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PubMed2002

Two cases of polymorphic ventricular tachycardia induced by the administration of verapamil against paroxysmal supraventricular tachycardia.

Verapamil is widely used for the termination of paroxysmal supraventricular tachycardia (PSVT) with little proarrhythmic effect. We describe two cases of PSVT that changed to non-sustained polymorphic ventricular tachycardia after administration of verapamil. Electrophysiological study revealed atrioventricular nodal reentrant tachycardia in the first case, and atrioventricular reentrant tachycardia due to a concealed left lateral accessory pathway in the second case. Catecholamine-induced automaticity was one of the possible mechanisms of VT in the first case, but the mechanism is unknown in the second case.

Anti-Arrhythmia Agents↗
PubMed2005

[Tachycardia with rSr' <110 ms in lead V1 -- is it always an atrio-ventricular nodal tachycardia?].

We present a case of a 15-year old girl in whom supraventricular tachycardia (SVT) with rSr' pattern in lead V1 and the QRS width of less than 110 ms, suggesting typical slow-fast AVNRT, was the presenting arrhythmia. During sinus rhythm no preexcitation was observed. Considerable variability of the tachycardia cycle length (240-370 ms), attributable to the presence of the fast and slow nodal pathways, was also observed. However, during the electrophysiological study only orthodromic atrio-ventricular reciprocating tachycardia with the left-sided superior accessory pathway as the retrograde limb was documented. Thus, rSr' pattern was due to incomplete right bundle branch block. We describe how the correct diagnosis and the site of the atrial insertion of the accessory pathway could be inferred from the careful analysis of the P' wave morphology during the tachycardia.

Adolescent↗
PubMed1993

A case of tachycardia-induced cardiomyopathy due to chronic ectopic atrial tachycardia.

Only a few reports exist that chronic supraventricular tachycardia causes ventricular dilation and poor left ventricular contraction--so-called "tachycardia-induced cardiomyopathy." Clinical and electrophysiologic features of chronic supraventricular tachycardia including chronic persistent ectopic atrial tachycardia (EAT) in adults have also been described by a few investigators. We report a rare case of long follow-up of chronic EAT-induced severe cardiomyopathy and mitral regurgitation that was well controlled after medical treatment.

Cardiac Catheterization↗
PubMed2002

Anti-tachycardia therapy can improve altered cardiac adrenergic function in tachycardia-induced cardiomyopathy.

We investigated whether anti-tachycardia therapy might improve the altered cardiac adrenergic and systolic function in tachycardia-induced cardiomyopathy (TC) in contrast to dilated cardiomyopathy (DCM). The subjects were 23 patients with heart failure, consisting of 8 patients with TC (43.6 +/- 10.0 yrs) and 15 with DCM (45.3 +/- 8.2 yrs). TC was determined as impairment of left ventricular function secondary to chronic or very frequent arrhythmia during more than 10% of the day. All patients were receiving anti-tachycardia treatment. Cardiac 123I-MIBG uptake was assessed as the heart/mediastinum activity ratio (H/M) before and after treatment. LVEF was also assessed. In the baseline study, H/M and LVEF showed no difference between TC and DCM (2.21 +/- 0.44 vs. 2.10 +/- 0.42, 35.3 +/- 13.1 vs. 36.0 +/- 10.9%, respectively). After treatment, the degree of change in H/M and LVEF differed significantly (0.41 +/- 0.34 vs. 0.08 +/- 0.20, 20.5 +/- 14.4 vs. -2.1 +/- 9.6%, p < 0.01). In TC, heart failure improved after a shorter duration of treatment (p < 0.05). In conclusion, anti-tachycardia therapy can improve altered cardiac adrenergic function and systolic function in patients with TC over a shorter period than in those with DCM.

3-Iodobenzylguanidine↗
PubMed1981

Termination of circus movement tachycardia utilizing an accessory atrioventricular pathway by retrograde concealed penetration of the atrioventricular node through the bundle branch system. A mechanism of tachycardia termination in Wolff-Parkinson-White syndrome.

