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At least 127 records · Page 7Linked to original sources
PubMed1999

Radiofrequency catheter ablation of coexistent atrioventricular reciprocating tachycardia and left ventricular tachycardia originating in the left anterior fascicle.

Coexistence of supraventricular tachycardia and ventricular tachycardia is rare. A patient with no structural heart disease and wide QRS complex tachycardia with a right bundle block configuration and right-axis deviation underwent electrophysiological examination. A concealed left atrioventricular pathway (AP) was found, and atrioventricular reciprocating tachycardia (AVRT) and left ventricular tachycardia (VT) originating in or close to the anterior fascicle of the left ventricle were both induced. Radiofrequency (RF) catheter ablation of the concealed left AP was successfully performed. Ten months later, VT recurred and was successfully ablated using a local Purkinje potential as a guide. Coexistent AVRT and idiopathic VT originating from within or near the left anterior fascicle were successfully ablated.

Adult↗
PubMed2004

[Paroxysmal tachycardia in a patient with a permanent form of junctional reciprocating tachycardia. A case report].

Junctional reciprocating tachycardia is an atrioventricular reentrant tachycardia whose anterograde conduction occurs via the His Purkinje and the retrograde conduction via an accessory pathway with slow conduction. The most common form is incessant tachycardia but a paroxysmal form also exists. We report a 35 years old female with recurrent paroxysmal tachycardia, that underwent electrophysiological evaluation. A left posterolateral accessory pathway was documented. Reciprocating paroxysmal tachycardia was induced by electrical stimulation and a successful pathway ablation was performed.

Adult↗
PubMed1990

Sinus tachycardia masquerading as ventricular tachycardia.

We describe here a 87-year-old male who came to the emergency room with the chief complaints of dyspnea and chest pain. His electrocardiogram showed a wide QRS tachycardia with a heart rate of 140 beats/min, a left bundle branch block pattern and low voltage in leads I, aVL, V5 and V6. A long strip showed a premature ventricular complex, and the sinus beat just after the extrasystole showed P waves which were positive in leads I, II, III and a VF similar in shape to those in sinus rhythm. Therefore, a diagnosis of sinus tachycardia with tachycardia dependent left bundle branch block was made. The low voltage in the left lateral leads was ascribed to pneumothorax of the left lung. When a wide QRS tachycardia is encountered in an emergency situation, marked sinus tachycardia with coexistent bundle branch block or aberrant ventricular conduction should be taken into consideration.

Aged↗
PubMed1989

Wide QRS tachycardia in the conscious adult. Ventricular tachycardia is the most frequent cause.

Hemodynamic stability during wide QRS tachycardia is commonly, albeit erroneously, taken as evidence for a supraventricular mechanism. To determine the magnitude for potential misdiagnosis in applying this notion clinically, we analyzed 20 consecutive cases of regular wide QRS tachycardia in conscious adult patients (mean age, 64 years). The most common heart disease was atherosclerotic (75%), with an associated history of remote myocardial infarction in 73% of the cases. Tachycardia was sustained for a mean of 4.8 hours prior to medical evaluation, with a mean rate of 186 beats per minute and mean systolic blood pressure of 111 mm Hg. A diagnosis of ventricular tachycardia (VT) was established in 17 cases (85%). In the patients with VT, atrioventricular dissociation was recognized on the 12-lead electrocardiogram in 38%, with Wellens' morphological features favoring the diagnosis in 73%. Following conversion to sinus rhythm, electrophysiological testing in 17 patients reproduced the clinical arrhythmia in 94% (with a replication rate of 100% in 15 patients with VT), with at least one additional unsuspected VT morphology induced in 53% of patients with VT. Thus, VT should be considered the most likely cause of regular wide QRS tachycardia in the conscious adult patient, especially with a history of remote myocardial infarction. Recognition of this simple principle and careful examination of the 12-lead electrocardiogram may help to prevent the misapplication of pharmacotherapy in the vast majority of these patients.

Aged↗
PubMedDate not supplied

Supraventricular tachycardia that mimics ventricular tachycardia. Part II.

