Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q96S42 (nodal)
 22,877 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a series of 48 patients undergoing electrophysiological investigation for attacks of reciprocating tachycardia related to concealed or overt Wolff-Parkinson-White syndrome in sinus rhythm, 4 patients were found to have duality of nodal conduction. This association was responsible for several tachycardia circuits: in 2 patients the activation passed constantly retrogradely through the accessory pathway and then either through the slow nodal pathway or the rapid nodal pathway in the anterograde direction. In the other two patients, in addition to classical orthodromic tachycardia, purely intranodal reciprocating rhythms giving rise to sustained tachycardia in one case and to simple echos in the other, were observed.
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PMID:[Obvious or inapparent Wolff-Parkinson-White syndrome associated with duality of nodal conduction. Apropos of 4 cases]. 11 32

Four members of a family presenting with sinus bradycardia, a short P-R interval, intraventricular conduction defects, recurrent supraventricular tachycardia (SVT), syncope, and cardiomegaly had His bundle studies and were found to have markedly shortened A-H intervals (30 to 55 msec.) with normal H-V times (35 to 50 msec.). Right atrial pacing at rates as high as 170 to 215 per minute failed to increase the A-H or H-V intervals significantly. The data are compatible with the presence of an A-V nodal bypass tract (James bundle) or even complete absence of an A-V node. Ventricular pacing and spontaneous ventricular premature beats resulted in a short ventriculoatrial conduction time (110 msec.) suggesting that if A-V nodal bypass tracts exist, they are utilized in an antegrade and retrograde fashion. None of the features of WPW syndrome was present. The mechanism of syncope in the mother and daughter was intermittent third-degree heart block. Both went on to develop permanent complete heart block despite electrophysiologic studies demonstrating 1:1 A-V conduction at extremely rapid atrial pacing rates and both required implantation of permanent pacemakers. The mechanism of syncope in the two brothers was possibly marked sinus bradycardia, but transient complete heart block has not been ruled out. Permanent pacemaker therapy was recommended for both. The nature of the cardiomegaly, which was mild in three patients, is not known. Although not well documented, several maternal relatives have had enlarged hearts, SVT, complete heart block, and syncope.
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PMID:Familial occurrence of sinus bradycardia, short PR interval, intraventricular conduction defects, recurrent supraventricular tachycardia, and cardiomegaly. 13 66

The electrophysiological effects of an intravenous dose of disopyramide phosphate (2 mg per kg body weight) were studied in 17 patients. Studies were performed with the patients fasting, unpremedicated, and off all medication for three days. Blood samples for estimation of serum levels of disopyramide were collected in 15 of these patients. The effects of intravenous disopyramide were maximal at five minutes, less marked at 20 minutes, and largely gone by 30 minutes after administration of the drug. Sinus cycle length and corrected sinus node recovery time were shortened significantly. No index of atrioventricular nodal function was significantly changed. Both atrial and ventricular effective refractory periods were significantly prolonged. Further impairment of intraventricular conduction occurred in six patients with bundle branch block on electrocardiogram or prolonged HV interval. In one of two patients with Wolff-Parkinson-White syndrome, the bypass effective refractory period was prolonged. These electrophysiological changes are similar to quinidine and quinidine like drugs. It is recommended that disopyramide should be used cautiously in patients with evidence of His Purkinje system disease since it may lead to higher degrees of intraventricular block.
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PMID:Electrophysiology of disopyramide in man. 28 51

The phrase paroxysmal supraventricular tachycardia describes a group of arrhythmias with similar electrocardiographic features but different mechanisms that have been clarified in recent years with specialized intracardiac recording and pacing techniques. Reentry accounts for most cases and has been localized to the A-V node and less frequently to the sinus node, the atria themselves, and A-V nodal bypass tracts (Wolff-Parkinson-White syndrome). These forms of supraventricular tachycardia are initiated by premature beats that dissociate conduction between two pathways and permit the establishment of circulating electrical activity that spreads to atrial and ventricular myocardium. Paroxysms cease when the conducting properties of the reentrant circuits are disturbed by changes in autonomic tone or the application of certain drugs, pacing, or cardioversion. Supraventricular tachycardia may also result from abnormal automaticity in atrial tissues. Such automatic atrial tachycardias are often associated with A-V block ("paroxysmal atrial tachycardia with block") and may be due to digitalis intoxication. This arrhythmia is treated by withdrawal of digitalis or administration of antiarrhythmic drugs that decrease automaticity.
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PMID:Supraventricular tachycardia: mechanisms and management. 33 25