A 30 year old woman with Wolff-Parkinson-White syndrome underwent electrophysiologic study for investigation of circus movement tachycardia utilizing the accessory pathway for retrograde conduction. The accessory pathway was located on the right side. Episodes of circus movement tachycardia with left and right bundle branch block were induced. Some episodes of circus movement tachycardia with left bundle branch block terminated spontaneously. Two episodes of spontaneous termination at the level of the atrioventricular (A-V) node were preceded by prolongation of the H-V interval causing delay in atrial activation. This delayed atrial cycle was then followed paradoxically by spontaneous termination of the tachycardia in the A-V node. A similar phenomenon could be demonstrated reproducibly with single echo beats induced by coronary sinus extrastimuli. It appears that retrograde concealed penetration of the A-V node through the bundle branch system during anterograde left bundle branch block is the most likely mechanism for this phenomenon.

Adult↗
PubMed1975

Pacing techniques in the management of supraventricular tachycardias. Part 1. The use of high frequency stimulation (HFS) in the management of paroxysmal supraventricular tachycardia.

Using techniques for programmed electrical stimulation of the heart, seven patients with paroxysmal supraventricular tachycardia have been studied and shown to have a reciprocal mechanism as the most likely basis for the tachycardia. In four patients it was found that the tachycardia could be terminated by single right atrial premature beats and in three patients two right atrial premature beats were required. A variable zone for tachycardia termination was found when single or double stimuli were used and so a system for introducing high frequency stimuli at 100 or 1000 stimuli/sec for a given duration is described. Using this system a wider range of the cardiac cycle could be covered, thereby increasing the likelihood of producing correctly timed premature beats. The results of using this system are presented and its practical usage discussed.

Adult↗
PubMed1986

Programmed electrical stimulation studies for ventricular tachycardia induction in humans. I. The role of ventricular functional refractoriness in tachycardia induction.

Closely coupled extrastimuli are frequently necessary to induce ventricular tachycardia at electrophysiologic study. Although induction usually requires propagated extrastimuli, systematic evaluations of minimal coupling intervals have focused on nonpropagated measures (effective refractory periods) rather than on propagated measures (functional refractory periods). The effects of procedural factors on ventricular functional refractory periods were examined in 10 patients. Like the effective refractory period, the functional refractory period shortens with rapid pacing cycle lengths (281 +/- 12 ms at a cycle length of 600 ms; 260 +/- 15 ms at a cycle length of 400 ms) and with multiple extrastimuli (279 +/- 16 ms with one extrastimulus; 214 +/- 16 ms with two extrastimuli). The effects of multiple extrastimuli exceed those of shortening pacing cycle length. Unlike the effective refractory period, the functional refractory period is affected by recording site (increasing as the distance from the pacing site increases) but is not affected by increasing the stimulus intensity above twice diastolic threshold (282 +/- 14 ms at 2 times threshold; 282 +/- 13 ms at 16 times threshold) or by increasing the pulse width above 2 ms (282 +/- 13 ms at a pulse width of 2 ms; 282 +/- 14 ms at a pulse width of 5 ms). The effect of varying stimulus intensity on ventricular tachycardia induction was examined in a second group of 11 patients with documented, spontaneous ventricular tachycardia. No change in ventricular tachycardia inducibility accompanied changes in stimulus intensity from 2 to 10 times threshold.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Paroxysmal fascicular tachycardia and ventricular tachycardia due to mechanical stimulation by a mitral valve prosthesis.

Electrophysiologic studies were performed in a woman who had two varieties of paroxysmal wide QRS tachycardia after mitral valve replacement with a Starr-Edwards prosthesis. One tachycardia originated in the left anterior fascicle; QRS complexes were 100 ms wide and resembled right bundle branch block with left posterior fascicular block, and a His bundle potential preceded each QRS by an interval of 20 ms (compared with 50 ms during sinus rhythm). The other tachycardia originated in the left ventricle. Clinical and echocardiographic observations suggested that the tachycardias were caused by mechanical stimulation of the interventricular septum by the mitral prosthesis.