Concealed WPW is a newly described clinical entity. The existence of this syndrome can be ascertained only through specific electrophysiologic intracardiac studies. From the clinical standpoint, the existence of an accessory unidirectional A-V pathway anatomically located in the general area of the Kent bundle should be suspected in those patients with chronic BBB who have recurrent paroxysmal atrial tachycardias initiated by sinus arrhythmias or premature atrial beats. It should be noted that functional BBB can occur following a premature atrial beat. This will also set the stage for the initiation of a reciprocating tachycardia in concealed WPW. Pharmacological therapy aimed at preventing the recurrent tachycardias is disappointing. Pacemaker implantation appears to be successful by rendering one of the bundle branches refractory through concealed conduction. With chronic block of the remaining bundle branch, the natural pathway of A-V conduction is totally blocked at a critical time during the tachycardias, thus eliminating the reciprocating tachycardia.

Adult↗
PubMedDate not supplied

Resolution of tachycardia-induced cardiomyopathy following ablation of verapamil-sensitive idiopathic left ventricular tachycardia.

Few reports have described tachycardia-induced cardiomyopathy secondary to ventricular tachycardia. We present a 12-year-old boy with dilated cardiomyopathy and incessant verapamil-sensitive idiopathic left ventricular tachycardia. Twelve-lead electrocardiogram showed right bundle branch block QRS morphology with superior axis during tachycardia. Electrophysiology study confirmed the diagnosis, and radiofrequency ablation was done and successfully terminated and prevented induction of ventricular tachycardia. During the follow-up period of 18 months, the patient remained free of symptoms and arrhythmia. Three months after ablation, left ventricular ejection fraction improved and cardiac silhouette became normal on chest x-ray.

Cardiomyopathy, Dilated↗
PubMed1983

Influence of tachycardia cycle length and antiarrhythmic drugs on pacing termination and acceleration of ventricular tachycardia.

We examined the influence of ventricular tachycardia (VT) cycle length and antiarrhythmic drugs on the frequency of VT termination and acceleration by single and double extrastimuli and right ventricular burst pacing. In 57 patients, 89 episodes of sustained VT (32 control, 57 drug) were induced by programmed electrical stimulation. Overall, 60 of 89 (67%) episodes of ventricular tachycardia were terminated by means of programmed electrical stimulation. In patients with relatively slow ventricular tachycardia (VT cycle length greater than or equal to 350 msec) pacing terminated 37 of 44 (84%) episodes but terminated only 24 of 45 (51%) episodes of more rapid VT (VT cycle length less than or equal to 349 msec, p less than 0.005). Pacing successfully terminated VT in nine of 49 (18%) episodes using a single extrastimulus, 22 of 52 (42%) episodes using double extrastimuli, and 40 of 66 (61%) episodes using burst right ventricular pacing. VT acceleration occurred in none of 49 attempts with a single extrastimulus, in eight of 52 (15%) attempts with double extrastimuli, and in 12 of 66 (18%) attempts using burst right ventricular pacing. During therapy, the frequency of either ventricular tachycardia termination or acceleration did not change regardless of the pacing termination method used. However, by prolonging the mean VT cycle length from 311.1 +/- 82.2 msec to 401.9 +/- 103.5 msec (p less than 0.01), drugs increased the overall frequency of VT termination. We conclude that: (1) pacing terminates VT more frequently if the VT cycle length is long and if right ventricular bursts are used, (2) burst right ventricular pacing increases the risk of VT acceleration, and (3) drugs increase the frequency of ventricular tachycardia termination by prolonging VT cycle length but do not affect frequency of VT acceleration.

Adult↗
PubMed1979

Carotid sinus massage induced elimination of rate related bundle branch block during paroxysmal atrial tachycardia: a simple method of proving bypass tract participation in the tachycardia.

Four cases of paroxysmal atrial tachycardia are described in whom rate related left bundle branch block (LBBB) was often present which persisted indefintely and showed no signs of spontaneous disappearance. Transient slowing of the tachycardia by carotid sinus massage in each case eliminated LBBB and this led to tachycardia acceleration. The tachycardia acceleration was traceable to a shortening in ventriculoatrial conduction. These observations proved the participation of a left sided bypass tract in the tachycardia circuit in each of these cases.

Bundle-Branch Block↗
PubMed1979

Transfer of coupling of premature ventricular contractions to an ectopic ventricular tachycardia: a mechanism for atypical bidirectional tachycardia.

