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PubMed1990

Prognostic role of inducible ventricular tachycardia in patients with dilated cardiomyopathy and asymptomatic nonsustained ventricular tachycardia.

We studied the prognostic relevance of inducible ventricular tachycardia in 32 patients with dilated cardiomyopathy and spontaneous nonsustained asymptomatic ventricular tachycardia. Programmed ventricular stimulation included basic drive cycle lengths of 600, 500, 430, 370, 330 and 300 msec at single, double, and triple extrastimuli. Ventricular tachycardia (greater than or equal to 6 beats) was initiated in 7 patients (22%), with sustained monomorphic ventricular tachycardia being seen in 4 of them. During median follow-up of 21 months (13-44), 14 patients died. Sudden cardiac death occurred in two of the seven patients with inducible tachycardia and in only one of the 25 patients in whom it was not possible to induce tachycardia. Although patients with inducible tachycardia did not differ clinically from those in whom tachycardia could not be induced, the projected mean survival time was significantly shorter in those with inducible tachycardia (10 months vs. 32 months, P = 0.04). For late sudden cardiac death, the positive predictive value of inducible tachycardia was 28%. The negative predictive value was 96%. We conclude that induction of ventricular tachycardia by programmed stimulation might indicate poorer prognosis in patients with dilated cardiomyopathy.

Adult↗
PubMed1994

Radiofrequency ablation of fascicular tachycardia: efficacy of pace-mapping and implications on tachycardia origin.

Verapamil-sensitive but adenosine resistant left ventricular tachycardia (fascicular tachycardia) is a recognised cause of ventricular tachycardia occurring in patients without overt cardiac disease. This study addresses (1) the efficacy of radiofrequency ablation guided by pace-mapping technique in the treatment of this tachycardia, and (2) the location of this tachycardia in the left ventricle as assessed by simultaneous ventriculography. Five patients (two women and three men, mean age 25 +/- 8 years) with ventricular tachycardia exhibiting a right bundle branch block and left axis deviation morphology, with documented response to verapamil but resistance to intravenous adenosine triphosphate were studied. Biplane left ventricular cineangiography was first performed to visualise the topography of the left ventricle. Pace-mapping at a rate within 10 beats/min of the tachycardia rate was performed, and the concordance of paced QRS configuration with that of the induced tachycardia was compared for each of the 12 leads for major or minor differences. A perfect pace-map could be achieved in all five patients (two in posteroseptal left ventricle and three in the posterior left ventricular wall). Five of eight applications at an identical pace-map resulted in suppression of tachycardia induction, whereas none of the 39 applications at sites with a less identical map was successful (P < 0.001). After a successful procedure, there was no recurrence as assessed clinically, by non-invasive monitoring (event recording, Holter monitoring and exercise testing for all patients) and repeat electrophysiology testing (three patients) during a follow-up of 12 +/- 3 months. Thus radiofrequency ablation guided by pace-mapping technique is a highly efficacious treatment for fascicular tachycardia. The response to radiofrequency ablation suggests the origin of tachycardia as reentry circuits involving the lower septum or posterior part of the left ventricle close to or within the endocardial surface.

Adult↗
PubMed1995

Localisation of ventricular tachycardia substrates by analysis of the surface QRS recorded during ventricular tachycardia.

