特发性左室流出道室性心律失常的心电图特点

探讨特发性左室流出道室性心律失常患者的心电图特点。对 7例特发性左室流出道室性早搏 (简称室早 )、室性心动过速 (简称室速 )患者进行心电图分析 ,并行心内电生理检查及射频消融治疗 ,同时对 10例预激综合征患者成功消融房室旁道后行主动脉瓣上及瓣下起搏 ,记录同步 12导联起搏心电图。对比分析两组病例体表心电图QRS波图形特点。结果 :7例左室流出道室早、室速患者经心内电生理检查证实 6例起源于冠状动脉窦内 ,1例起源于左室流出道主动脉瓣右瓣下方 ,所有患者经射频消融成功治疗室性心律失常。对照组 10例在主动脉瓣下起搏(其中 6例同时在主动脉瓣上起搏 )获得同步 12导联起搏心电图。两组病例体表心电图共同特点为 :QRS波额面电轴向下 ,Ⅱ、Ⅲ、aVF导联主波向上 ,QRS波在V2 或V3 前移行为Rs或R型。结论 :左室流出道为特发性室早、室速发生部位之一 ,体表心电图有其独特性 ,导管射频消融治疗安全有效。     

Use of electrophysiologic testing in patients with nonsustained ventricular tachycardia: prognostic and therapeutic implications

Forty patients with coronary artery disease and nonsustained ventricular tachycardia on ambulatory electrocardiographic monitoring underwent programmed electrical stimulation. In 22 patients, monomorphic ventricular tachycardia was induced at baseline drug-free electrophysiologic testing; 9 of these patients subsequently developed a clinical sustained ventricular tachyarrhythmia. In 18 patients, no tachycardia could be induced, and none of these 18 had subsequent tachycardia. In 25 of the 40 patients, arrhythmia management was guided by the results of electrophysiologic testing; this group included 11 patients who received antiarrhythmic therapy for induced ventricular tachycardia and 14 patients without inducible ventricular tachycardia who did not receive antiarrhythmic therapy. In the remaining 15 patients, arrhythmia management was not based on the results of electrophysiologic testing. Only two episodes of clinical sustained tachyarrhythmia occurred in the group receiving electrophysiologically guided therapy compared with seven episodes in the group treated without electrophysiologic guidance (p less than 0.01). Thus, in patients with coronary artery disease with nonsustained ventricular tachycardia on ambulatory electrocardiography, electrophysiologic testing can identify those at high and low risk for subsequent clinical tachycardia events. Furthermore, results of such testing can be used to optimize arrhythmia management in these patients.     

Patient activated asynchronous ventricular pacing at normal rates for termination of ventricular tachycardia

Ventricular pacing has been used to prevent or convert ventricular tachycardia. We report the use of patient-activated asynchronous mode ventricular pacing at normal rates for conversion of ventricular tachycardia by competitive pacing impulses. Following electrophysiologic studies, a specially constructed pacemaker was inserted. Routine function mode resulted in no output but activation of the reed switch resulted in V00 (asynchronous) pacing at 80/min. Patient-initiated conversion of ventricular tachycardia was documented by ambulatory electrocardiographic monitoring. The patient reports an average of two episodes per month converted over a four year period.     

Development of the implantable transvenous cardioverter

The development of the transvenous cardioverter, from the initial animal studies, to the clinical studies using temporary leads, to the initial permanent implants is described. Shocks less than or equal to 2.0 joules synchronized to the QRS complex and delivered through a specially designed catheter electrode placed in the apex of the right ventricle successfully terminate most episodes of ventricular tachycardia in patients. The implanted unit which also serves as a demand ventricular pacemaker, can be used to perform programmed electrophysiologic studies. Future devices must be capable of defibrillation and more accurate arrhythmia detection.     

