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)

Anterograde and retrograde pathways are the two major components of the reentry circuit in patients with paroxysmal supraventricular reentrant tachycardias. Therefore, the capacity of each pathway to maintain 1:1 conduction would be expected to determine the cycle length (CL) of the tachycardia. In this study, the possible relationship between the CL of reentrant tachycardia and the maximum capacities of anterograde and retrograde conduction in the maintenance of a 1:1 response during atrial and ventricular pacing were examined. This relationship was analyzed in 26 patients with orthodromic reentrant tachycardia due to Wolff-Parkinson-White syndrome (group 1) and compared with that in 26 patients with atrioventricular nodal reentrant tachycardia (group 2). There were no statistically significant differences between the two groups in the shortest tachycardia CLs (mean +/- SD, 325 +/- 44 versus 329 +/- 52 ms); in the shortest ventricular pacing CLs with 1:1 response (314 +/- 63 versus 319 +/- 38 ms); nor in the CLs that produced retrograde atrioventricular block (306 +/- 62 versus 301 +/- 37 ms). In contrast, the longest atrial pacing CL that produced Wenckebach's phenomenon and the shortest atrial pacing CL with 1:1 response were significantly shorter for group 1 than for group 2 patients (290 +/- 38 versus 390 +/- 88 ms, P less than 0.001) and (305 +/- 38 versus 406 +/- 90 ms, P less than 0.001), respectively. It was concluded that the CL of orthodromic tachycardia can best be predicted from the shortest atrial pacing CL that maintains 1:1 anterograde conduction via the normal pathway.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tachycardia cycle length and maximum capacity of anterograde and retrograde atrioventricular conduction in paroxysmal supraventricular tachycardia. 337 96

The hypothesis that production of ischemia or cooling of an arrhythmogenic area or pathway could interrupt tachycardias was tested by subselective catheterization of the coronary artery supplying the site of origin of ventricular tachycardia (9 patients), the accessory pathway (2 patients) and the site of origin of atrial tachycardia (1 patient). Ventricular tachycardia was reproducibly terminated and reinduction temporarily prevented in 8 of the 9 patients by occlusion of the artery or administration of iced isotonic saline. Block in the accessory pathway was obtained in 1 of the 2 patients with Wolff-Parkinson-White syndrome. Selective cooling through the atrioventricular nodal artery in 1 patient terminated his circus movement tachycardia. Reproducible termination of a continuous atrial tachycardia was obtained by cooling of the atrial branch supplying the site of origin of the arrhythmia. These data demonstrate the feasibility of identification and selective catheterization of the coronary artery branch supplying blood to an arrhythmogenic area or pathway and suggest a new possibility for treatment of tachycardias by permanently blocking the blood supply to the site of origin or pathway of a tachycardia.
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PMID:Termination of tachycardias by interrupting blood flow to the arrhythmogenic area. 341 15

We evaluated the effects of intravenous and long-term oral sotalol treatment in 17 patients with an accessory atrioventricular (AV) pathway. All patients had a history of symptomatic supraventricular tachycardia. During electrophysiologic study intravenous (1.5 mg/kg body weight) and oral (240 to 320 mg/day) sotalol caused significant increases of sinus cycle length, AV nodal conduction time, and refractory periods of atrial and ventricular myocardium and accessory pathway. AV reciprocating tachycardia, which was inducible and sustained in 15 patients at control, was still inducible after intravenous sotalol in 14 patients, including one in whom it was not inducible at control. However, tachycardia became nonsustained in 10 patients. In seven patients who underwent repeat drug testing while on oral sotalol, results were the same as after intravenous sotalol. Sixteen patients were followed-up for 36 months (median value). Fifteen of them were clinically free of symptoms or experienced marked improvement, despite recurrences of tachycardia in two. In a third patient sotalol had to be withdrawn because of recurrent supraventricular tachycardia. Orthostatic hypotension occurred in five patients and required withdrawal of sotalol in one. To predict the long-term clinical outcome of patients, exercise testing and Holter monitoring were of little or no value. Programmed electrical stimulation predicted clinical outcome in 63% after intravenous and in 86% after oral sotalol. This study shows that long-term treatment with sotalol is highly effective in patients with the Wolff-Parkinson-White syndrome and regular supraventricular tachycardia.
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PMID:Sotalol in patients with Wolff-Parkinson-White syndrome. 356 5

