Inducible multiform ventricular tachycardia in Wolff-Parkinson-White syndrome.

The induction of ventricular tachycardia by ventricular stimulation was investigated in 46 patients with isolated Wolff-Parkinson-White syndrome (10 concealed) and 36 control patients with normal electrocardiograms and conduction systems. None of those studied had spontaneous ventricular arrhythmias or myocardial or valve disease. Single and double ventricular extrastimuli were delivered at 3 cycle lengths (sinus, 600 ms, 400 ms). In the controls ventricular simulation induced one episode (3%) of non-sustained ventricular tachycardia. Ventricular stimulation in patients with Wolff-Parkinson-White syndrome induced two episodes of ventricular fibrillation and 15 episodes of non-sustained multiform ventricular tachycardia (37%). Ventricular arrhythmias were induced only in patients with overt Wolff-Parkinson-White syndrome. In 14 patients the conformation of the electrocardiogram at the start of ventricular tachycardia resembled that of major pre-excitation. The absence of inducible ventricular tachycardia in patients with concealed Wolff-Parkinson-White syndrome suggests that anterograde conduction via an atrioventricular accessory pathway is required to initiate the ventricular arrhythmias: the ventricular tachycardia may be associated with reentry of impulses via atrioventricular connection during the phase of ventricular vulnerability. The similarity between the start of ventricular tachycardia and pre-excitatory complexes may also indicate local reentry into the ventricular area occupied by the bypass tracts. Patients with Wolff-Parkinson-White syndrome and anterograde pre-excitation are more likely to have inducible multiform ventricular tachycardia than individuals without Wolff-Parkinson-White syndrome.     

Development of multiform ventricular tachycardia during atrioventricular nodal reentrant tachycardia

A woman of 18 presented with a supraventricular tachycardia, subsequently shown to be caused by atrioventricular nodal reentry, which abruptly deteriorated to a multiform ventricular tachycardia. She had not received any antiarrhythmic drugs nor did she have any of the disorders that are usually associated with this atypical ventricular tachycardia.     

Development of multiform ventricular tachycardia during atrioventricular nodal reentrant tachycardia.

A woman of 18 presented with a supraventricular tachycardia, subsequently shown to be caused by atrioventricular nodal reentry, which abruptly deteriorated to a multiform ventricular tachycardia. She had not received any antiarrhythmic drugs nor did she have any of the disorders that are usually associated with this atypical ventricular tachycardia.     

Electrophysiologic mechanisms of orthodromic tachycardia initiation during ventricular pacing in the Wolff-Parkinson-White syndrome

Orthodromic tachycardia is the most common arrhythmia in patients with Wolff-Parkinson-White syndrome. It is often initiated during incremental ventricular pacing that requires the onset of retrograde block along the normal pathway (that is, atrioventricular [AV] node-His-Purkinje system) with concomitant retrograde atrial activation by way of the accessory pathway. However, the site of retrograde block, that is, the AV node versus the His-Purkinje system, during incremental ventricular pacing and, hence, the mechanism of orthodromic tachycardia initiation have not been systematically elucidated. The mechanisms of orthodromic tachycardia induction were studied in 17 patients with Wolff-Parkinson-White syndrome using a specially designed pacing protocol. A beat by beat analysis indicated that the retrograde His-Purkinje system block was the most common initiating mechanism of orthodromic tachycardia in 14 of the 17 cases. In two cases, AV node block preceded the onset of orthodromic tachycardia, whereas the data in the remaining case suggested that both mechanisms were operative but at different pacing cycle lengths. The orthodromic tachycardia induction with His-Purkinje system block occurred within the first two cycles in most cases. When orthodromic tachycardia initiation was delayed beyond the first two cycles of the ventricular train it represented either a 2:1 block in the His-Purkinje system; a linking phenomenon in the His-Purkinje system; or a block in the AV node. These data have methodologic, mechanistic and therapeutic implications for patients with the Wolff-Parkinson-White syndrome.     

Paroxysmal ventricular tachycardia in Wolff-Parkinson-White syndrome: Case report and review of the literature

A case with Type A Wolf f-Parkinson-White pattern and recurrent sustained ventricular tachycardia is presented. Because of ventricular pre-excitation, electrocardiographic clues suggestive of ventricular tachycardia were ignored and the diagnosis of supraventricular tachycardia with conduction to the ventricles over the accessory pathway was made during reach admission to the hospital. Ventricular tachycardia was suspected only when programmed stimulation studies performed twelve years after initial presentation and many hospitalizations failed to induce a tachycardia with a QRS pattern similar to that of spontaneously occurring tachycardia. The diagnosis of ventricular tachycardia was later confirmed by intracardiac recordings made during a spontaneous episode of tachycardia. Tachycardia was unresponsive to all conventional antiarrhythmic agents but was controlled with amiodarone.The differential diagnosis of wide QRS complex tachycardia in patients with Wolff-Parkinson-White syndrome, the implications of correctly diagnosing the tachycardia, and the usefulness of intracardiac electrophysiologic studies in differentiating supraventricular tachycardia with aberrant conduction from ventricular tachycardia are discussed.     

Monomorphic ventricular tachycardia related to Wolff-Parkinson-White surgery.

Monomorphic ventricular tachycardia (MVT) is well described in patients who have had a ventricular scar due to repair of congenital heart disease. A 54-year-old woman presented with MVT 20 years after WPW surgery for a left-sided accessory pathway. The circuit was mapped to an area at the base of the left ventricle consistent with the incision described in the operation report. Entrainment confirmed the re-entrant circuit. Successful radiofrequency ablation was performed in a zone of slowed conduction consistent with the circuit isthmus. Any iatrogenic ventricular scar may form the substrate for MVT and be treated with standard electrophysiology techniques.     