Atypical ventricular tachycardia as a manifestation of disopyramide toxicity

An unusual ventricular tachyarrhythmia developed in a 57 year old woman with recurrent ventricular tachycardia and toxic disopyramide plasma concentrations. The rhythm was similar to the patient's previous ventricular tachycardia, but the rate was slower and the QRS complex was markedly widened, mimicking the electrocardiographic changes associated with electrolyte abnormalities. Disopyramide, which has electrophysiologic properties similar to those of quinidine, probably caused the arrhythmia and should be added to the list of drugs associated with atypical ventricular tachycardia.     

Determinants of QRS alternans during narrow QRS tachycardia

This study was designed to prospectively determine the incidence of QRS alternans during various types of narrow QRS tachycardia and to clarify the determinants of QRS alternans. An electrophysiologic study was performed in 28 consecutive patients with a narrow QRS tachycardia. Persistent QRS alternans was observed in 6 (43%) of 14 patients during orthodromic reciprocating tachycardia, 5 (71%) of 7 patients during atrial tachycardia and 3 (43%) of 7 patients during atrioventricular (AV) node reentrant tachycardia. Incremental atrial pacing during sinus rhythm resulted in QRS alternans in patients who had QRS alternans during tachycardia, unless the shortest pacing cycle length associated with 1:1 AV conduction exceeded the tachycardia cycle length. In patients without QRS alternans during narrow QRS tachycardia, incremental atrial pacing during sinus rhythm resulted in persistent QRS alternans in five patients in whom the shortest pacing cycle length associated with 1:1 AV conduction was 60 to 180 ms less than the tachycardia cycle length. In an additional 20 patients without a narrow QRS tachycardia, persistent QRS alternans was observed during incremental atrial pacing in 11 (55%) of the patients. In six of six patients who had QRS alternans during abrupt rapid atrial pacing, QRS alternans was not observed when the same pacing rates were achieved gradually. Among the patients with narrow QRS tachycardia, the mean tachycardia cycle length in those who had QRS alternans (mean +/- SD 288 +/- 44 ms) was significantly shorter than in those who did not (369 +/- 52 ms, p less than 0.001). The presence of QRS alternans was not related to the tachycardia mechanism, relative or functional refractory period of the His-Purkinje system (at a drive cycle length of 500 ms), age, presence of structural heart disease, direction of input into the AV node or concealed retrograde conduction in the His-Purkinje system. In conclusion, QRS alternans during narrow QRS tachycardias is a rate-related phenomenon that depends on an abrupt increase to a critical rate and is independent of the tachycardia mechanism.     

Termination of ventricular tachycardia with bursts of rapid ventricular pacing

Bursts of rapid ventricular pacing used during 573 episodes of ventricular tachycardia in 23 patients terminated 5 12 episodes (89 percent), with burst rates averaging 56 beats/min above the ventricular tachycardia rate, for 5 to 10 captures. Tachycardia was accelerated by pacing bursts to rates below 300 beats/min in 16 episodes (3 percent); 10 of these terminated spontaneously or responded to further bursts. Acceleration of heart rate to more than 300 beats/min or ventricular fibrillation occurred six times (1 percent), each episode requiring direct current cardioversion. Pacing bursts had no effect in 38 instances (7 percent), mostly in patients with terminal cardiogenic shock. Implantable pacemakers delivering bursts of rapid ventricular pacing were placed in two patients who have used these units at home. No deaths were associated with bursts of rapid ventricular pacing, which is an effective, rapid, pleasant alternative to repeated direct current cardioversion and a useful tool during electrophysiologic testing in patients with recurrent tachycardia.     