BACKGROUND: Analysis of the surface ECG can predict the locations of pacing foci but is of limited value for locating arrhythmogenic substrates causing ventricular tachycardia because of the effects of myocardial infarction, ischaemia, and bundle branch block on ventricular activation. AIM: To determine whether analysis of the initial 60 ms segment of the surface QRS improves the accuracy of the ECG for predicting ventricular tachycardia origin we correlated the locations of 37 arrhythmogenic areas present in 20 patients with the 3D vectors of the ventricular tachycardias generated by each respective area. METHODS: The 3D vector of each ventricular tachycardia morphology was calculated from the integrals of the initial 60 ms of the surface vectorcardiogram and from the entire QRS recorded in each lead of the Frank orthogonal lead vectorcardiogram. Sixty eight-morphologies of ventricular tachycardia were mapped using simultaneous recordings from 60 catheter electrodes. RESULTS: Ventricular tachycardias with 3D vectors directed inferiorly and posteriorly or superiorly and anteriorly were more likely to originate from the septum, P = 0.04, whereas tachycardias directed superiorly and to the right were more likely to originate from the inferior wall and the cardiac apex, P = 0.001. However, the same arrhythmogenic area could generate multiple ventricular tachycardias with different 3D vectors. In addition, ventricular tachycardias with similar 3D vectors were generated by arrhythmogenic areas in the septal, apical and inferior walls. The variances of the mean 3D vectors of ventricular tachycardias originating from each of 12 different cardiac regions were no different when based on the initial 60 ms of the surface QRS than on the entire surface QRS. CONCLUSION: Analysis of the surface ECG provides only an approximate guide to the locations of arrhythmogenic areas generating ventricular tachycardia even when analysis is restricted to the initial forces in the surface QRS. Therefore, detailed mapping is needed to accurately determine the number and location of arrhythmogenic areas.

Bundle-Branch Block↗
PubMed1988

Fast-slow type of atrioventricular nodal reentrant tachycardia: horizontal dissociation of the AV node during tachycardia.

Two patients with recurrent supraventricular tachycardia are presented. The tachycardia was initiated and terminated by atrial extrastimulation beyond the atrial relative refractory period and the atrial activation sequence during the tachycardia was low to high. The induction of tachycardia was dependent on a critical AH interval. In patient 1 who had ventriculoatrial conduction, the tachycardia was initiated by the premature ventricular stimulation followed by double atrial response. In patient 2 the ventriculoatrial conduction was not observed. In both patients, the unchanged atrial cycle length during the tachycardia with antegrade Wenckebach AH block was observed. When AH block occurred during tachycardia the first AH interval was shorter than the subsequent HA interval. In patient 2 verapamil (5 mg) prolonged the atrial cycle length during tachycardia and rapid intravenous injection of adenosine triphosphate (10 mg) terminated the tachycardia. Oral diltiazem (180 mg/day) suppressed the tachycardia in patient 1. These findings suggest that the mechanism of tachycardia may be fast-slow type of AV nodal reentry in the upper portion of the AV node and this type of arrhythmia has tendency to show incessant form.

Adenosine Triphosphate↗
PubMed2004

Heart failure and sudden death in patients with tachycardia-induced cardiomyopathy and recurrent tachycardia.

BACKGROUND: Tachycardia-induced cardiomyopathy is a reversible cause of heart failure. We hypothesized that although left ventricular ejection fraction measurements normalize after heart rate or rhythm control in patients with tachycardia-induced cardiomyopathy, recurrent tachycardia may have abrupt and deleterious consequences. METHODS AND RESULTS: Patients with tachycardia-induced cardiomyopathy that developed over years were evaluated and treated. Tachycardia episodes and outcomes were assessed. Twenty-four patients were identified. All had NYHA functional class III heart failure or greater on presentation. One third were heart transplant candidates. There were 17 men and 7 women with a mean age of 46+/-16 years and mean left ventricular ejection fraction of 0.26+/-0.09 at the index visit. The cause was atrial fibrillation (n=13), atrial flutter (n=4), atrial tachycardia (n=3), idiopathic ventricular tachycardia (n=1), permanent junctional reciprocating tachycardia (n=2), and bigeminal ventricular premature contractions (n=1). Within 6 months of rate control or correction of the rhythm, left ventricular ejection fraction improved or normalized and symptoms abated in all. Five patients had tachycardia recur. In these patients, left ventricular ejection fraction dropped precipitously and heart failure ensued within 6 months, even though the initial impairment took years. Rate control eliminated heart failure and improved or normalized ejection fraction in 6 months. Three of 24 patients died suddenly and unexpectedly. CONCLUSIONS: Tachycardia-induced cardiomyopathy develops slowly and appears reversible by left ventricular ejection fraction improvement, but recurrent tachycardia causes rapid decline in left ventricular function and development of heart failure. Sudden death is possible.

