Factors regulating ventricular rates during atrial flutter and fibrillation in pre-excitation (Wolff-Parkinson-White) syndrome.

Castellanos, Agustín; Myerburg, Robert J.; Craparo, Karen; Befeler, Benjamin; Agha, Abdul S.

doi:10.1136/hrt.35.8.811

Cited by 93 publications

(10 citation statements)

References 6 publications

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“…As shown in figure 3 Q prevented atrial re-entry, which prior toC) created refractoriness in the atrial part of the tachycardia pathway. Widening of the QRS complex by [10][11][12][13][14][15][16][17][18][19][20] wvas observed in the effective refractory period of the A-V node in the three patients in whom this could be studied. In these three patients the H-V interval increased by 10 to 15 msee.…”

Section: Quinidinementioning

confidence: 99%

Effect of Procaine Amide, Quinidine, and Ajmaline in the Wolff-Parkinson-White Syndrome

1974

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SUMMARYUsing the single test stimulus method, atrioventricular (A-V) conduction, ventriculo-atrial conduction, the refractory period of right atrium and right ventricle, and the mechanism of tachycardia were studied in 16 patients with the Wolff-Parkinson-White syndrome. The same studies were repeated at least four times during the hour following intra-atrial administration of 10 mg procaine amide/kg body weight (six patients), 4 mg quinidine gluconate/kg body weight (six patients), or 50 mg ajmaline (four patients).Following procaine amide the refractory period of the accessory pathway increased in all patients, with temporary complete block of the accessory pathway in four patients. There was an increase in H-V interval during antegrade conduction through the A-V node-His pathway. The effective refractory period of the A-V node showed no appreciable change. In three of four patients tachycardia could not be produced by pacing in contrast to the pacing effect found prior to procaine amide.Quinidine gluconate increased the refractory period of the accessory pathway in four patients, causing temporary complete block in two patients. The H-V interval increased in three patients. The refractory period of the A-V node showed no change in three patients, lengthened in one, and shortened in the other two. Ouinidine gluconate prevented pacing-induced initiation of tachycardia in two out of four patients.Ajmaline' increased the refractory period of the accessory pathway in all four patients, with temporary complete block in three patients. The H-V interval also lengthened. No change was observed in the refractory period of the A-V node. Ajmaline prevented initiation of tachycardia in one out of two patients. In the other patient tachyeardias could still be initiated despite disappearance of pre-excitation during atrial pacing.In one patient in each group tachycardia could be produced during pacing following drug administration where no tachycardia could be produced under control conditions. In two patients re-entry in the A-V node during ventricular pacing caused this phenomenon. In the other patient administration of the drug prevented atrial re-entry during atrial pacing. This re-entrant beat had previously created refractoriness in the atrial part of the tachycardia pathway. The changes following procaine amide, quinidine gluconate, and ajmaline were clearly short term; their effects disappeared after one hour in 15 of the 16 patients studied.

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Section: Quinidinementioning

confidence: 99%

Effect of Procaine Amide, Quinidine, and Ajmaline in the Wolff-Parkinson-White Syndrome

1974

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“…1 to 5 confirm that the essential electrophysiological feature of an AV nodal bypass tract in patients with recurrent supraventricular tachyarrhythmias is the presence of a short (or at the lower limits of normal) AH interval which shows an abnormal response to atrial stimulation at increasing rates and/or with the extrastimulus method (Coumel et al, 1972;Castellanos et al, 1973;Caracta et al, 1973;Bissett et al, 1973;Denes et al, 1974b;Befeler et al, 1976).…”

Section: Atrio-his Bundle Bypass Tract With Normal Pr Intervalmentioning

confidence: 91%

Intermittent AV conduction disturbances in patients with AV nodal bypass tracts. Possible mechanisms of unusual variant of tachycardia-bradycardia syndrome.