The authors report two cases of "true" consecutive double ventricular response caused by a single premature atrial stimulation; both were young men with Wolff-Parkinson-White syndrome. In both cases, the presence of a bundle of Kent was confirmed. The phenomenon of double ventricular response arising successively from the bundle of Kent and node-His pathway is rare, being mentioned in only two cases in the literature. It is only found when there is the combination of a good bundle of Kent, fair forward conduction, and a relative ventricle-His retrograde block. Amongst the other mechanisms for double ventricular repsonse, re-entry from branch to branch presents the most difficult differential diagnosis. From our observations, the forward characteristics of the spread through the bundle of His which always procedes the bundle of His which always precedes the second ventricular complex have been confirmed, especially in view of the freat variation in the position of this potential which can easily be explained by variations in intra-nodal conduction. In one of these cases, the atriogram, taken after the second ventriculogram, was provided by retrograde activity in the bundle of Kent.
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PMID:[The double ventricular response phenomenon in 2 cases of Wolff-Parkinson-White syndrome]. 41 84

In a patient with the Wolff-Parkinson-White Syndrome we observed atrial fibrillation and three distinct paroxysmal re-entrant tachycardias. Intracardiac electrograms obtained during the tachycardias showed the mechanisms to be A-V nodal, accessory pathway and sinus node re-entry. When P wave morphology, R-P relationship and QRS configuration are considered, it is illustrated how these four tachyarrhythmias may be successfully diagnosed on the surface electrocardiogram. The therapeutic implications of multiple arrhythmias with different mechanisms in the Wolff-Parkinson-White Syndrome are discussed.
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PMID:Multiple mechanisms of tachycardias in a patient with the Wolff-Parkinson-White syndrome. 45 92

Seventeen patients with recurrent symptomatic arrhythmias were treated with oral disopyramide (DP). Fifteen of the 17 patients had received other currently conventional anti-arrhythmic therapy, to which only 1 patient responded, yet 13 of these 15 patients with resistant arrhythmias responded to DP. Electrophysiological studies were performed on 9 patients. The most impressive electrophysiological findings were the depressant effect of DP on ventricular automaticity and its action in slowing conduction through the His-Purkinje system (including the bundle branches) without depressing sino-atrial rate and atrioventricular (AV) nodal conduction time. Retrograde ventriculo-atrial (VA) conduction was markedly prolonged in 4 patients with reciprocating supraventricular tachycardia (SVT), including 2 patients with Wolff-Parkinson-White syndrome. All 4 patients with reciprocating SVT appear to be cured of their arrhythmia, probably by this mechanism.
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PMID:Clinical and electrophysiological observations with disopyramide in drug-resistant and recurrent symptomatic arrhythmias. 74 66

Five patients, age 3 weeks to 11 years, presented with supraventricular tachycardia that remained uncontrolled following adequate digitalization. Four of these patients underwent invasive electrophysiologic studies to determine the mechanism of the arrhythmias. Of these four patients, three had concealed Wolff-Parkinson-White syndrome, and one patient had evidence of dual A-V nodal pathways. Propranolol was added to the medical treatment and was administered orally in doses ranging from 7 to 14 mg/kg/day (average 9 mg/kg/day). All five children remain free of their tachycardia except for one patient who occasionally has supraventricular tachycardia with febrile illnesses. No adverse reactions to these high doses of propranolol were encountered.
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PMID:High-dose propranolol therapy in the management of supraventricular tachycardia. 75 96

Stimulation of the bundle of His and of the uppermost portion of the interventricular septum gives us an opportunity to make a precise study of capture phenomena in patients with paroxysmal nodal tachycardia. According to whether the capture is correctly timed, delayed, or unusually premature, the inferior junction point of the reentry circuit can be located precisely by reference to the H wave and the onset of the R wave. Out of a series of 65 patients, only 30 of whom had a true WPW syndrome, it was shown that 43 cases had a bundle of Kent which ensured retrograde conduction during the tachycardia, and was therefore the seat of a unidirectional block in 13 cases. In 22 cases (33.8%) the diagnosis of WPW syndrome was excluded, but the reentry circuit was nevertheless not of nodal origin. The inferior junction point of the circuit was effectively situated between H and R in 12 cases, and at H in 5. In only 5 cases (7.8%) might there have been a reciprocal intra-nodal rhythm, which should not necessarily be taken as proof of its existence. The validity of the classical criteria in localising the reentry circuit is discussed.
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PMID:[Paroxysmal junctional tachycardia. Determination of the inferior point of junction of the reentry circuit. Dissociation of the intra-nodal reciprocal rhythms]. 81 83

Accurate electrocardiographic diagnosis of myocardial ischemia or infarction is difficult in patients with the Wolff-Parkinson-White syndrome; however, myocardial ischemia may also have profound effects on the electrophysiologic characteristics of the bypass tract in these patients. Comparison of studies performed during and two months following an episode of significant myocardial ischemia demonstrated substantial prolongation of the refractoriness of the bypass tract during the period of ischemia. Bypass refractoriness was prolonged by 196 msec, yet atrioventricular nodal refractoriness was not significantly different from normal. These studies, therefore, suggest that, on occasion, the presence of acute myocardial ischemia may, in fact, obscure the electrocardiographic diagnosis of the Wolff-Parkinson-White syndrome.
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PMID:Wolff-Parkinson-White syndrome. Alterations in electrophysiologic characteristics of the bypass tract secondary to ischemia. 88 79


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