Atrial Pacing in Ventricular Tachycardia and Supraventricular Tachycardia with Aberrant Intraventricular Conduction: Diagnostic and Therapeutic Implications*

Summary: The diagnostic and potential therapeutic value of rapid right atrial pacing in ventricular tachycardia and supraventricular tachycardia with aberrant intraventricular conduction, was examined. The effect of right atrial pacing at incremental rates beginning 10 bpm above the rate of the tachycardia was studied in five patients with ventricular tachycardia, and in four patients with supraventricular tachycardia with rate-related bundle branch block aberration, the mechanism of tachycardia having been demonstrated at electrophysiology study. Atrial pacing resulted in persistent (four) or occasional (one) normalisation of the QRS complexes to that seen in sinus rhythm in those five patients with ventricular tachycardia. The intraventricular conduction pattern persisted with atrial pacing in those patients with supra-ventricular tachycardia and aberrant intraventricular conduction. This confirms that atrial pacing is a useful and simple diagnostic test in wide QRS tachycardia, which does not require sophisticated electrophysiological facilities. In three of the patients with ventricular tachycardia, atrial pacing terminated the arrhythmia, suggesting potential therapeutic use of rapid atrial pacing in such patients.     

Chronic Recurrent Ventricular Tachycardia—An Electrophysiological Study*

Summary: Electrophysiological techniques were used to study 17 patients with chronic recurrent ventricular tachycardia. Twelve of the patients had coronary disease, while eight had pre-existing intraventricular conduction defects. The site of origin of the tachycardia as deduced by analysis of the QRS morphology correlated well with the electrocardiographic evidence of the site of the old infarction. Ventricular tachycardia was induced by pacing techniques in eight patients while it occurred spontaneously during the study in two others. In only four of the eight patients in whom tachycardia was induced, could the arrhythmia be reinduced; the arrhythmia could not be reproduced in one, while reproducibility was not assessed in the remaining three. Tachycardia was terminated by pacing techniques in six patients and by DC cardioversion in four. Ventricular tachycardia was initiated with a run of “torsade de pointes” in four patients. Ventricular tachycardias with varying morphology were observed in three patients. Electrophysiological study was of significant benefit in patient management in 14 of the 17 patients, particularly those with pre-existing intraventricular conduction defects, undocumented tachycardia or undocumented syncope.     

Incidence of reentry with an excitable gap in ventricular tachycardia: a prospective evaluation utilizing transient entrainment

The demonstration of transient entrainment has been proposed as evidence of reentry, with an excitable gap as the probable mechanism of tachycardia. A prospective series of 27 consecutive patients with sustained ventricular tachycardia induced by programmed electrical stimulation was studied to determine the frequency with which transient entrainment can be demonstrated and to define the optimal location of pacing and recording electrodes. In all patients, electrodes for pacing and recording were placed in both the left and right ventricles during electrophysiologic study. Among the 19 patients in whom the response to rapid pacing could be evaluated (25 episodes of ventricular tachycardia), transient entrainment was demonstrated in 79% (76% of episodes). Ten of 12 episodes of ventricular tachycardia with a left bundle branch block QRS configuration in lead V1 and 9 of 13 episodes with a right bundle branch block QRS configuration could be transiently entrained (p = NS). Transient entrainment was demonstrated for 8 of 11 episodes of ventricular tachycardia with a left bundle branch block configuration during pacing from the left ventricle, but for only 2 of 10 episodes during pacing from the right ventricular apex (p less than 0.05). Conversely, 9 of 13 episodes of ventricular tachycardia with a right bundle branch block configuration were transiently entrained during pacing from the right ventricular apex, but 0 of 10 episodes were transiently entrained by left ventricular pacing (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Spectrum of regular tachycardias with wide QRS complexes in patients with accessory atrioventricular pathways