Adult↗
PubMed1995

Recurrent tachycardia after selective ablation of slow pathway in patients with atrioventricular nodal reentrant tachycardia.

Recurrence rate of atrioventricular (AV) nodal reentrant tachycardia after successful radiofrequency ablation varies widely, and the determinants of recurrent AV nodal reentrant tachycardia remain controversial. Furthermore, true or pseudorecurrence of tachycardia after successful ablation in patients with different forms of AV nodal reentrant tachycardia has not been evaluated systematically. Three hundred sixty-two patients (161 men and 201 women [mean age 52 +/- 16 years]), including 314 patients with typical-form, 10 patients with atypical-form, 4 patients with variant-form, and 34 patients with multiple-form AV nodal reentrant tachycardias, received selective radiofrequency ablation of the anterograde and/or retrograde slow AV nodal pathway. During a mean follow-up of 27 +/- 11 months, 9 patients (2.5%) experienced recurrent AV nodal reentrant tachycardia (true recurrence, group A), and 8 (2.2%) had inappropriate sinus tachycardia or paroxysmal atrial tachyarrhythmias (pseudorecurrence, group B). Neither the true nor pseudorecurrence rate was different among the 4 different forms of tachycardia. Factors including presence of residual slow pathway conduction, a single AV nodal reentrant echo beat, absence of an accelerated junctional rhythm during successful ablation, facilitating induction of tachycardia by isoproterenol, radiofrequency pulse number, and successful ablation site were not associated with an increased risk of recurrent AV nodal reentrant tachycardia. The onset time of recurrent tachycardia was significantly late in group B patients (30 +/- 21 vs 292 +/- 240 days, p = 0.04). Thus, this study demonstrated that both true and pseudorecurrence could occur after successful ablation.

Adolescent↗
PubMed1986

A single atrial extrastimulus can distinguish sinus tachycardia from 1:1 paroxysmal tachycardia.

We have developed a tachycardia detection scheme for use in an antitachycardia pacemaker in which the use of a properly timed atrial extrastimulus provides a means of discriminating sinus tachycardia from pace-terminable 1:1 tachycardias. An atrial extrastimulus is delivered in late diastole (80 ms premature), and the ventricular response is monitored. In sinus tachycardia, the ventricular response is expected to appear early as well, but in pace-terminable tachycardias, such as AV reentrant and ventricular with VA conduction, the ventricular rhythm will be unperturbed. Testing of the algorithm was performed in 34 patients. In 29 patients, atrial extrastimuli were delivered during sinus tachycardia, and in 22 patients during various types of 1:1 paroxysmal tachycardia. In one patient the procedure was completely automated, i.e., delivery of the atrial extrastimuli and diagnosis were microcomputer controlled. In 28/29 cases, the delivery of an atrial extrastimulus 80 to 120 ms early during sinus tachycardia elicited a ventricular response at least 28 ms early. In 22/22 patients with 1:1 paroxysmal tachycardia, atrial extrastimuli 80 to 120 ms early failed to produce a significant change in ventricular cycle length. This technique appears to be promising for prevention of inadvertent pacing of sinus tachycardia in an antitachycardia pacemaker.

Diagnosis, Computer-Assisted↗
PubMed1975

Junctional reciprocating tachycardias. The permanent and paroxysmal forms of A-V nodal reciprocating tachycardias.

