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)

Electrophysiological studies were performed in 22 patients with intraventricular conduction delay before and after intravenous infusion of disopyramide (Norpace), 2 mg/kg. Mean control maximal sinus node recovery time (1039 +/- 187 msec), atrioventricular nodal conduction time (113 +/- 28 msec), and atrioventricular nodal effective refractory periods (349 +/- 67 msec) did not change significantly after administration of disopyramide (1073 +/- 284 msec, 112 +/- 31 msec, and 342 +/- 42 msec, respectively). Mean spontaneous cycle length (756 +/- 146 msec) decreased significantly 5 minutes after disopyramide (717 +/- 124 msec) (p less than 0.05), but not after 30 minutes (734 +/- 142 msec). A small but statistically significant (p less than 0.05) increase occurred after disopyramide in the mean atrial effective refractory period (259 +/- 51 to 280 +/- 53 msec), ventricular effective refractory period (253 +/- 23 to 275 +/- 33 msec), as well as the relative refractory period of the ventricular specialized conduction system (six patients) 433 +/- 78 to 479 +/- 62 msec). Although mean control infranodal conduction time (67 +/- 35 msec) increased 5 minutes after disopyramide (79 +/- 41 msec) (p less than 0.001) (18%), no spontaneous episodes of second-degree or third-degree atrioventricular block were observed. In six patients with premature ventricular depolarizations (greater than or equal to 1/min), the arrhythmia was totally abolished in four, markedly reduced in one, and remained unchanged in one. Disopyramide resulted in significant prolongation of infranodal conduction time as well as in atrial and ventricular refractoriness, but nevertheless appears to be safe in patients with bundle branch block.
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PMID:Electrophysiological effects of disopyramide in patients with bundle branch block. 75 89

The effects on A-V conduction of dehydrobenzperidol (Droperidol) 0.35 and 1.0 mg/kg i.v.) and disopyramide (1, 5 and 10 mg/kg i.v.) were tested in anesthetized, open chest and paced dogs. His's bundle electrograms were recorded by means of a catheter electrode or by a sutured electrode-bearing plaque in the A-V nodal region. Droperidol at the lower dose did not modify conduction time, while 1.0 mg/kg (3 times the usual clinical dose), prolonged atrial-His conduction without modifying H-V interval. Disopyramide 1 mg/kg caused a non-significant decrease in atrial-His concuction time, while in doses of 5 and 10 mg/kg it prolonged both conduction times (S-H and H-V), due to a predominant direct depressant effect, which is opposite to the atropinic actions of the drug.
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PMID:Dehydrobenzperidol and disopyramide in A-V conduction. 95 32

Disopyramide is a Vaughan-Williams class Ia antiarrhythmic, which is distinguished by its anticholinergic activity, which is due to its active metabolite: mono-N-alkyl disopyramide. In cells with a rapid response, such as those in the His-Purkinje tissue, it depresses conduction. In slow-responding cells (sinus node and Tawara's node) direct depression of conduction and automatism, and anticholinergic stimulation have opposing effects. In terms of clinical electrophysiology, this is a Touboul class IIa compound: and action mainly on the His-Purkinje system involving extension of the conduction time and of the refractory time. Nodal conduction is improved according to measurement of the alternate Wenckebach; according to studies of the denervated heart in transplanted patients, there is a depressant effect on automatism and conduction at all levels, but the vagolytic effect corrects this activity at Tawara's node. Clinical trials have demonstrated the absence of any deterioration, and in some cases and actual improvement of nodal conduction disorders in response to disopyramide and good safety in the presence of non-major intraventricular conduction problems (such as bundle branch block). In practice, these properties mean that moderate nodal conductive disorders and simple bundle branch block do not constitute an obstacle to the use of disopyramide. In junctional tachycardia, it is particularly indicated for use in tachycardia involving an accessory pathway, but is also effective in intranodal tachycardia due to its twofold action.
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PMID:[Effects of disopyramide on normal and pathological atrioventricular conduction]. 129 85