Adult↗
PubMed2003

Inducible atrioventricular nodal reentry tachycardia in infants with a history of neonatal orthodromic reciprocating tachycardia.

Atrioventricular nodal reentry tachycardia (AVNRT) is an uncommon mechanism of supraventricular tachycardia in neonates in whom orthodromic reciprocating tachycardia (ORT) predominates. We report three patients with structurally normal hearts who presented with neonatal ORT, documented by transesophageal electrophysiology studies at 2 to 3 weeks of age. At follow-up study at 8-12 months of age, no infant had inducible ORT, suggesting spontaneous regression of congenital accessory pathways; however, each had inducible tachycardia consistent with the typical form of AVNRT. The clinical significance of this finding is unknown and warrants further study.

Anti-Arrhythmia Agents↗
PubMed2000

[Idiopathic right ventricular tachycardia or arrhythmogenic right ventricular tachycardia?].

HISTORY: While cycling a 38-year-old man suddenly experienced palpitations associated with marked weakness. 90 min later his general practitioner, having diagnosed a ventricular tachycardia (VT) with a rate of 218/min, terminated it by a drug injection. INVESTIGATIONS: Electrocardiography (ECG), echocardiography and biventricular cardiac catheterization with right ventricular contrast injection failed to provide any evidence of structural abnormality. However, ergometry and EPS with programmed ventricular stimulation induced VT of identical morphology (left bundle branch bloc [LBBB] with right axis deviation [RAD]). TREATMENT AND COURSE: Idiopathic right-ventricular outflow tract tachycardia (IRVT) having been diagnosed, the patient was put on a maintenance dose of 50 mg/d atenolol. After 6 months without symptoms he again experienced several attacks of tachycardia. Resting ECG merely revealed an epsilon potential and negative T waves in V1-V3. Right ventricular contrast injection revealed inferolateral dyskinesia. EPS demonstrated both the known VT and a second, morphologically different one (LBBB with LAD). These findings indicated arrhythmogenic right-ventricular cardiomyopathy (ARCV). A cardioverter/defibrillator was implanted (ICD) and over the subsequent 8 months he had six episodes of VT which were quickly terminated by the ICD. CONCLUSION: At first presentation of right-ventricular outflow tract tachycardia it is often not possible to differentiate between IRVT and arrhythmogenic RV cardiomyopathy. The two being significantly different in prognosis and treatment, follow-up monitoring is essential to establish the definitive diagnosis.

Adult↗
PubMed1984

Tachycardia-termination algorithm: a valuable feature for interruption of pacemaker-mediated tachycardia.

A 45-year-old man who had been implanted with a VVI pacemaker for sinus arrest complained of syncope, dizziness and throbbing in the neck. His pacemaker function was normal, but during ventricular pacing, retrograde V-A conduction was observed. This pacer was replaced by a DVI unit which caused periodic abdominal muscular contractions. We replaced this unit with an Intermedics Cosmos DDD-M pacemaker. This type of pacemaker in a patient with V-A conduction may cause pacemaker-mediated tachycardia (PMT). However, the Cosmos has a tachycardia-termination algorithm which detects continued pacing at the ventricular tracking rate, allows it to proceed for 15 consecutive pace events, and inhibits the 16th ventricular output pulse, thus breaking the reentry loop. The Cosmos pacer has a number of features to prevent initiation of PMT, and is also able to terminate the tachycardia when it occurs because of the tachycardia-termination algorithm. This feature is valuable in DDD-M pacemakers implanted in patients with V-A conduction. Whether this algorithm will be effective in all cases remains to be determined.

Abdominal Muscles↗
PubMed2004

Retrograde cycle length alternans during supraventricular tachycardia: an unusual tachycardia mechanism.