Stimulation technics have demonstrated a reciprocating mechanism in many supraventricular tachycardias previously classified from a purely morphologic point of view. Three conditions are required for the creation of a circus movement: a potential circuit pathway, undirectional block in this curcuit, and slowed conduction. While all three conditions are readily apparent in reciprocating tachycardias of the WPW syndrome, two or even all of these factors may be concealed in the others forms. Paroxysmal reciprocating tachycardias are characterized by prolongation of the P-R interval in the beat immediately preceding the tachycardia, and are generally accepted as being related to longitudinal dissociation of the A-V node, though the possibility of unidirectional (anterograde) block of an extra-nodal accessory pathway should be appreciated. Permanent reciprocating tachycardias start after a normal P-R interval when the sinus cycle reaches a critical value. Both paroxysmal and permanent forms of reciprocating tachycardia must be differentiated from tachycardias located in the atria: one of the most reliable features of reciprocating tachycardia is the existence of a 1:1 A-V relationship which cannot be altered without interrupting the tachycardia. Study of capture phenomena during the tachycardia, and the modes of termination not only permit the demonstration of the reentry mechanism but may also determine more precisely the actual location of the circus movement.

Adult↗
PubMed1999

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.

Adrenergic beta-Antagonists↗
PubMed1982

Termination of ventricular tachycardia: role of tachycardia cycle length.

The mode of termination of ventricular tachycardia (VT) and its relation to tachycardia cycle length was evaluated in 139 patients. Tachycardia was terminated by programmed stimulation in 110 patients (79%) and cardioversion was required in 29 patients (21%). Single, double, and triple ventricular extrastimuli terminated the tachycardia in 23 of 85 (27%), 39 of 62 (63%), and 7 of 16 patients (44%), respectively. In all patients requiring 1 extrastimulus, in 35 patients (90%) requiring 2 extrastimuli, and in 6 patients (86%) requiring 3 extrastimuli, the tachycardia cycle length exceeded 300 ms. Rapid ventricular pacing terminated tachycardia in 41 of 54 patients (76%). In 21 (51%) of these patients the tachycardia cycle length exceeded 300 ms. However, rapid ventricular pacing caused acceleration of the arrhythmia in 19 patients (35%). The ability of procainamide to modify the termination of VT was studied in 23 patients. In 7 of these patients (30%) procainamide increased the tachycardia cycle length by 49 +/- 42 ms (p less than 0.01) and did not modify the mode of termination. In 6 patients (26%) procainamide increased cycle length by 142 +/- 108 ms (p less than 0.01), but termination was more difficult. In 10 patients (44%) procainamide increased the cycle length by 138 +/- 110 ms (p less than 0.001) and termination was easier. We conclude that termination of VT by timed extrastimuli requires a tachycardia cycle length longer than 300 ms. Rapid pacing or cardioversion is usually required when the cycle length is less than 300 ms. Although procainamide slows tachycardia, it can unpredictably make termination more difficult in 1 of 4 patients.

Adolescent↗
PubMed1979

Atrial pacing in ventricular tachycardia and supraventricular tachycardia with aberrant intraventricular conduction: diagnostic and therapeutic implications.

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 supraventricular 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.

Adult↗
PubMed1986

Spontaneous termination of paroxysmal supraventricular tachycardia following disappearance of bundle branch block ipsilateral to a concealed atrioventricular accessory pathway: the role of autonomic tone in tachycardia diagnosis.

We present a case of an 18-year-old man with a history of palpitations in whom episodes of paroxysmal supraventricular tachycardia were easily initiated by administered atrial premature beats. In all 15 control episodes of tachycardia, functional left bundle branch block (LBBB) seen at the onset, resolved within 10-20 cycles (mean, 13.1 +/- 0.95). The tachycardia ended with the normalized QRS complex in each episode. Eleven episodes ended because of block within the antegrade pathway (ended with a P-wave), and four episodes stopped because of block within the retrograde pathway (ended without a P-wave). During the administration of isoproterenol (1 mg/min IV) all six episodes of tachycardia had LBBB but these did not end when LBBB disappeared spontaneously. When LBBB subsided, the mean tachycardia cycle interval shortened from 328.5 +/- 1.4 to 264.2 +/- 2.1 ms (p less than 0.001). Each episode of tachycardia was then terminated by carotid sinus massage. The disappearance of LBBB in control conditions presented the retrograde and antegrade limbs of the reentrant circuit with an early impulse that stopped the tachycardia. After isoproterenol administration, the tachycardia did not end following disappearance of LBBB, thus enabling the tachycardia cycle interval to shorten by a mean of 64.3 +/- 1.9 ms. This extent of tachycardia acceleration is diagnostic of the participation of a concealed, left free-wall bypass tract.