Reciprocating tachycardia and atrial flutter or fibrillation are the rhythm disorders most frequently documented in patients with accessory atrioventricular (A-V) pathways. Reciprocating tachycardia typically results in a regular tachycardia (140 to 250/min) with a normal QRS pattern, although on occasion bundle branch block aberration occurs. Atrial flutter or fibrillation may result in an irregular ventricular response, with the QRS configuration being normal or exhibiting bundle branch block or various degrees of ventricular preexcitation, or both. Although much less common than either reciprocating tachycardia or atrial flutter/fibrillation, regular tachycardias with a wide QRS complex suggestive of ventricular preexcitation are observed in patients with accessory pathways. Excluding functional or preexisting bundle branch block, several arrhythmias may cause these electrocardiographic findings which may mimic those of ventricular tachycardia.In the present study a variety of arrhythmias that resulted in tachycardias with a wide QRS complex were examined in 163 patients with accessory pathways who underwent clinical electrophysiologic study for evaluation of recurrent tachyarrhythmias. Twenty-six patients (15 percent) manifested a regular tachycardia with a wide QRS complex suggesting ventricular preexcitation. Atrial flutter with 1:1 anterograde conduction over an accessory pathway (15 of 26 patients, 58 percent) was the most frequent arrhythmia and was usually associated with a heart rate of 240/min or greater (12 of 15 patients). Reciprocating tachycardia with conduction in the anterograde direction over an accessory pathway (antidromic reciprocating tachycardia) occurred in 7 of 26 patients (27 percent), and resulted in a slower ventricular rate than atrial flutter (217 ± 22 versus 262 ± 42, P < 0.01). Other arrhythmias included reciprocating tachycardia with reentry utilizing a fasciculoventricular or nodoventricular connection (two patients, 8 percent), reciprocating tachycardia with reentry in the atrium or A-V node and anterograde accessory pathway conduction (one patient, 4 percent) and ventricular tachycardia (one patient, 4 percent).In this study the clinical electrophysiologic diagnostic features of several arrhythmias which cause tachycardias with a wide QRS compex suggesting ventricular preexcitation are outlined. It is apparent that definitive arrhythmia diagnosis during these tachycardias is often complex and usually requires careful study using intracardiac electrode catheter techniques.     

Clinical and electrophysiologic assessment of oral flecainide acetate for recurrent ventricular tachycardia: Evidence for exacerbation of electrical instability

Four patients with recurrent, symptomatic ventricular tachycardia (VT) refractory to conventional antiarrhythmic agents were given flecainide acetate to control arrhythmias. Ventricular stimulation studies were performed in all patients before and 1 to 2 weeks after initiation of oral flecainide therapy. Before flecainide, all patients had easily inducible VT that was morphologically identical to their spontaneously occurring arrhythmia. Flecainide increased the mean PR interval (from 0.17 to 0.23 second), mean QRS duration (from 0.08 to 0.12 second) and mean ventricular effective refractory period (from 235 to 270 ms). Mean corrected QT interval did not change (0.51 second).In 2 patients, VT could not be induced during follow-up stimulation studies. One patient has been treated successfully for 10 months, with no clinically apparent episodes of VT. One patient had recurrent nonsustained VT and was withdrawn from the study as a treatment failure after 6 months of therapy. Two patients had inducible, polymorphous VT that degenerated into ventricular fibrillation that required 2 countershocks before the successful restoration of sinus rhythm. One of these patients had VT stimulation by atrial pacing at a cycle length of 320 ms in the postflecainide electrophysiologic study. VT was not inducible by atrial pacing during this patient's preflecainide study.Thus, sustained oral flecainide administration may precipitate serious electrical instability in susceptible patients, and ventricular stimulation studies and other clinical variables may be useful in selecting patients with recurrent VT who may benefit or may be endangered by oral flecainide therapy.     

Idiopathic sustained left ventricular tachycardia: clinical and electrophysiologic characteristics

Electrophysiologic studies were performed in 16 patients 11 to 45 years old (mean 33 years) with idiopathic sustained (lasting more than 5 min) ventricular tachycardia (VT) originating from the left ventricle. Endocardial mapping during VT showed that the earliest site of activation was at the apical inferior portion of the left ventricle in 14 patients whose QRS morphology during VT showed a right bundle branch block pattern and left-axis deviation, but at the apical anterosuperior portion of the left ventricle in two patients whose QRS morphology during VT showed a right bundle branch block and right-axis deviation. Single programmed ventricular stimulation induced VT in 13 patients, and rapid ventricular pacing induced VT in the remaining three patients. Rapid ventricular pacing terminated VT in all patients. The relationship between the coupling interval and the echo interval was inverse in all eight patients with a wide VT inducible zone. Entrainment was recognized in three of six patients. The initiation of VT by constant pacing depended on the number of pacing beats but not the duration of pacing in all four patients tested. Intravenous verapamil terminated the VT in 13 of 14 patients. Long-term oral verapamil was also effective in all five patients who required long-term oral therapy for their symptoms associated with VT. In conclusion (1) idiopathic left ventricular tachycardia has unique electrocardiographic, electrophysiologic, and electropharmacological properties, (2) the electrophysiologic characteristics suggest that the mechanism is reentry, and (3) verapamil is effective in both the short- and long-term treatment of VT.     