Iatrogenic ventricular fibrillation in Wolff-Parkinson-White syndrome

Wolff-Parkinson-White (WPW) syndrome is the most common manifestation of ventricular pre-excitation syndrome and is mostly found in individuals with no structural heart disease. Although the risk of malignant arrhythmias is low, sudden cardiac death (SCD) as the first clinical manifestation of WPW syndrome is well documented, and atrial fibrillation (AF) with a rapid ventricular response is the main mechanism involved. Unfortunately, the signs of pre-excitation and arrhythmias are sometimes under-diagnosed and under-treated. We describe the case of a 31-year-old man who was admitted with an irregular wide complex tachycardia consistent with pre-excited AF, which was not promptly diagnosed, and who developed ventricular fibrillation (VF) after administration of atrioventricular (AV) nodal blockers, as a primary manifestation of WPW syndrome. Blocking the AV node in patients with pre-excited AF may increase the ventricular rate and potentially result in hemodynamic instability. Among patients with WPW syndrome who survive an episode of SCD, catheter ablation of the accessory pathway is the treatment of choice.     

Phase mapping of radionuclide gated biventriculograms in patients with sustained ventricular tachycardia or Wolff-Parkinson-White syndrome

Summary Accuracy of Fourier phase mapping of radionuclide gated biventriculograms in detecting the origin of abnormal ventricular activation was studied during ventricular tachycardia or preexcitation. Group I included six patients suffering from clinical recurrent VT; 3 gated blood pool studies were acquired for each patients with Wolff-Parkinson-White syndrome and recurrent paroxysmal tachycardia; 3 gated blood pool studies were acquired for each patient: during sinus rhythm, right atrial pacing and orthodromic reciprocating tachycardia. Each acquisition lasted 5 min, in 30–40 left anterior oblique projection.In Group I, the Fourier phase mapping was consistent with QRS morphology and axis during VT (5/6), except in one patient with LV aneurysm and LBBB electrical pattern during VT. Origin of VT on phase mapping was located in the right ventricle (n=2) or in left ventricle (n=4), at the border of wall motion abnormalities each time they existed (5/6).In Group II, the phase advance correlated with the location of the accessory pathway determined by ECG and endocardial mapping (n=6) and per-operative epicardial mapping (n=1). Discrimination between anterior and posterior localisation of paraseptal pathways and location of intermittent preexcitation was not possible.We conclude that Fourier phase mapping is an accurate method for locating the origin of VT and determining its etiology. It can help locate the site of ventricular preexcitation in patients with only one accessory pathway; its accuracy in locating multiple accessory pathways remains unknown.     

Inducible monomorphic sustained ventricular tachycardia in the conscious pig

Sustained monomorphic ventricular tachycardia (VT) is of clinical importance but has not been readily modeled in conscious animals. Eleven pigs had myocardial infarction induced by pulling snares previously placed around the left anterior descending (LAD) coronary artery. Six days after occlusion, bipolar pacing catheters were inserted in the right ventricular apex for induction of VT. Testing was repeated in conscious pigs on 6 out of 8 to 19 days after infarction. Monomorphic VT was induced in each animal during each session, using three to four extrastimuli. VT was terminated by burst pacing in 74% of trials; average VT rate was 362 +/- 26 beats/min. VT was prevented in four of eight animals by procainamide and in five of eight animals by magnesium, but was not prevented by lidocaine or metoprolol. The model may be useful in the study of potentially malignant ventricular tachyarrhythmias, important prodromes for sudden death.     

Long-term control of reciprocating paroxysmal tachycardia by ventricular pacing in a case of Wolff-Parkinson-White syndrome.

A patient is described with a complex electrocardiographic pattern, including preexcitation, grade 1 atrioventricular block, reciprocal rhythm of atrial origin, and frequent attacks of reciprocating tachycardia at a rate of about 135 beats per minute. Long-term control of these attacks was obtained by synchronous ventricular pacing at 80 beats a minute, which was below the rate during the attacks of tachycardia and above the spontaneous heart rate between the attacks.     

MAST conversion of paroxysmal supraventricular tachycardia in Wolff-Parkinson-White syndrome

A 48-year-old man with Wolff-Parkinson-White syndrome presented with paroxysmal supraventricular tachycardia. Prior episodes had required inpatient drug therapy or cardioversion. Attempts at conversion to normal sinus rhythm with vagal maneuvers were unsuccessful. Inflation of military antishock trousers resulted in rapid termination of the arrhythmia and avoidance of hospitalization.     

Cardioversion of recurrent postoperative supraventricular tachycardia in Wolff-Parkinson-White syndrome

A man whose electrocardiograms disclosed evidence of the Wolff-Parkinson-White syndrome had five attacks of supraventricular tachycardia after operation for relief of small bowel obstruction. Quinidine, digoxin and potassium chloride neither prevented nor terminated the recurrent episodes of tachycardia. However, each attack of supraventricular tachycardia was terminated by electric cardioversion administered without general anesthesia.     

Atrial reciprocal rhythm and reciprocating tachycardia in Wolff-Parkinson-White syndrome

In an infant with type A Wolff-Parkinson-White syndrome, atrial reciprocal beats and attacks of reciprocating tachycardia were repeatedly recorded. Their dependence on a prolongation of the P-R interval could be well demonstrated during Wenckebach periods. Because of the normal aspect of the QRS complex during arrhythmia, the short ventriculo-atrial conduction time (0.08 sec), and the vectorial orientation of the secondary P wave, it was concluded that retrograde reactivation of the atria probably took place via the anomalous bundle. The versatility of the conduction through the accessory bundle is shown by the fact that its direction may change from antegrade in one beat to retrograde in the next. The importance of a circus movement in the genesis of some types of tachycardia in the WPW syndrome is discussed.