Bidirectional tachycardia was observed on Holter tracings recorded from a dog three days after the production of a small freeze lesion on the wall of the left ventricle. A bigeminal rhythm with fixed coupling of ventricular premature contractions was interrupted by a burst of ventricular tachycardia of different morphology. The ventricular premature contractions, originally coupled to the sinus beats, became coupled to the new ventricular tachycardia with an identical coupling interval. This resulted in a dibirectional tachycardia, created by the "transfer" of coupling of premature ventricular contractions to a separate ectopic ventricular tachycardia.

Animals↗
PubMed1984

Resetting of tachycardia cycle by single and double ventricular extrastimuli in recurrent sustained ventricular tachycardia.

In two cases with recurrent sustained ventricular tachycardia (VT) due to re-entry, the response pattern to extrastimuli during the tachycardia was studied. In each case, right ventricular extrastimuli with longer coupling intervals during VT were followed by fully compensatory pauses and with shorter coupling intervals reset the tachycardia cycle. In one case, a plateau was produced by a single extrastimulus, resembling that seen in the response curve of sinus node automaticity as well as ectopic atrial tachycardia. Two successive stimuli produced three definite zones, i.e., fully compensatory, reset producing a plateau, and progressive prolongation zones with shortening of the coupling intervals between the two stimuli, and terminated the tachycardia with further shortening of the coupling intervals. In conclusion, resetting phenomenon was confirmed on two cases with re-entrant VT. This phenomenon cannot be used as a criterion to determine the mechanism responsible for VT.

Adult↗
PubMed1990

Termination of ventricular tachycardia by nonpropagated local depolarization: further observations on entrainment of ventricular tachycardia from an area of slow conduction.

A 60-year-old woman with a large left ventricular apical aneurysm underwent preoperative catheter mapping of ventricular tachycardia. A zone of slow conduction with marked decremental conductive properties was identified between the left ventricular aneurysmal pouch and the right ventricular septum. Pacing from the right ventricular septum produced a QRS on the surface electrocardiogram of the same morphology as that of spontaneous ventricular tachycardia, while pacing from the left ventricular aneurysm caused tachycardia entrainment without fusion. Termination of ventricular tachycardia invariably occurred in association with an unpropagated left ventricular capture, followed by a change in ventricular activation to an opposite direction. This case provides a direct demonstration of reentrant ventricular tachycardia termination by orthodromic block in a zone of slow conduction.

Bundle-Branch Block↗
PubMed2003

Differential diagnosis of slow/slow atrioventricular nodal reentrant tachycardia from atrioventricular reentrant tachycardia using concealed posteroseptal accessory pathway by 12-lead electrocardiography.

Slow pathways are used as both antegrade and retrograde conduction pathway in slow/slow atrioventricular nodal reentrant tachycardia (SS-AVNRT), and patients with SS-AVNRT have tachycardia ECGs mimicking atrioventricular reentrant tachycardia using concealed posteroseptal accessory pathway (PS-AVRT). Therefore, SS-AVNRT can be misdiagnosed as PS-AVRT, and the differential diagnosis is clinically important. Standard 12-lead ECGs during tachycardia were analyzed in patients with SS-AVNRT (n = 10) and PS-AVRT (n = 10). All these patients were diagnosed by electrophysiological study and underwent successful catheter ablation. Differences of the RP' intervals (dRP') between V1 and the inferior leads were evaluated. SS-AVNRT had significantly longer RP' intervals measured in V1 (167 +/- 25.2 vs 137 +/- 26.8 ms, SS-AVNRT vs PS-AVRT, respectively, P = 0.02), longer dRP' between V1 and II (dRP'[V1-II], 37 +/- 14 vs 17 +/- 6.7 ms, P = 0.0007), longer dRP'[V1-III] (39 +/- 14 vs 17 +/- 9.9 ms, P = 0.0011), and longer dRP'[V1-aVF] (39 +/- 13 vs 20 +/- 9.5 ms, P = 0.0008). The following criteria were suggested for differential diagnosis of SS-AVNRT from PS-AVRT: dRP'[V1-II] >25 ms (sensitivity and specificity: 80% and 100%, respectively), dRP'[V1-III] >23 ms (90% and 90%), dRP'[V1-aVF] >30 ms (90% and 90%). Differences of the RP' intervals between V1 and the inferior leads in the tachycardia ECGs were useful for differential diagnosis of SS-AVNRT from PS-AVRT.

