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Query: UNIPROT:Q96S42 (nodal)
 22,877 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-three patients with atrial fibrillation associated with the Wolff-Parkinson-White (WPW) syndrome were studied to determine the relation of sinus bradycardia and atrial fibrillation. In seven patients the sinus rate was less than 40 beats/min and sinus nodal disease was considered a cause of the periods of bradycardia. Ventricular fibrillation of functional cardiac arrest was documented in four instances. Twenty-six patients demonstrated a type A and seven a type B WPW pattern during periods of sinus rhythm. Male patients predominated. The average age was 38.5 years among patients with a type A pattern compared with 25.3 years among those with a type B pattern. The shortest R-R cycle length in this group was 130 msec during a period of atrial fibrillation. Five thousand serial microscopic sections were studied in one patient who demonstrated ventricular fibrillation. Three anomalous pathways were located in this patient with the widest tract, 380 mu, containing about 400 muscle cells. Most of the sinoatrial node was replaced by collagen elastic fibers, and there was widespread destruction of the atria with a marked increase in fibrous connective tissue. Ventricular fibrillation or functional cardiac arrest is not a rare arrhythmia in patients with atrial fibrillation associated with the WPW syndrome and may be responsible for sudden death in patients with these arrhythmias. Hence, precise electrophysiologic studies and pharmacologic or surgical management, or both, are suggested to prevent sudden death in patients with short refractory periods associated with atrial fibrillation and the WPW syndrome.
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PMID:Sinus bradycardia and atrial fibrillation associated with the Wolff-Parkinson-White syndrome. 95 59

In two patients with WPW syndrome Type A suffering from syncopes and dizziness intermittent high degree A-V block was observed. The analysis of the surface Ecg revealed in the first case a complete A-V block within the normal conduction system at the level of the A-V node. In the second case there was a constant left bundle branch block with intermittent block in the right fascicle (intermittent trifascicular block). In both cases the preexcitation syndromes could be best explained by accessory tracts bypassing the normal nodal system left side. One-to-one conduction through the bypass occurred only at a distinct range of cycle lengths, at lower frequencies the accessory tracts were refractory and a IInd or IIIrd degree A-V block occurred. However, outside this frequency zone some P waves were conducted through the accessory tracts without changes in cycle lengths. The findings support the thesis of at least two functionally different atrioventricular pathways in patients with preexcitation syndrome.
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PMID:[Severe atrioventricular block in 2 cases with pre-excitation syndrome]. 96 Sep 77

In a patient whose electrocardiogram (ECG) initially (1966) showed a Type A Wolff-Parkinson-White pattern, recurrent supraventricular tachycardia (SVT) developed but never subsequently showed antegrade bypass conduction. Intracardiac pacing studies (1975) revealed that premature high right atrial (induced 250-450 msec after atrial depolarization) or coronary sinus depolarization (250-550 msec) resulted in SVT. Late coronary sinus depolarization resulted in SVT without A-H prolongation. During SVT, P wave morphology changed and the coronary sinus atrial electrogram preceded that from the low right atrium; retrograde ventriculoatrial conduction time was 240 msec. Neither pacing the high right atrium or coronary sinus up to rates of 200 beats/min nor progressive atrial premature depolarizations from the high right atrium or coronary sinus resulted in antegrade bypass conduction. Failure of antegrade bypass conduction does not preclude SVT due to retrograde preexcitation and must be distinguished from atrioventricular (A-V) nodal reentry. Atrial effective refractory period (200 msec) was shorter than the minimal time required for an atrial impulse to return to the atrium (380 msec), suggesting concealed antegrade bypass conduction. Stimulation of the atrium linked to the A-V bypass results in earlier bypass activation and recovery and explains the differing high right atrial vs coronary sinus echo zones.
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PMID:Right atrial versus left atrial echo zones: a proposed new criterion for determining the atrial site of retrograde preexcitation. 97 86

