Bedside Termination of Sustained Ventricular Tachycardia by Transesophageal Atrial Pacing

Transesophageal atrial pacing was used to terminate hemodynamically stable sustained monomorphic ventricular tachycardia in two patients. The procedure was performed at the bedside, no anesthesia was required, there were no complications, and one of the patients went home after the procedure was performed. This method should be considered prior to using direct current cardioversion in patients with hemodynamically stable sustained monomorphic ventricular tachycardia.     

Treatment of Drug Refractory Ventricular Tachycardia by Biventricular Pacing

GARRIGUE, S., et al. : Treatment of Drug Refractory Ventricular Tachycardia by Biventricular Pacing. In a patient with severe congestive heart failure and ischemic disease, frequent episodes of ventricular tachycardia were completely suppressed by an implantable cardioverter defibrillator with biventricular pacing     

Demonstration of Right and Left Atrial Dissociation by Atrial Rapid Pacing or Extrastimulation During Fast-Slow (Uncommon) Form of Atrioventricular Nodal Reentrant Tachycardia

Some recent works suggest that extranodal atrial fibers may form part of the reenlry circuit in the atrioventricular (AV) nodal reentrant tachycardia (AVNRT). This hypothesis is based on the fact that the perinodal dissection successfully abolished AVNRT while preserving intact AV conduction. Apart from the surgical success, the electrophysiological evidence supporting this hypothesis has not been demonstrated, especially in the uncommon (fast-slow) form of AVNRT. We present some electrophysiological evidence suggesting atrial participation in eight patients with the fast-slow form of AVNRT. During the tachycardia, rapid pacing or extrastimulation was done from the orifice of the coronary sinus (CS) and the right atrium (RA), while recording the electrograms of the CS and the low septal RA. In seven patients, right and left atrial dissociation was demonstrated during pacing from the RA, while in the remaining one this was demonstrated from the CS. The interatrial dissociation will be unlikely if the intranodal reentry circuit connects with the atria via a single upper common pathway. This suggests that the upper turnaround of the reentry circuit involves atrial tissue and that the extranodal accessory pathway with long conduction times may form the ascending limb of the circuit (atrionodal reentry). Alternatively, the reentry circuit is entirely intranodal and two or more connecting pathways are present between the atria and the circuit.     

Rapid Atrial Pacing Does Not Decrease the Atrial Defibrillation Threshold

The aim of the study was to evaluate the effect of preshock atrial pacing on the atrial defibrillation threshold (DFT) during internal cardioversion of AF. The implantable atrial defibrillator has been added to the therapeutic options for patients with recurrent episodes of persistent AF. Although the device is efficient in restoring sinus rhythm, patient discomfort is a limitation. Methods that lower the ADFT are needed. Eleven patients with AF underwent internal cardioversion. In a randomized, crossover design, ADFT testing was performed, applying a step-up protocol starting at 100 V. Rapid atrial pacing was performed with a right atrial catheter for 20 seconds at 90% of the average cycle length of the fibrillatory waves and was immediately followed by a biphasic defibrillation shock. At each energy level, pacing + shock was compared to shock only, until the level at which sinus rhythm was restored by both modes. The step-up protocol was thereafter repeated using the inverse sequence of the two modes. A total of 19 ADFTs were obtained. For 10 the ADFT was lower with pacing + shock, in 4 equal and in 5 higher, than with shock only. The ADFT (mean ± SD) with pacing + shock was   260 ± 84   V   (3.4 ± 2.9 J)   and did not differ from shock only:   268 ± 85   V   (3.8 ± 3.0 J) (P > 0.05)   . The coefficient of variation and the coefficient of reproducibility for pacing + shock was 16% and 60 V, respectively, and for shock only 17% and 61 V. Rapid atrial pacing did not influence the internal ADFT in AF. The randomized, crossover protocol used was reproducible between different modes, and seems useful when testing the impact of different interventions on the ADFT. (PACE 2003; 26[Pt. I]:1461–1466)     

Rapid Ventricular Tachycardia Due to His-Purkinje Reentry

Two patients developed rapid His-Purkinje reentrant tachycardia during programmed ventricular stimulation for evaluation of recurrent ventricular tachycardia. In Patient 1, His-Purkinje reentry induced a morphologically distinct ventricular tachycardia which may have been a reentrant circuit operating independently for several cardiac cycles. His-Purkinje reentry was not inducible in Patient 2 until lidocaine was given. Following lidocaine administration, sustained His-Purkinje reentrant tachycardia was initiated by 2 premature ventricular stimuli. The tachycardia was rapid (240 beats per minute) and required cardioversion.     