Cycle length alternans is occasionally seen during supraventricular tachycardia due to oscillations in the antegrade atrioventricular nodal (AVN) refractoriness. However, alternans due to retrograde variation in AVN conduction has not been reported. This report describes the case of a 36-year-old man with atypical AVN reentry tachycardia (AVNRT) whose episodes of tachycardia were characterized by continuous oscillations in retrograde AVN conduction. Ablation at one spot eliminated the tachycardia. Cycle length alternans due to oscillations in retrograde AVN conduction, although rare, can be seen during atypical AVNRT and should be considered.

Adult↗
PubMed2006

Latent atriofascicular pathway participating in a wide complex tachycardia: differentiation from ventricular tachycardia.

Accessory pathways with anterograde decremental conduction properties usually are characterized by presence of antegrade preexcitation during atrial pacing. We report a 38-year-old man with frequent episodes of palpitation. No evidence of ventricular preexcitation was seen during sinus rhythm or atrial pacing. All electrophysiologic maneuvers were compatible with an antidromic tachycardia using atriofascicular pathway as the antegrade limb and the atrioventricular nodal pathway as retrograde limb. Radiofrequency ablation at recording site of accessory pathway potential resulted in cure of tachycardia with no recurrence during 3-month follow-up. This report indicated that atriofascicular pathway-mediated tachycardia should be considered in differential diagnosis of all cases of wide complex tachycardia with left bundle branch morphology and left axis.

Adult↗
PubMed1976

Intractable paroxysmal tachycardia caused by a concealed retrogradely conducting Kent bundle. Demonstration by epicardial mapping and cure of tachycardias by surgical interruption of the His bundle.

Electrophysiological and epicardial mapping studies are described in a patient without pre-excitation who had intractable recurrent paroxysmal supraventricular tachycardia. Electrophysiological studies revealed fixed VA conduction times during both rapid ventricular pacing and coupled ventricular stimulation. Catheter mapping of atrial activation during retrograde conduction and during induced paroxysmal supraventricular tachycardia revealed early distal coronary sinus activation (posterior left atrium) relative to the low septal, low lateral, and high lateral right atrium. These studies suggested the presence of a concealed left-sided bypass tract. The patient underwent surgical interruption of the His bundle for control of paroxysmal supraventricular tachycardia. Epicardial mapping of the atria (during ventricular pacing) confirmed the presence of a concealed left-sided bypass tract. Surgery produced antegrade av block (while retrograde conduction was maintained) and total cure of paroxysmal supraventricular tachycardia. This is the first reported case of a concealed retrograde extranodal pathway documented by epicardial mapping.

Adult↗
PubMed2002

Characterization of reentrant circuits in left atrial macroreentrant tachycardia: critical isthmus block can prevent atrial tachycardia recurrence.

BACKGROUND: Left atrial macroreentrant tachycardia (LAMRT) has not been characterized in detail. METHODS AND RESULTS: Twenty-eight patients with LAMRT, including 4 patients with ablated typical atrial flutter (AFL), underwent electroanatomic mapping of the left atrium (LA) between February 1999 and October 2001. LA maps were performed during LAMRT in 26 patients and during sinus rhythm in 2 patients. Electrically silent areas or continuous lines of double potentials were identified as acquired anatomic barriers in all patients. In 23 of 26 patients with LAMRT mapping, 42 reentry circuits with a protected isthmus were identified. The isthmus was 11.8+/-5.9 mm wide, with the maximal amplitude of 0.07 to 3.61 mV. Radiofrequency pulses terminated all LAMRTs in 23 patients and resulted in conduction block across the isthmus in 20 patients. In 2 patients with sinus mapping, all identified isthmuses were ablated. Additionally, AFL was induced and ablated in 6 patients. Atrial tachycardia recurred in 4 patients: 3 patients without validated block across the isthmus presented with recurrence of the same LAMRT, and 1 patient without ablated cavotricuspid isthmus presented with AFL. All tachycardias were abolished during a second procedure. Of 25 patients with identified isthmuses, 20 patients were without atrial arrhythmia and 5 had only atrial fibrillation during a median follow-up of 14 months. CONCLUSION: The reentry circuit with a protected isthmus can be identified in 89% patients with LAMRT by electroanatomic mapping. The isthmuses were amenable to radiofrequency applications in most patients. No atrial tachycardia recurred in any patients with isthmus block.