Adult↗
PubMed1996

Bundle branch reentry tachycardia and possible sustained interfascicular reentry tachycardia with a shared unusual induction pattern.

A case of bundle branch reentry tachycardia with an unusual induction pattern is presented. Unlike typical cases of this arrhythmia in which tachycardia is usually inducible with routine programmed ventricular stimulation and/or short-long sequences, tachycardia in this case was inducible only with atrial stimulation. It also arose spontaneously during atrial flutter and during isoproterenol administration. After ablation of the right bundle, possible interfascicular reentry tachycardia with a similar induction pattern was observed. This tachycardia was successfully ablated in the region of the posterior fascicle of the left bundle branch.

Aged↗
PubMed2006

Tachycardia-induced cardiomyopathy in a young Boxer dog with supraventricular tachycardia due to an accessory pathway.

A 1-year-old male Boxer dog presented with sustained supraventricular tachycardia and tachycardia-induced cardiomyopathy. Conversion to sinus rhythm was achieved initially with intravenous lignocaine and subsequently with oral procainamide. Oral procainamide treatment was relatively successful in maintaining normal sinus rhythm with no side effects apart from a reversible change in coat colour. Electrophysiological studies demonstrated the presence of an accessory pathway connecting the right atrium to the right ventricle and confirmed the diagnosis of orthodromic atrioventricular reciprocating tachycardia. Radiofrequency catheter ablation of the accessory pathway led to permanent resolution of the supraventricular tachycardia and for 9.5 years the dog has had no further signs of cardiac disease. The successful treatment of this condition highlights the importance of differentiating tachycardia-induced cardiomyopathy from dilated cardiomyopathy.

Animals↗
PubMed1994

Ventricular tachycardia: an unusual pacemaker-mediated tachycardia.

A 74 year old man had recurrent ventricular tachycardia, which was well controlled with amiodarone, and complete heart block for which a VVI permanent pacing system had previously been implanted. After an elective increase in the programmed pacemaker rate from 70 to 82 beats/min, there was recurrence of frequent episodes of ventricular tachycardia. Each episode of tachycardia was initiated by a fusion beat consisting of a ventricular extrasystole and a paced beat. When the pacemaker rate was reprogrammed to 70 beats/min the episodes of tachycardia ceased abruptly. It is proposed that the fusion of a ventricular extrasystole with a pacemaker beat may have induced ventricular tachycardia, even though neither of these beats occurring separately was sufficient to cause this.

Aged↗
PubMedDate not supplied

Adenosine-sensitive wide-complex tachycardia: an uncommon variant of idiopathic fascicular ventricular tachycardia--a case report.

Most wide-complex tachycardias encountered in the emergency department (ED) are ventricular in origin, most commonly associated with structural heart disease. Ventricular tachyarrhythmias range in severity from life-threatening rhythms (eg, ventricular fibrillation and hemodynamically compromising ventricular tachycardia [VT]) to idiopathic forms of VT, which have a benign clinical course and a more favorable prognosis. The authors present the case of a 34-year-old woman who presented to the ED, with a wide-complex tachycardia with a right-bundle-branch block (RBBB) morphology and a right inferior axis, which was terminated with adenosine. The patient was previously misdiagnosed as suffering from a paroxysmal supraventricular tachycardia (SVT), which was unresponsive to beta-blocker therapy. Although the tachycardia responded to adenosine, suggestive of an SVT, the patient was referred to the arrhythmia service, where further work-up revealed an uncommon form of an idiopathic VT, originating from the left anterior fascicle. The authors discuss the unique electrocardiographic and electrophysiologic properties and useful diagnostic maneuvers required to properly identify this form of VT.

Adenosine↗
PubMed1988

[Termination of idiopathic ventricular tachycardia with QRS morphology of right bundle branch block and anterior fascicular hemiblock (fascicular tachycardia) by vagal maneuvers. Presentation of 4 cases].

We present 4 patients aged 51, 19, 22 and 16 years respectively, with no overt heart disease. They complained of recurrent episodes of paroxysmal sustained tachycardia with QRS morphology of right bundle branch block and left fascicular hemiblock. The analysis of the electrocardiogram during the tachycardia and, in two cases, the electrophysiologic study showed a complete a-v dissociation and capture beats confirming the ventricular origin of the arrhythmia. In all the patients the interruption of the tachycardia was obtained by the vagal maneuvers; in two of them the tachycardia was also sensitive to verapamil iv. These cases demonstrate the efficacy of the vagal maneuvers in the termination of fascicular tachycardia and support the hypothesis of slow-response nodal-like fibers, distally displaced, as the anatomical substrate of this arrhythmia.