Permanent Rapid Atrial Pacing to Control Supraventricular Tachycardia

A case is reported of a patient who had continuous supraventricular tachycardia with a ventricular rate of about 170. The arrhythmia was refractory to drugs and DC countershock, and did not convert with atrial pacing. Rapid atrial stimulation controlled the ventricular rate by simulating atrial fibrillation (pacing at 300-400/min), or by simulating a faster atrial tachycardia with 2:1 conduction (pacing at 205-210/min). This form of therapy was used on a permanent basis for more than five months.     

Acceleration of Ventricular Tachycardia by Rapid Overdrive Pacing Combined with Extrastimuli

A case of attempted termination of ventricular tachycardia using rapid overdrive pacing combined with double extrastimuli resulted in acceleration of the ventricular tachycardia. This case demonstrates the potential for acceleration of ventricular tachycardia when pacing termination is utilized.     

Serum Electrolytes and Catecholamines After Cardioversion From Ventricular Tachycardia and Atrial Fibrillation

We have observed hypokalemia after cardioversion from spontaneous out-of-hospital ventricular fibrillation and induced ventricular tachycardia. To test the hypothesis that the hormone response to the hemodynamic stress of the arrhythmia initiated the change in potassium, we compared the electrolytes and hormones in three groups of patients. We observed a decrease in serum potassium and magnesium after cardioversion from ventricular tachycardia induced by programmed Stimulation but not after normal programmed stimulation of the ventricle or after cardioversion from stable atrial fibrillation. These changes were preceded first by a rise in norepinephrine and epinephrine then a rise in glucose, followed by a rise in insulin. The stimulus for these changes was probably the hypotension associated with ventricular tachycardia. The sequence of changes suggests that the decrease of potassium and magnesium after ventricular tachycardia was due to a shift of the electrolytes into cells related to the insulin-mediated movement of glucose from the blood into cells.     

Pacing for Ventricular Tachycardia

Plusieurs problèmes restent à résoudre avant que les stimulateurs puissent jouer un rôle majeur dans le traitement de la tachycardie ventriculaire. Nous citons des exemples pour illustrer quelques difficultés à résoudre. les mécanismes qui contribuent au succès ou à l'échec de la stimulation antitachycardie sont discutés. L'avenir de cette stimulation sera plus assuré dès que ces appareils serent équipés d'un cardioverteur-défibrillateur de secours.     

Adenosine-Sensitive Atrial Tachycardia

Limited data suggest that adenosine termination of atrial tachycardia is uncommon. To investigate further the effect of adenosine on atrial tachycardia, adenosine (6–12 mg) was administered during sustained atrial tachycardia in 17 patients. All patients underwent electrophysiological study to exclude other mechanisms of supraventricular tachycardia. Mean patient age was 51 ± 20 years (range 18–82 years). Seven patients had no structural heart disease. The mean atrial tachycardia cycle length was 390 ± 80 msecs (range 260–580). Sustained atrial tachycardia was induced with atrial extrastimuli in 8 patients, and was either incessant at baseline or developed spontaneously during isoproterenol infusion in 9 patients. Adenosine terminated atrial tachycardia in 3 patients (18%), transiently suppressed atrial tachycardia in 4 patients (23%), and produced AV block without affecting tachycardia cycle length in the remaining 10 patients. Adenosine sensitivity was observed in 3 of 8 patients with tachycardias initiated and terminated by atrial extrastimuli, and in 4 of 9 patients with spontaneous, but not inducible tachycardias including 3 of 4 patients with isoproterenol facilitated tachycardias. Of multiple clinical and electrophysiological variables examined as potential predictors of adenosine sensitivity, only isoproterenol facilitation of spontaneous or inducible sustained tachycardia predicted adenosine sensitivity (P = 0.02). These observations suggest that adenosine-sensitive atrial tachycardia may be more common than previously recognized. Adenosine sensitivity does not appear to be specific for tachycardia mechanism and cannot be predicted by response to pacing. Atrial tachycardias dependent on β-adrenergic stimulation are most likely to be terminated by adenosine.     