Adolescent↗
PubMed1986

Incidence of symptomatic tachycardia in untreated patients with paroxysmal supraventricular tachycardia.

The purpose of this article is to investigate the occurrence of symptomatic paroxysmal supraventricular tachycardia (PSVT) in untreated patients and to assess factors that influenced its occurrence. We studied 34 patients with this arrhythmia during an observation period in which they received no antiarrhythmic drug therapy for up to 90 days. Recurrence of PSVT was documented by telephone transmission of the electrocardiogram. Each patient was allowed to have exactly one episode of tachycardia before being removed from the study. We measured how long patients remained free of their tachycardia (the tachycardia-free period) and heart rate during tachycardia. Twenty-nine of the 34 patients had an attack of symptomatic tachycardia within the 90-day observation period. The proportion of patients who had not had any symptomatic PSVT by each day of follow-up was calculated using the Kaplan-Meier method as follows: 75% by day 3, 50% by day 19, 25% by day 36, and 17% by day 90. Patients with any other heart or lung disease had significantly shorter tachycardia-free periods. The mean heart rate during spontaneous tachycardia was 203.5 +/- 34.9 beats per minute (range, 142 to 288 beats per minute). Patients with longer tachycardia-free periods had significantly faster heart rates during tachycardia.

Adult↗
PubMed1988

Ventricular tachycardia masquerading as supraventricular tachycardia: a wolf in sheep's clothing.

It is generally assumed that if a wide QRS complex tachycardia has the same morphology on the 12-lead electrocardiogram as during sinus rhythm, the tachycardia is supraventricular. The author presents unique electrocardiographic data on four patients with QRS complex morphologies that are nearly identical during ventricular tachycardia and during sinus rhythm. The QRS complex duration during sinus rhythm was 140-180 msec and was the same as that of the tachycardia. The QRS complex morphology on the electrocardiogram was a right bundle branch block, left axis in three patients and right bundle branch block, normal axis in one patient. The mean ventricular tachycardia cycle length was 345 msec. The diagnosis of ventricular tachycardia was established by electrophysiologic testing in two patients and by atrial electrograms demonstrating AV dissociation in two patients. Thus, if the 12-lead electrocardiogram morphology of a wide QRS complex tachycardia is similar to that during sinus rhythm, it does not necessarily imply that the tachycardia is supraventricular. Ventricular tachycardia can occur with the same QRS complex morphology as occurs during sinus rhythm.

Adult↗
PubMed2003

Usefulness of ST-segment elevation in lead aVR during tachycardia for determining the mechanism of narrow QRS complex tachycardia.

In the present study, we analyzed ST-segment elevation in lead aVR during tachycardia to differentiate the narrow QRS complex tachycardia. A total of 338 12-lead electrocardiograms during narrow QRS complex tachycardia were analyzed. Each patient underwent a complete electrophysiologic study. There were 161 episodes of atrioventricular nodal reentrant tachycardia (AVNRT), 165 episodes of atrioventricular reciprocating tachycardia (AVRT), and 12 episodes of atrial tachycardia (AT). The prevalence of aVR ST-segment elevation was 71% for AVRT, 31% for AVNRT, and 16% for AT. For ST-T changes in different leads, logistic regression analysis showed aVR ST-segment elevation was the only significant factor to differentiate the types of narrow QRS complex tachycardia (p<0.001 for AVRT and AVNRT; p=0.02 for AVRT and AT). The sensitivity, specificity, and accuracy of aVR ST-segment elevation to differentiate AVRT from AVNRT and AT were 71%, 70%, and 70%, respectively. Among 117 episodes of AVRT with aVR ST-segment elevation, there were 76 (65%) left side, 23 (20%) right side, 14 (12%) posterior septal, and 4 (3%) antero- and mid-septal accessory pathways (p=0.002). In conclusion, aVR ST-segment elevation during narrow QRS complex tachycardia favors the atrioventricular reentry through an accessory pathway as the mechanism of the tachycardia.