Incidence and clinical significance of induced ventricular tachycardia

Five hundred twenty-nine patients were studied with programmed ventricular stimulation for evaluation of supraventricular and ventricular tachyarrhythmias. Eighty-six patients had clinical ventricular tachycardia. Sustained ventricular tachycardia was induced in 52 (91 percent) of the 57 patients with a sustained form of the arrhythmia clinically. Nonsustained ventricular tachycardia was induced in 18 (62 percent) of 29 patients with a symptomatic nonsustained form clinically, in 2 (4 percent) of 57 patients with a sustained form and in 3 (0.7 percent) of the 443 patients with no documented spontaneous ventricular tachycardia. Ventricular tachycardia (sustained or nonsustained) was induced by double right or left ventricular extrastimuli in 47 patients (63 percent) and by single right ventricular extrastimuli in 23 (31 percent); in 5 (7 percent), it was inducible only by rapid ventricular pacing and in 9 (12 percent) only by left ventricular stimulation.All 52 patients with induced sustained ventricular tachycardia had the sustained form clinically. Of the 23 patients with induced nonsustained ventricular tachycardia, 18 (78 percent) had the nonsustained form clinically. Four hundred fifty-four patients had no induced ventricular tachycardia; only 14 (3 percent) of these had the arrhythmia spontaneously. The morphologic features, axis and cycle length of 54 of 62 episodes of induced ventricular tachycardia in 43 patients were similar to those of the clinically observed arrhythmia. It is concluded that ventricular tachycardia resembling the clinical variety can be induced in the laboratory in almost all patients with sustained ventricular tachycardia clinically, in the majority of those with symptomatic nonsustained ventricular tachycardia clinically, and only rarely in patients with no previously documented ventricular tachycardia. Conversely, induction of ventricular tachycardia implies the likelihood of spontaneous episodes of this arrhythmia.     

Electrocardiographic observations on the termination of supraventricular tachycardia by verapamil.

The effect of intravenous verapamil on the termination of supraventricular tachycardia (SVT) was studied by continuous electrocardiographic monitoring of 27 episodes of SVT. Progressive increase of the cycle length heralded conversion in eight episodes while cycle-length alternation preceded cessation of the arrhythmia in 13 episodes. In five patients the arrhythmia was either stopped or closely followed by a ventricular premature beat (VPB), followed by further VPBs in three. Runs of bizarre ventricular tachycardia followed initial sinus-beats in two patients. Sinus standstill, lasting 30 seconds, was observed in one patient. The first post SVT beats had an aberrant QRS configuration with a normal P-R interval in four cases and an aberrant QRS complex with a short P-R interval, resembling Wolff-Parkinson-White complexes, in a further seven patients. The possible mechanisms causing this variability of pre- and post-conversion period are discussed. It is suggested that some aspects of verapamil action may be explained by a parasympaticomimetic effect on the myocardium.     

Polymorphous ventricular tachycardia: clinical features and treatment.