Entrainment of Ventricular Tachycardia in Arrhythmogenic Right Ventricular Tachycardia

In two patients with arrhythrnogenic right ventricular dysplasia (ARVDJ, sustained ventricular tachycardia (VT) was induced by programmed stimulations during serial drug testings. One patient had five and the other had two VT morphologies, and the sites of origin were determined by endocardial catheter mappings. When overdrive pacing was performed, constant fusion in the QflS complex was observed in the two patients. Constant fusion of a different degree was also observed at different paced cycle lengths. Both patients had dilated right ventricles and wall-motion abnormality, and the diagnosis of ARVD was further confirmed by the specimen resected at the site of origin of VT. Therefore, VT in ARVD can be entrained and reentry is the most likely mechanism of such VT.     

Successful Treatment of Ventricular Tachycardia by Physiological Pacing

The case is presented of a young patient with atrioventricular (AV) block but no evidence of other disease; in this patient exercise or stress-related syncope continued after implantation of a ventricular inhibited (VVI) pacemaker. Investigation revealed exercise-induced limited rapid multiform ventricular tachycardia (VT) which was associated with faintness or syncope. Temporary atrial triggered ventricular inhibited ventricular (VDD) pacing resulted in enhanced exercise tolerance with no significant arrhythmia. A permanent full function dual chamber [DDD] pacemaker was implanted and prevented the VT. There have been no further exercise-related symptoms during two years 0f follow up.     

Atrial Tachycardia Facilitating Initiation of Ventricular Tachycardia

A 17-year-old male was studied because of clinically documented tachycardias showing narrow and wide QRS complexes. He was found to suffer from an atrial and a ventricular tachycardia. It was demonstrated that initiation of ventricular tachycardia occurred on reaching a critical ventricular rate during atrial tachycardia. Our study illustrates the value of electrophysiological studies in patients suspected of suffering from double or multiple tachycardias. It also shows that the occurrence of one type of tachycardia may be critically related to another type of tachycardia.     

Pacing Techniques in the Prophylaxis of Junctional Reentry Tachycardia

Atrial premature beats (APBs) which encounter sufficient AV delay may initiate junctional reentry tachycardia (JRT). This form of initiation may be prevented by rendering part of the reentry circuit refractory by artificial stimulation following an APB which would otherwise initiate JRT. Two such approaches have been suggested: preexcitation pacing, that is, ventricular stimulation with a short AV delay triggered by atrial depolarization; and preemptive pacing, which consists of early atrial stimulation coupled to the initiating APB. We compared these approaches and describe them as follows. Ten patients with JRT (six with atrioventricular reentry and four with AV nodal reentry) were studied. Against a background of regular atrial drive, the range of coupling intervals over which a stimulated APB initiated JHT (tachycardia initiation window) was determined (control). The tachycardia initiation window was also measured when a second atrial stimulus followed the initiating APB 20 ms after atrial recovery (preemptive pacing) or when a ventricular stimulus closely followed the initiating APB with an AV delay of 65 ms (preexcitation pacing). The tachycardia initiation window in response to an isolated APB was also assessed following regular AV pacing with a short (65 ms) AV delay (preconditioning pacing) and the effect of preexcitation pacing following the initiating APB was also assessed after a similar drive (combined preconditioning and preexcitation pacing). All protocols were performed at two basic drive cycle lengths. The results are arranged for the slow and fast drives, respectively, and were as follows: control initiating windows—49.5, 28.5 ms; preemptive pacing initiation windows—151, 38 ms; preexcitation pacing initiation windows—26, 23.5 ms; preconditioning pacing initiation windows—45.5, 35 ms; combined preconditioning and preexcitation pacing initiation windows—10.0, 2.5 ms. Whereas preemptive pacing tended to widen the tachycardia initiation windows (a proarrhythmic effect) the combination of preconditioning and preexcitation pacing considerably reduced the possibility of JRT initiation by an atrial premature beat.     