Penticainide is a new class I antiarrhythmic agent. Its electrophysiological effects and pharmacokinetic properties were studied in 28 patients undergoing endocavitary exploration for paroxysmal supraventricular tachycardia (10 cases), WPW syndrome involving an accessory pathway (5 cases), and unexplained dizziness (13 cases). Increasing doses of penticainide were infused in the first 18 patients (0.12 up to 3.5 mg kg-1). The next ten patients received 4 mg kg-1 over a 30 minute period. Penticainide shortened the sinus cycle length and increased the transnodal conduction time. The ventricular conduction time tended to increase. Atrial functional refractory period increased when atrioventricular nodal and ventricular refractory periods remained unchanged. In patients with previous supraventricular tachycardias all triggered arrhythmias were prevented with dosages higher than 2 mg kg-1 and related blood levels higher than 3 mg l-1. A dose-dependency of plasma and renal clearance was documented. Average Cmax values after 4 mg kg-1 was 7.37 +/- 1.28 mg l-1. No adverse events occurred during the trial and penticainide proved to be well tolerated.
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PMID:Electrophysiologic effects and pharmacokinetics of intravenous penticainide (CM 7857). 362 42

Effects of intravenous injection of 0.6 mg/kg sotalol, a beta-blocking agent with additional class III properties, were studied by means of electrophysiologic techniques in 14 patients, seven with the Wolff-Parkinson-White syndrome and seven with concealed atrioventricular (AV) accessory pathways. Sotalol brought about a significant increase in the retrograde effective refractory period of the anomalous pathway, whereas changes in the antegrade effective refractory period were more variable. In five of nine patients with electrically induced reciprocating tachycardia sotalol prevented the initiation of sustained reentry. In most cases the suppression of the circus movement was the result of the development of AV nodal block. Thus our data support the use of sotalol for the treatment of tachycardias incorporating anomalous AV conduction pathways.
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PMID:Effects of intravenous sotalol in patients with atrioventricular accessory pathways. 363 Aug 95

In this study we sought to determine whether characteristics of ventricular-induced atrial preexcitation during reciprocating tachycardia could help differentiate atrioventricular (AV) nodal reentry from orthodromic AV reentry using an accessory pathway and to identify the site of accessory pathways in patients with Wolff-Parkinson-White syndrome. Fifty-five patients with orthodromic AV reciprocating tachycardia and 22 patients with AV nodal reentrant tachycardia were studied with standard electrophysiologic techniques. There were 24 left free wall, 23 posterior septal, seven anterior septal, and one right free wall accessory pathways. Progressively premature right ventricular complexes (V2) were introduced during reciprocating tachycardia (V1V1). The V1V1 interval during tachycardia minus the longest V1V2 at which atrial preexcitation occurred defined a preexcitation index (PI). Atrial preexcitation occurred in 49 of 55 (89%) patients with AV reentry compared with only three of 22 (14%) patients with AV nodal reentry (p less than .001). In the three patients with AV nodal reentry who demonstrated atrial preexcitation, the PI was distinct from that of the septal pathways and was in the upper range of values for left free wall pathways. The percentage of tachycardias demonstrating atrial preexcitation was not different between the free wall and septal pathways, but His bundle activation was visible at the time of atrial preexcitation in only six of 17 (35%) left free wall compared with 13 of 16 (81%) posterior septal and seven of seven (100%) anterior septal pathways (p less than .05 free wall vs posterior or anterior septal).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The preexcitation index: an aid in determining the mechanism of supraventricular tachycardia and localizing accessory pathways. 374 51

To assess the antiarrhythmic efficacy of intravenous propafenone, 20 patients with inducible sustained supraventricular tachycardia received propafenone, 2 mg/kg body weight, or placebo in a double-blind, randomized, crossover study. Three patients had intra-atrial reentrant tachycardia, 3 had atrioventricular nodal reentrant tachycardia, and 14 had atrioventricular reciprocating tachycardia associated with the Wolff-Parkinson-White syndrome. Termination of supraventricular tachycardia occurred in 15 of the 20 patients receiving propafenone but 0 of the 11 patients receiving placebo (p less than 0.01). Propafenone prolonged refractoriness and slowed conduction of the atrium, the atrioventricular node, and accessory atrioventricular bypass tracts, and these effects provided antiarrhythmic action to halt tachycardia. No adverse effects were observed in any patient. We conclude that intravenous propafenone is safe and effective in the acute treatment of various forms of reentrant supraventricular tachycardia.
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PMID:Intravenous propafenone for termination of reentrant supraventricular tachycardia. A placebo-controlled, randomized, double-blind, crossover study. 376 46