Castellanos¹,

Sung²,

Befeler³

et al. 1977

Heart

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His bundle recordings were performed in 2 patients in whom AV nodal bypass tracts coexisted with intermittent A V conduction disturbances occurring below the sitefrom which the His bundle deflection was recorded. Case 1 had: (a) tachycardia dependent right bundle-branch block, (b) persistent HV prolongation, and (c) bradycardia dependent A V block. Case 2 showed: (a) intra-atrial conduction delay, (b) tachycardia dependent left bundle-branch block with HV prolongation, (c) bradycardia dependent HV conduction disturbance, (d) tachycardia-bradycardia syndrome of an unusual type; the latter presumably resulted, during atrial.flutter, from the alternation of rapid AH conduction through the bypass tract with intermittent (complete) distal His bundle block or bilateral bundle-branch block.In a previous communication in this journal , we discussed the occurrence of bundle-branch block and normal PR intervals in patients with AV nodal bypass tracts. It appeared justified, in view of the very few existing publications (Krishnaswani and Geraci, 1974;Brechenmacher, 1975), to report the association of AV conduction disturbances with AV nodal bypass tracts (in absence of coexisting Mahaim tracts). In addition the possible mechanisms of an unusual type of tachycardia-bradycardia syndrome are discussed. Subjects and methodsHis bundle recordings were obtained in 2 patients referred to the Cardiovascular Laboratory for evaluation of recurrent supraventricular tachycardias. The procedure was explained and informed consent obtained. The normal values in our department for the various conduction intervals are as follows (Castellanos et al., 1975;Befeler et al., 1976): PA=20-45 ms; AH=55-120 ms; HV= 35-55 ms.

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“…The incidence of AF in patients with WPW syndrome is reported to be 10-30% [3][4][5]. No relationship between the onset of AF and localization of accessory pathways has been reported [6], and successful ablation of the accessory pathway prevents the recurrence of AF in the majority of patients.…”

Section: Explanations Of the Arrhythmiamentioning

confidence: 99%

Irregular wide QRS complex tachycardia without structural heart disease

Kobayashi

Ikeda

2012

Journal of Arrhythmia

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Case presentationA 64-year-old female presented to the emergency room with persistent dizziness that began early that morning. She had a 30-year history of palpitations and known electrocardiogram (ECG) abnormalities. Her pulse was irregular at 130-270 min À 1 and blood pressure was 90/40 mmHg. There were no other abnormalities on physical examination. A chest X-ray was normal and without cardiomegaly. Echocardiography revealed normal left ventricular contraction without structural abnormalities. Blood chemistry evaluation, including electrolytes and cardiac enzymes, was within normal limits. Twelve-lead ECG showed irregular wide QRS tachycardia of various configurations (Fig. 1).How would you diagnose her tachycardia? CommentaryThe patient's ECG shows wide QRS tachycardia with a rate from 150 to 300 beats/min. The RR intervals are irregularly irregular and no P wave preceding QRS was confirmed. The QRS complex has beat-beat variations in morphology. At this point, some of the arrhythmias that should be considered are: (1) irregular ventricular tachycardia (such as torsades des pointes or polymorphic ventricular tachycardia); (2) atrial fibrillation (AF) with bundle branch block; (3) AF in Wolff-Parkinson-White (WPW) syndrome (pseudo-ventricular tachycardia). The QRS complex shows right axis deviation during tachycardia with no progressive change in cardiac axis, thus polymorphic ventricular tachycardia and torsades des pointes associated with QT prolongation are excluded. Polymorphic ventricular tachycardia associated electrolyte abnormality and myocardial ischemia could not be totally excluded by this ECG, however laboratory examination did not indicate myocardial ischemia or an electrolyte abnormality.The representative arrhythmia of the patient's irregular heart rate is AF, which is the most common cardiac arrhythmia. When the ventricular rate is slow, AF can be easily diagnosed. However if the ventricular rate is rapid, AF is difficult to appreciate because QRS complexes are clustered together and fibrillatory waves become more difficult to evaluate. The QRS complexes during AF with bundle branch block usually do not have beat-beat variation, and both an Rr 0 pattern in lead V 1 and R oS amplitude in V 6 are uncommon for the ECG of right bundle branch block. On the other hand, the QRS complexes during AF in WPW syndrome are extremely bizarre and broad because the QRS complex reflects varying degrees of fusion of ventricular activation via the atrioventricular (AV) node and accessory pathways.To terminate AF and block the accessory pathway, procainamide was given intravenously at a dose of 400 mg over 30 min. It is important to note that AV nodal blocking agents are contraindicated in treatment of AF in patients with WPW syndrome. AV nodal blocking agents, for example verapamil and digoxin, decrease the number of impulses conducted through the His-Purkinje system and enhance conduction across accessory pathways, thus increasing the ventricular rate during AF. If the patient is hemodynamically unstable, elect...

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Factors regulating ventricular rates during atrial flutter and fibrillation in pre-excitation (Wolff-Parkinson-White) syndrome.

Cited by 93 publications

References 6 publications

Effect of Procaine Amide, Quinidine, and Ajmaline in the Wolff-Parkinson-White Syndrome

Effect of Procaine Amide, Quinidine, and Ajmaline in the Wolff-Parkinson-White Syndrome

Intermittent AV conduction disturbances in patients with AV nodal bypass tracts. Possible mechanisms of unusual variant of tachycardia-bradycardia syndrome.

Irregular wide QRS complex tachycardia without structural heart disease

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