A Prospective Evaluation of Single and Dual Current Pathways for Transvenous Cardioversion in Rapid Ventricular Tachycardia

By using a prospective randomized study design, we compared the clinical efficacy and safety of single unidirectional and bidirectional transvenous cardioversion shocks for termination of rapid ventricular tachycardia (VT) having cycle lengths less than 300 ms. A Medtronic 6880 catheter was placed in the right ventricular apex and an R2 skin patch electrode was placed over the left scapula. Patients were randomized into two groups. Group A patients received unidirectional transvenous shocks using the two catheter electrodes (right ventricular apical cathode and superior vena caval anode) which resulted in a single current pathway. Group B patients received bidirectional transvenous shocks using a common cathode (right ventricular apex) and two separate anodes (superior vena caval and R2 patch) resulting in two current pathways. Identical shocks with total energies of 2.7, 5.0 and 10.0 J and waveform tilt of 27% were delivered to Groups A and B. In selected Group B patients, delivered shock currents through the right ventricular apex/superior vena caval and right ventricular apex/R2 patch electrode pairs were measured. We analyzed the initial episode of VT with a cycle length less than 300 ms in 33 patients with organic heart disease (mean age, 64 +/- 9 years; mean VT cycle length, 248 +/- 37 ms) who underwent programmed electrical stimulation. Transvenous cardioversion shocks terminated 31% of 16 VT episodes in Group A and 41% of 17 VT episodes in Group B (p greater than .2). The mean successful shock energy was 6.1 +/- 3.7 J in Group A and 3.0 +/- 0.9 J in Group B (p less than .05). Forty percent of all successfully cardioverted episodes in Group A and 86% of all successfully cardioverted VT episodes in Group B were terminated at an energy of 2.7 J (p = .09). Analysis of shock waveforms in Group B revealed 47 to 74% of the total current was transmitted through the right ventricular apex/superior vena caval electrodes and 26 to 53% through the right ventricular apex/R2 electrodes. We conclude that single bidirectional transvenous shocks are effective for rapid VT termination in selected patients. Dual current pathways decrease energies needed for successful transvenous cardioversion in this patient population.     

Chronic Rapid Atrial Pacing to Maintain Atrial Fibrillation: Use to Permit Control of Ventricular Rate in Order to Treat Tachycardia Induced Cardiomyopathy

LR was a patient, followed over a 16-year period, who presented with an atrial tachycardia which was initially intermittent, but became incessant. Neither the atrial tachycardia nor the associated rapid ventricular response rate could be treated successfully with available drug therapy, resulting in a dilated cardiomyopathy and New York Heart Association (NYHA) class III-IV congestive heart failure. Acute induction of atrial fibrillation with rapid atrial pacing demonstrated that the associated ventricular rate could be satisfactorily slowed with digitalis therapy. Initially, short bursts from an implanted, radiofrequency controlled, patient activated pacemaker programmed to a rate of 600 bpm and connected to a permanent endocardial atrial J lead successfully interrupted the tachycardia and precipitated atrial fibrillation. Over a period of 3 months, this therapy changed the patient's heart failure to NYHA class II status. Subsequently, precipitation of atrial fibrillation with this technique failed, resulting in return to NYHA class III-IV congestive heart failure. Therefore, a custom-designed, high rate, rate-programmable pacemaker was implanted to pace the atria rapidly and continuously to maintain atrial fibrillation. A pacing rate of 375 bpm plus digoxin slowed the ventricular rate to 70-80 bpm, with stabilization of the congestive heart failure to NYHA class II. The pacemaker generator was replaced 6 months later, and after another 5 months, pacing was discontinued. The patient's subsequent rhythm remained stable atrial fibrillation with clinically successful control of both the ventricular rate and heart failure (NYHA class II) until the patient's death 72 months later. This unique case demonstrates another form of chronic therapy which, in selected cases, can be used for the long term control of rapid ventricular response rates to supraventricular arrhythmia.     