Adolescent↗
PubMed1999

Electrophysiological delineation of the tachycardia circuit in atrioventricular nodal reentrant tachycardia.

BACKGROUND: The exact boundaries of the reentry circuit in atrioventricular nodal reentrant tachycardia (AVNRT) have not been convincingly defined. METHODS AND RESULTS: To define the tachycardia circuit, single extrastimuli were delivered during AVNRT to 8 sites of the right intra-atrial septum: 3 arbitrarily divided sites of the AV junction extending from the His bundle (HB) site to the coronary sinus ostium (CSOS) (sites S, M, and I) and the superior (S-CSOS), inferior (I-CSOS), posterior (P-CSOS), and posteroinferior (PI-CSOS) portions of the CSOS and the CSOS in 18 patients. The mean tachycardia cycle length (TCL) was 368+/-52 ms. Retrograde earliest atrial activation was observed at the HB site in all patients. The longest coupling intervals of single extrastimuli that reset AVNRT at sites S, M, I, I-CSOS, CSOS, S-CSOS, P-CSOS, and PI-CSOS were 356+/-51, 356+/-51, 355+/-52, 357+/-51, 318+/-47, 305+/-53, 311+/-56, and 312+/-56 ms, respectively, and the following return cycles at these sites were 368+/-52, 368+/-53, 367+/-53, 367+/-53, 407+/-66, 431+/-73, 415+/-55, and 412+/-56 ms, respectively. The longest coupling intervals at sites S, M, I, and I-CSOS did not differ from each other and were longer than those at CSOS and S-, P-, and PI-CSOS (P<0.0001). The return cycles at sites S, M, I, and I-CSOS did not differ from the TCL, whereas those at CSOS and S-, P-, and PI-CSOS were longer than the TCL (P<0.0001). CONCLUSIONS: The perinodal atrium extending from the HB site to I-CSOS was involved in the tachycardia circuit. I-CSOS was thought to be the entrance of the slow pathway.

Adult↗
PubMed1975

Prolongation of the tachycardia zone: a possible mechanism for medical failure in paroxysmal supraventricular tachycardia.

Paroxysmal supraventricular tachycardia in man has been considered to be due to either development of reentry utilizing AV junctional tissue or the presence of an ectopic pacemaker located within the atrium. Most contemporary information suggests that AV junctional reentry is the dominant mechanism for this arrhythmia in man. This present study identifies that the frequence of tachycardia episodes may be correlated with the width of a tachycardia zone as determined by the atrial extrastimulus technique. Moreover, pharmacological therapy directed toward the elimination of this arrhythmia can be assessed utilizing this atrial stimulation technique. Findings in this present study identify that, in patients with widened tachycardia zones, propranolol therapy may not be efficacious. This latter finding is no contrast to the previous observations suggesting that propranolol therapy is the drug of choice for reentrant arrhythmias in man.

Atrioventricular Node↗
PubMed1975

The mechanism of supraventricular tachycardia induced by a single premature beat in the isolated left atrium of the rabbit. II. The termination of the tachycardia.

Tachycardias induced by a single stimulus in the left atrium of the rabbit, are based on a circus movement of the impulse through the atrial myocardium. Circus movement often stopped spontaneously after only one beat ("coupled extrasystole") or after a small number of beats. This frequent early cessation of circus movement is explained by the relatively high conduction velocity and relatively long refractory period in the early stage of tachycardia. As an exception tachycardia lasted for a longer period. The circulating impulse then could always be interrupted by the application of a properly timed stimulus. In this case the circulating impulse will encounter the activation wave elicited by the stimulus. This resulted either in termination or resetting of the tachycardia.

Action Potentials↗