A description is given of the principles of re-entry and circus movement, which were originally formulated on the basis of experiments on jellyfish and play an important role in cardiac arrhythmias. The essential features of re-entry are 1) the existence of two conducting pathways which communicate at their proximal and distal ends, and 2) the occurrence of uni-directional block in one pathway while conduction is maintained in the other. A retrograde wavefront may then be set up in the pathway where block was present, and the tissue from which the impulse came may be re-excited. Once this sequence is set up it may continue as a circus movement leading to tachycardia. Long re-entry circuits are present in Wolff-Parkinson-White syndrome, in which two connections between atria and ventricles exist. Micro-re-entry may occur in a variety of cardiac tissues. An example of supraventricular tachycardia due to micro-re-entry in the atrio-ventricular node of an isolated rabbit heart is shown, in which simultaneous recording of transmembrane potentials of AV nodal cells unraveled the events. The principles of the termination of circus movement tachycardias by electrically induced premature beats are discussed.
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PMID:Pathophysiological basis of tachyarrhythmias--re-entry. 99 76

The authors report two clinical cases (one with WPW syndrome) of paroxysmal supraventricular tachycardia caused, in one case, by sino-atrial node or perisinusal nodal tissue re-entrance and in the other case by re-entry in the lower atrium and the high part of the A-V node junction. Both present A-V node Wenckebach periodism, which can be distinct from reciprocating tachycardias, through an anomalous pathway or within the A-V node, which have a typical A-V conduction in the ratio of one to one. But A-V node Wenckebach periodism makes it hard to differentiate between reciprocating and ectopic atrial tachycardias, as the latter often has an A-V block. The effects of two antiarrhythmic drugs (Verapamil, Amiodarone) on echo-zone duration, on initiation and on prophylactic long-term treatment of paroxysmal tachycardias are also reported and discussed.
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PMID:[Tachycardia caused by sinus-node and atrial re-entry with associated depression of A-V conduction]. 102 3

Stimulation technics have demonstrated a reciprocating mechanism in many supraventricular tachycardias previously classified from a purely morphologic point of view. Three conditions are required for the creation of a circus movement: a potential circuit pathway, undirectional block in this curcuit, and slowed conduction. While all three conditions are readily apparent in reciprocating tachycardias of the WPW syndrome, two or even all of these factors may be concealed in the others forms. Paroxysmal reciprocating tachycardias are characterized by prolongation of the P-R interval in the beat immediately preceding the tachycardia, and are generally accepted as being related to longitudinal dissociation of the A-V node, though the possibility of unidirectional (anterograde) block of an extra-nodal accessory pathway should be appreciated. Permanent reciprocating tachycardias start after a normal P-R interval when the sinus cycle reaches a critical value. Both paroxysmal and permanent forms of reciprocating tachycardia must be differentiated from tachycardias located in the atria: one of the most reliable features of reciprocating tachycardia is the existence of a 1:1 A-V relationship which cannot be altered without interrupting the tachycardia. Study of capture phenomena during the tachycardia, and the modes of termination not only permit the demonstration of the reentry mechanism but may also determine more precisely the actual location of the circus movement.
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PMID:Junctional reciprocating tachycardias. The permanent and paroxysmal forms of A-V nodal reciprocating tachycardias. 108 33

His bundle electrograms were recorded in a patient with Wolff-Parkinson-White syndrome (type B) during atrial pacing studies and during the induction of premature atrial depolarization at varying coupling intervals. Early ventricular depolarization (preexcitation) occurred simultaneously with the His depolarization, suggesting that conduction occurred via both the Kent and the normal A-V nodal-His-Purkinje pathway during sinus rhythm. Atrial pacing at increasing rates showed progressive advance of the His spike into the QRS and increasing duration of the delta wave until the appearance of broad bizarre QRS complexes with prolonged P-J intervals, suggesting major, if not total, depolarization of the ventricle by the Kent pathway. PAD's induced at coupling intervals of 360, 330, and 300 msec caused progressive delay of the His bundle depolarization, with the His spike occurring after the QRS at S(1)-H intervals of 230, 265, and 325 msec, respectively, and Q-H intervals of 123, 160 and 220 msec, respectively. These findings suggest that during sinus rhythm the QRS was a fusion beat. With early premature atrial stimulation, conduction occurred solely via the Kent pathway, with conduction via the normal A-V nodal pathway encountering increasing delay. The finding of His depolarization occurring after the QRS suggests retrograde myocardial-His block, and may explain the absence of paroxysmal supraventricular tachycardias in this patient.
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PMID:Wolff-Parkinson-White syndrome type B with His depolarization occurring after the QRS. Further evidence that WPW-QRS is a fusion beat. 112 73