Atrial Fibrillation with Rapid Ventricular Response Resulting from Low-Voltage Electrical Injury

Background

Cardiac dysrhythmias after electrical injury have been reported previously, however, atrial fibrillation after low-voltage electrical injury is extremely rare. We present a case of atrial fibrillation with rapid ventricular response resulting from a low-voltage electrical injury. Case Report: A 24-year-old active duty Navy sailor presented to the emergency department after an electrical shock from a 440-V furnace. He experienced severe pain in both hands and a racing sensation in his chest. He denied other symptoms. An electrocardiogram was performed demonstrating atrial fibrillation with a rapid ventricular response (132 beats/min). After analgesia and sedation, synchronized cardioversion (100 J) was performed with complete resolution of cardiac symptoms and restoration of normal sinus rhythm (75 beats/min). Cutaneous wounds were bandaged and the patient was discharged with cardiology follow-up. At follow-up, the patient reported no symptoms and an echocardiogram revealed no structural abnormalities. Conclusions: Atrial fibrillation in the setting of electrical injury is rarely reported in the published medical literature. In patients without history suggestive of cardiac structural abnormalities, synchronized cardioversion is a potential option for restoration of normal sinus rhythm and resolution of symptoms after electrical injury−induced atrial fibrillation with rapid ventricular response.     

Prevention of Intra-Atrial Reentry by Chronic Atrial Pacing

The authors describe a cose of so-called "intra-atrial reentry," associoted with sinus node dysfunction. The spontaneous initiation of the tachycardia was always preceded by a sinus pause, and external atrial pacing prevented the appearance of tachycardia. Thus an atrial pacemaker was implanted, and after several months, the atriaJ dysrhythmias disappeared completely, despite interruption of the antiarrhythmic drugs. When a pacemaker dysfunction occurred, the sinus node dysfunction and the tachycardia reappeared. This is analogous with the "incessant" tachycardias seen in the WPW syndrome, and must be differentiated from the usual forms of the sick sinus syndrome which require both a pacemaker and antiarrhythmic drugs.     

Termination of Ventricular Tachycardia by Programmed Extrastimuli from an Externally-Activated Permanent Pacemaker

Two patients with hemodynamically well-tolerated recurrent ventricular tachycardia, drug resistant and previously requiring numerous external electrical cardioversions, had a permanent pacemaker implanted which could be programmed to deliver extrastimuli to convert the ventricular tachycardia to normal sinus rhythm. The patient- or physician-activated device can be programmed to induce or terminate ventricular tachycardia with extrastimuli delivered at the predetermined intervals which consistently induced or terminated the arrhythmia in the electrophysiology laboratory, allowing repeated evaluation of drug regimens. The pacemaker has reliably, painlessly, and consistently induced and terminated repeated episodes of ventricular tachycardia. This programmable pacemaker offers an alternative therapy for patients with hemodynamically well-tolerated refractory ventricular tachycardia.     

Safety and Efficacy of Pacing for Ventricular Tachycardia

This study was undertaken to determine the safety and efficacy of three different pacing modalities on the termination of ventricular tachyarrhythmias. Thirty-two patients were studied in the electrophysiology laboratory. Three randomized pacing modalities were selected for attempted conversion: auto increment, auto burst, and random burst. In all three groups, arrhythmias with cycle lengths shorter than 230 ms required DC shock, with one exception. Those longer than 230 ms were terminated by pacing in 85% of cases. There was a 15% rate of acceleration. Thus, antitachycardia pacing for ventricular tachyarrhythmias should be considered only with defibrillating back-up.