The acute electrophysiologic effects of pirmenol are reported in 8 normal subjects and in 8 patients with Wolff-Parkinson-White (WPW) syndrome. Standard electrophysiologic testing was performed before and after a 50-mg intravenous bolus and a 60-minute infusion of 150 mg of pirmenol. After pirmenol administration, AH interval, atrial refractory period, atrioventricular (AV) nodal functional refractory period and Wenckebach cycle length did not change; however, sinus cycle length decreased from 743 +/- 169 to 650 +/- 133 ms (p less than 0.001), sinoatrial conduction time from 103 +/- 35 to 78 +/- 37 ms (p less than 0.05) and AV nodal effective refractory period from 308 +/- 51 to 272 +/- 23 ms (p less than 0.01). Pirmenol increased the HV interval from 43 +/- 5 to 48 +/- 6 ms (p less than 0.05) and ventricular functional refractory period from 247 +/- 21 to 260 +/- 21 ms (p less than 0.005). Anterograde effective refractory period of the accessory AV pathway increased in 4 of 6 patients with ventricular preexcitation and retrograde effective refractory period increased in all patients. Pirmenol treatment prolonged the shortest preexcited RR interval from 253 +/- 38 to 459 +/- 19 ms (p less than 0.05) and the average RR interval from 354 +/- 26 to 421 +/- 60 ms (p less than 0.01) during atrial fibrillation in all 6 patients with preexcitation. Pirmenol did not influence the inducibility or cycle length of AV reciprocating tachycardia in the patients with WPW syndrome. The pirmenol infusions were well tolerated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute electrophysiologic effects of pirmenol in normal subjects and in patients with Wolff-Parkinson-White syndrome. 396 64

Successful surgical treatment of all forms of supraventricular tachyarrhythmias is dependent on accurate electrophysiologic guidance. Surgery for WPW syndrome is no longer experimental and should be offered to (1) patients with medically refractory reciprocating tachycardia associated with the syndrome, (2) patients with spontaneous atrial fibrillation who are at risk for sudden death, (3) patients with drug intolerance, and (4) young, otherwise healthy patients with symptoms that warrant more than minimal medical therapy. The current results of surgery for WPW syndrome would seem to lessen the likelihood that a major new method of superior nonpharmacologic treatment will emerge in the near future. Surgery for most other types of supraventricular tachyarrhythmias remains experimental and should be applied only under the most controlled circumstances and after satisfying the most rigid criteria for surgical intervention, the main indication being absolute medical refractoriness. The single exception at the present time is surgery for AV node reentry tachycardia, which appears to be easily cured by the new technique of discrete cryosurgery of the peri-AV nodal region of the lower right atrial septum. In a majority of patients, ventricular tachycardia can be successfully ablated surgically without the use of electrophysiologic mapping to guide the surgeon. If such an approach is taken, however, the surgical treatment of these complex arrhythmias becomes a completely service-oriented exercise. Although delivery of such a service is of undeniable importance, the potential for learning more about these complex and lethal arrhythmias is lost unless each patient is studied as comprehensively as possible.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The status of surgery for cardiac arrhythmias. 397 19

A comparison of the effects of several antiarrhythmic agents was made in a study of 70 patients - 15 with manifest Wolff-Parkinson-White (WPW) syndrome, 17 with concealed WPW syndrome, 18 with AV nodal re-entrant tachycardia, 14 with paroxysmal atrial fibrillation and 6 with paroxysmal atrial flutter - employing intracardiac stimulation and esophageal pacing. For the termination of paroxysmal supraventricular tachycardia, intravenous administration of verapamil or aprindine was more effective than that of disopyramide or procainamide. In AV nodal re-entrant tachycardia, verapamil was the most effective for termination. In the manifest WPW syndrome, disopyramide or aprindine was indicated especially for patients with the accessory pathways of the short antegrade refractory period, because these drugs lengthened the refractory period of the accessory pathways. For the purpose of converting atrial fibrillation or flutter to the sinus rhythm, type IA drugs such as disopyramide were indicated. However, verapamil was effective for slowing down the ventricular rate in atrial fibrillation or flutter except in cases of manifest WPW syndrome. A 6-month follow-up study showed that oral administration of verapamil was also useful for putting a stop to the attacks in 24 out of 32 patients with paroxysmal supraventricular tachycardia, while oral disopyramide prevented the recurrence of atrial fibrillation in only 4 of 10 patients.
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PMID:Usefulness of invasive and non-invasive electrophysiologic studies in the selection of antiarrhythmic drugs for the patients with paroxysmal supraventricular tachyarrhythmia. 398 93


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