolus administration. Its most prominent cardiac effect is impairment or blockade of atrioventricular nodal conduction, but other effects are depression of automaticity of the sinus node and attenuation of catecholamine-related ventricular after-depolarizations. The cardiac cell surface receptor is the A₁ purinoceptor. The therapeutic value of adenosine is predominantly in those arrhythmias in which the atrioventricular node forms part of a reentry circuit, as clearly demonstrated by the high success rate for termination of atrioventricular nodal reentry tachycardia and of atrioventricular reentry tachycardia involving an accessory pathway in the Wolff-Parkinson-White syndrome. Ventricular tachycardias are generally unresponsive, with the exception of right ventricular outflow tract tachycardia. A diagnostic role has emerged for adenosine. The transient blockade of the atrioventricular node that it causes can reveal important electrocardiographic features in arrhythmias, such as atrial flutter, or can unmask latent preexcitation. In wide-QRS tachycardias, adenosine can help to distinguish ventricular tachycardia from supraventricular tachycardia with QRS aberration. Unlike verapamil, adenosine is safe in ventricular tachycardia. A suggested dosing scheme is to give incremental doses at 1-minute intervals, starting at 0.05 mg/kg and continuing until complete atrioventricular block is induced or a maximum of 0.25 mg/kg is reached. Side effects are transient, sometimes uncomfortable, and not hazardous; dyspnea and chest discomfort are most frequent. A history of asthma is a relative contraindication. Aminophylline antagonizes and dipyridamole potentiates the effects of adenosine.     

Idiopathic left ventricular aneurysm associated with pleomorphic ventricular tachycardia: a case report

A 39-year-old Japanese woman presented with an idiopathic left ventricular aneurysm manifesting as recurrent episodes of palpitation. She was referred to our hospital for evaluation of sustained ventricular tachycardia. Echocardiography disclosed a dyskinetic well-defined wall bulge during both systole and diastole at the basal region of the interventricular septum, and reduced left ventricular wall thickness and severe hypokinesis at the anterolateral to posterolateral region. These appearances were confirmed by the angiographic findings. The sustained ventricular tachycardia was reproducibly induced by a single extrastimulus from the right ventricular apex. Subsequently, 4-type ventricular tachycardias were induced during the electrophysiological study and the mechanism of these ventricular tachycardias was considered reentry. Radiofrequency catheter ablation failed due to the changing QRS morphologies during the entrainment study. The patient was treated with cibenzoline 300 mg a day, and there has been no recurrence of tachycardia during the 18-month follow-up period.     

Fascicular tachycardia sensitive to calcium antagonists

Five patients with recurrent tachycardias exhibiting right bundlebranch block with left axis deviation were referred for investigation.In each case, a supraventricular mechanism was suspected. Duringsinus rhythm, the QRS morphology and axis (–10 to +60degrees) and HV intervals were normal. Tachycardia was initiatedby timed ventricular premature stimuli in 4 patients, rapidventricular pacing in 3 patients and rapid atrial pacing in2 patients. The tachycardia cycle length varied from 275 to380 ms with right bundle branch block and a leftward axis changeof 30 to 125 degrees at the onset of the tachycardia. The HVinterval ranged from +15 to –20 ms. In each patient ventriculoatrialdissociation occurred spontaneously or could be induced. Alltachycardias could be terminated or greatly slowed by calciumantagonists. These data are consistent with an unusual reentrantmechanism of tachycardia located in the posterior fascicle ofthe left bundle branch.