To study the pathway of tachycardia in patients with the Wolff-Parkinson-White (WPW) syndrome and reciprocal tachycardias, results from intracavitary recordings and atrial and ventricular stimulation were reviewed in 71 patients with the WPW syndrome and 54 patients without pre-excitation. In all patients a reproducible tachycardia could be initated and terminated by appropriately timed electrical stimuli. The following findings were accepted as suggesting the participation of an accessory pathway in the tachycardia circuit: 1) no increase in ventriculo-atrial conduction (V-A C) time following ventricular stimuli given with increasing prematurity; 2) activation of right or left atrium (depending upon the location of the atrial end of the accessory pathway) prior to activation of atrium in the His bundle lead; 3) slowing of tachycardia following bundle branch block to the ventricle in which the accessory pathway inserts; 4) V-A C time of early stimuli on the ventricle during the tachycardia equal to or less than the V-A c time following QRS complexes during tachycardia; 5) inability to initiate tachycardia or slowing of tachycardia following the administration of drugs affecting the accessory pathway. Accepted as suggestive for atrioventricular (A-V) nodal re-entry were the following factors: 1) activation of atrium following initiation of tachycardia by a single atrial premature beat after activation of the bundle of His but before or simultaneous with ventricular activation in first and subsequent beats of tachycardia; 2) initiation of tachycardia following a gradual increase in V-A C time with the appearance of a His bundle electrogram in between the premature beat and retrograde atrial activation; 3) gradual increase in V-A C time with the appearance of a His bundle electrogram following ventricular premature beats given with increasing prematurity; 4) two-to-one block distal to the A-V node or His bundle with persistance of tachycardia. If only positive findings were accepted, 51 patients of the WPW group used their accessory pathway during tachycardia. In eight patients re-entry was confined to the A-V node. In the remaining 12 patients the mechanism was not clear. Of the patients not showing pre-excitation in A-V direction, 47 patients seemed to have their re-entry circuit in the A-V node, five patients used an accessory pathway in V-A direction, and in two patients the pathway of tachycardia could not be identified.
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PMID:The role of an accessory atrioventricular pathway in reciprocal tachycardia. Observations in patients with and without the Wolff-Parkinson-White syndrome. 113 22

In patients with WPW syndrome the maximal ventricular rate attained during ectopic rapid supraventricular thythms depended on the type of arrhythmia as well as on the physiological properties of the AP. During reciprocating tachycardias the impulse is almost invariably conducted to the ventricles through the AV node. Therefore, the maxiaml ventricular rate is a function of the AV nodal ERP. On the other hand, when atrial flutter or atrial fibrillation were present the ventricular rate could be moderately elevated (when the ERP of the AP was longer than that of the AV node) or very rapid where the ERP of the AP was significantly short. Therefore, from the electrophysiological viewpoint, the AP appears to behave as His-Purkinje tissue in some cases and as ordinary artrial muscle in other patients. These assumptions await further documentation.
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PMID:Mechanisms determining the ventricular rate in wolff-parkinson-white arrhythmias. 113 85

Wolff, Parkinson, and White, in their initial description of the syndrome that bears their names, emphasized the association of tachycardias with the electrocardiographic abnormality. Subsequent investigations have identified, both anatomically and electrophysiologically, that dual pathways of atrioventricular (AV) conduction exist. Furthermore, experimental and clinical evidence has stressed that the mechanism of tachycardia production in the syndrome appears to reentry utilizing these dual pathways. However, recent studies have emphasized that other mechanisms of tachycardia production may be responsible for the arrhythmias seen in this syndrome. The present report identifies that AV nodal reentry may be the sole mechanism for tachycardia induction in the Wolff-Parkinson-White (WPW) syndrome. This finding may be of great clinical significance in light of the availability of surgical therapy for WPW patients with intractable arrhythmias.
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PMID:Atrioventricular nodal reentry in the Wolff-Parkinson-White syndrome. 115 36


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