Adult↗
PubMed1994

Coincident idiopathic left ventricular tachycardia and atrioventricular nodal reentrant tachycardia: control by radiofrequency catheter ablation of the slow atrioventricular nodal pathway.

A healthy 37-year-old male presented with a history of frequent palpitations and sustained wide QRS complex tachycardia with a right bundle branch block and left axis morphology. Serial electrophysiological studies revealed two inducible tachycardias, which were shown to represent atrioventricular nodal reentrant tachycardia and idiopathic left ventricular tachycardia. Transformation from one tachycardia to the other occurred spontaneously as well as following atrial or ventricular pacing. Radiofrequency catheter ablation of the slow atrioventricular nodal pathway resulted in cure of atrioventricular nodal reentrant tachycardia and the prevention of spontaneous recurrence of ventricular tachycardia, suggesting a role of atrioventricular nodal reentrant tachycardia in triggering the clinical episodes of ventricular tachycardia. The patient has remained asymptomatic without antiarrhythmic therapy for 8 months.

Adult↗
PubMed1998

[Ventricular tachycardia masquerading as supraventricular tachycardia].

To distinguish supraventricular tachycardia with aberrancy from ventricular tachycardia is sometimes difficult. It seems to be easy to distinguish the two forms in patients with preexisting bundle branch block: if the QRS morphology during tachycardia is identical to those during at rest the tachycardia is supraventricular, if different, ventricular. We present two cases with preexisting bundle branch block and wide complex tachycardia whose QRS morphologies were almost same to those during normal rest rhythm. The atrioventricular dissociation and the response to adenosine and lidocaine strongly suggests ventricular tachycardia. In these cases ventricular tachycardia masqueraded as supraventricular tachycardia and the identical QRS morphology with the preexisting bundle branch block may suggest a misdiagnosis of supraventricular tachycardia.

Aged↗
PubMed1998

"Cristal tachycardias": origin of right atrial tachycardias from the crista terminalis identified by intracardiac echocardiography.

OBJECTIVES: We sought to use intracardiac echocardiography (ICE) to identify the anatomic origin of focal right atrial tachycardias and to define their relation with the crista terminalis (CT). BACKGROUND: Previous studies using ICE during mapping of atrial flutter and inappropriate sinus tachycardia have demonstrated an important relation between endocardial anatomy and electrophysiologic events. Recent studies have suggested that right atrial tachycardias may also have a characteristic anatomic distribution. METHODS: Twenty-three consecutive patients with 27 right atrial tachycardias were included in the study. ICE was used to facilitate activation mapping in relation to endocardial structures. A 20-pole catheter was positioned along the CT under ICE guidance. ICE was also used to assist in guiding detailed mapping with the ablation catheter in the right atrium. RESULTS: Of 27 focal right atrial tachycardias, 18 (67%, 95% confidence interval [CI] 46% to 83%) were on the CT (2 high medial, 8 high lateral, 6 mid and 2 low). ICE identified the location of the tip of the ablation catheter in immediate relation to the CT in all 18 cases. The 20-pole mapping catheter together with echocardiographic visualization of the CT provided a guide to the site of tachycardia origin along this structure. Radiofrequency ablation was successful in 26 (96%) of 27 (95% CI 81% to 100%) right atrial tachycardias. CONCLUSIONS: This study demonstrates that approximately two thirds of focal right atrial tachycardias occurring in the absence of structural heart disease will arise along the CT. Recognition of this common distribution may potentially facilitate mapping and ablation of these tachycardias.

Adolescent↗