Thirty-four cases of ventricular tachyarrhythmia characterized by polymorphy of the QRS complexes with changing R-R intervals and a heart rate of 150 to 300 beats/min, termed polymorphous ventricular tachycardia, are described. The factors involved in the appearance of this arrhythmia were the administration of antiarrhythmic drugs (quinidine 22 patients, procainamide 5 patients, ajmaline 1 patient), antianginal drugs (prenylamine [Synadrin] 4 patients) and antidepressant drugs (thioridazine 1 patient). Twenty-one patients were treated for premature ventricular complexes, three for chronic recurrent ventricular tachycardia, six for atrial flutter and fibrillation, three for anginal pain and one patient for mental depression. All patients except one had a drug-induced prolonged corrected Q-T interval before the appearance of polymorphous ventricular tachycardia. Most of the patients with this arrhythmia were considered to have severe myocardial disease. Lidocaine and electric cardioversion were administered to all patients, but were effective only in seven patients whose tachycardia occurred in short, single episodes. The most effective treatment (17 patients) was temporary ventricular pacing at rates ranging from 100 to 140 beats/min. Intravenous isoproterenol proved to be successful in another 10 cases. It is concluded that patients with severe myocardial involvement receiving antiarrhythmic drugs for premature ventricular complexes, especially the multiform variety, are at high risk for the development of polymorphous ventricular tachycardia.     

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.     

Catheter ablation of idiopathic exercise-induced right bundle branch block and left axis deviation ventricular tachycardia

Catheter ablation of ventricular tachycardia was performed in a patient without evidence of structural heart disease. ECG showed ventricular tachycardia and a right bundle branch block QRS configuration with left axis deviation induced by exercise and atrial pacing. At electrophysiology, presystolic activation was found in the low septal region of the left ventricle. Radiofrequency energy delivered to this site failed to prevent tachycardia. Three direct current shocks (total energy 400 J) delivered in this region rendered the tachycardia noninducible. There were no complications. During the follow-up period of six months the patient has remained free from arrhythmia on no medication. This report expands the use of catheter ablation to patients with idiopathic ventricular tachycardia ('verapamil responsive' ventricular tachycardia) originating in the left ventricle.     

Permanent radiofrequency ventricular pacing for management of drug-resistant ventricular tachycardia

Three patients with frequent episodes of symptomatic, sustained ventricular tachycardia that often required physician intervention were treated with a permanent patient-activated radiofrequency ventricular pacemaker for self-termination of ventricular tachycardia. Before pacemaker implantation, electrophysiologic testing revealed the tachycardia to be resistant to all approved and several investigational antiarrhythmic drugs. In all three patients, ventricular tachycardia was reliably and reproducibly terminated with brief bursts of rapid right ventricular apical pacing over several hundred trials. No patient had rapid ventricular pacing-induced acceleration of ventricular tachycardia or pacing-induced ventricular fibrillation. Since the implantation of a radiofrequency ventricular pacemaker an average of 13.7 months ago, all episodes of ventricular tachycardia (average 43/patient) have been terminated successfully by radiofrequency pacing, and no patient has required hospitalization for an arrhythmia-related problem.     

Mechanisms of regular,wide QRS tachycardia in infants and children

A regular, wide QRS tachycardia was electrocardiographically documented in 32 patients aged 1 month to 18 years. The mechanisms of the tachycardia were evaluated using standard multicatheter electrophysiologic techniques. These mechanisms included (1) orthodromic reciprocating tachycardia with bundle branch aberration (seven patients), (2) antidromic reciprocating tachycardia using single (three patients), or multiple (three patients) atrioventricular connections (Kent bundles), (3) atrial flutter with ventricular preexcitation over accessory connections (eight patients), (4) reciprocating tachycardia using a nodoventricular connection (Mahaim fiber) (five patients), and (5) ventricular tachycardia (six patients). Regular, wide QRS tachycardias are not rare in pediatric patients. Their mechanisms can be quite complex, and electrocardiographic analysis with respect to QRS configuration, heart rate, or the presence or absence of ventriculoatrial dissociation is not sufficient for diagnostic purposes. Our results show that considerable understanding of the mechanism of regular, wide QRS tachycardias can be obtained by multicatheter electrophysiologic study. Understanding the mechanism is essential in order to make rational use of available therapeutic options.