Adolescent↗
PubMed1994

[Atrioventricular reciprocating tachycardia with QRS type left branch block in patients undergoing radiofrequency catheter ablation: analysis of the substrate and mechanism of tachycardia].

BACKGROUND: Among patients (pts) with atrioventricular accessory pathway (AP), some cases show wide complex arrhythmias with different QRS morphology. In a subset of these pts, an atrioventricular reentrant tachycardia with left bundle branch block morphology (LBBBM-AVRT) is observed. The aim of this study is: 1) to identify the substrate and the reentrant mechanism underlying the LBBBM-AVRT in pts undergoing radiofrequency catheter ablation (RFCA) of AP; 2) to report the results achieved by RFCA of the identified substrate. METHODS: From May 1991 to April 1993, among the 168 pts who underwent RFCA for arrhythmias related to an AP, 12 (7.1%) (8M, 4F, mean age 35 +/- 21 yrs, range 8-65) showed LBBBM-AVRT, alone or associated with other arrhythmias. Pts, in whom LBBBM was rate-related during orthodromic AVRT, were excluded from this study. During sinus rhythm, QRS complex was normal in 1 pt, while ventricular preexcitation due to a right-sided Kent bundle (KB) was present in 4 pts; among the other pts without preexcitation, 3 showed left bundle branch block (LBBB) and 4 right bundle branch block. In 2 pts, an Ebstein disease was present, while dilated cardiomyopathy was observed in another. The LBBBM-AVRT was iterative in 3 pts and in 6 pts it was the only arrhythmia observed; the mean tachycardia cycle length was 341 +/- 49 msec (range 250-428). In 1 pt, the LBBBM-AVRT was induced only after successful RFCA of a right-sided AP, responsible for orthodromic AVRT. All pts underwent diagnostic electrophysiologic study and RFCA during the same session. RESULTS: In 6/12 pts one or more KBs were observed, while in the remaining 6 an atrioventricular or atriofascicular "Mahaim like" bundle (MB) was present; the patient population was divided into 4 groups on the basis of the substrate and the reentrant mechanism responsible for LBBBM-AVRT. In Group 1, 3 pts were included: the LBBBM-AVRT was an orthodromic AVRT involving the nodal conduction antegradely (showing LBBB also during sinus rhythm) and a left-sided unidirectional KB, retrogradely. In all the 3 pts, the LBBBM-AVRT was iterative and not controlled by antiarrhythmic agents and RFCA of the KB abolished the arrhythmia. Two further pts were included in Group 2: in these pts with multiple bilateral KBs, the LBBBM-AVRT involved a right-sided KB antegradely and a left-sided one, retrogradely. In these 2 pts both KBs were successfully ablated. In 1 pt, considered in Group 3, the LBBBM-AVRT was sustained by an antidromic circuit involving a right-sided KB antegradely and the nodal conduction retrogradely; in this pt the KB was completely interrupted after two RFCA procedures. The remaining 6 pts with MB were included in Group 4: at least one associated electrophysiologic abnormality was present in all (dual A-V nodal pathway in 4/6 and a right-sided KB in 4/6); Ebstein disease was also observed in 2 of them. In 4/6 pts the LBBBM-AVRT was an antidromic tachycardia involving the nodal conduction retrogradely and the MB antegradely; in 3/4 pts the MB was ablated (along with a nodal reentrant tachycardia in 1 pt), while in the remaining pt in whom the non-sustained LBBBM-AVRT, inducible only after RFCA of a right-sided KB, had not been clinically observed, no further ablation was mandatory. In the remaining 2 pts in Group 4, the LBBBM-AVRT was due to the involvement of MB in other arrhythmias such as an AVRT due to a right-sided KB and a "slow-slow" nodal reentrant tachycardia, respectively; the LBBBM-AVRT were abolished by RFCA of these two underlying arrhythmias. All pts are asymptomatic during a 7.9 +/- 6.9 months follow-up. CONCLUSIONS: The LBBBM-AVRT is observed in a minority (7.1%) of the cases referred for RFCA of AP. (ABSTRACT TRUNCATED)

Adolescent↗