One case of Wolff-Parkinson-White Syndrome with paroxysmal supraventricular tachycardia related to orthodromic atrioventricular reentry using an accessory pathway for retrograde conduction an a rapidly conducting AV node for anterograde conduction is present. The pharmacological therapy with Digoxin, Propranolol, Quinidine, Disopyramide and Propafenone was not effective. An electrophysiologic study showed a reciprocating tachycardia induced by spontaneous ventricular beats. Both the effective refractory period of the AV node and the anterograde effective refractory period of the accessory pathway were minor or equal to 220 msec which made the control of the arrhythmia difficult. Amiodarone was able to suppress the premature ventricular beats, depress conduction and prolong refractoriness in both, the AV node and accessory pathway to prevent recurrences of atrioventricular reentry. In this patient a false positive test with ajmaline was documented. The electrophysiologic study showed the association of Wolff-Parkinson-White Syndrome with an enhanced atrioventricular nodal-conduction and allowed the selection of an appropriate antiarrhythmic agent.
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PMID:[Wolff-Parkinson-White syndrome with orthodromic supraventricular tachycardia associated with a "hyper-conductor" atrio-ventricular node. A therapeutic challenge]. 237 38

In the His bundle and ventricular electrograms of Langendorff-perfused guinea pig hearts driven at a cycle length of 450 or 700 msec, S-1389 (711389-S), a new antiarrhythmic agent, above 3 x 10(-7) or 10(-6) M increased the basal conduction times in the following order: His-Purkinje system greater than ventricular and atrial muscles greater than atrioventricular (AV) node. Slowing of the ventricular and AV nodal conduction of extrasystoles with variable coupling intervals was also caused by S-1389. S-1389 above 10(-6) or 3 x 10(-6) M significantly prolonged the functional and/or effective refractory periods of the AV node and ventricle. Disopyramide (3 x 10(-6)-3 x 10(-5) M) also produced similar effects, but they were much less potent than those of S-1389. Although disopyramide did not produce the rate-dependent increases in the atrial and AV nodal conduction times and in the AV nodal refractory period, S-1389 increased these parameters rate-dependently.
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PMID:Effects of S-1389 (711389-S), a new antiarrhythmic agent, on the conduction in perfused guinea pig hearts. 261 48

Cardiac drugs known to affect sinus function mostly exhibit negative chronotropic activity. However, impulse conduction within the sinus node can also be influenced. Recently we studied the direct effects of bepridil on rabbit sinus function. It appeared that sinoatrial impulse conduction was depressed markedly with drug concentrations that did not affect sinus automaticity. In the present study the direct effects of verapamil, diltiazem and disopyramide on rabbit sinus function and atrial conduction properties were studied. Verapamil (8.8 x 10(-8) M) reduced the sinoatrial impulse conduction velocity by 35% and prolonged sinoatrial refractoriness by 36%. On the other hand, the sinus rate and atrial conduction parameters were hardly affected. Diltiazem (5 x 10(-6) M) exerted similar actions on the sinoatrial impulse conduction velocity and caused a simultaneous reduction in the sinus rate of 48%. Atrial conduction remained unaffected. Disopyramide (5 x 10(-5) M) depressed both the atrial and nodal conduction properties markedly, whereas the sinus rate was reduced moderately, by almost 20%. Thus, verapamil, diltiazem and disopyramide act differently on sinus function and atrial conduction, whereby the predominant effect of verapamil and diltiazem on sinoatrial conduction properties favours the occurrence of a sinus exit block.
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PMID:Effects of verapamil, diltiazem and disopyramide on sinus function: a comparison with bepridil. 278 54

The electrophysiological effects of antiarrhythmic drugs were tested in 36 patients with recurrent paroxysmal supraventricular tachycardia (PSVT), 25 of whom had accessory pathway reentrant tachycardia (APRT) and 11 A-V nodal reentrant tachycardia (AVNRT; 10 of the slow-fast type one of the fast-slow type). The test drugs were procainamide (used in 19 patients), verapamil (in 27), disopyramide (in 31), and propranolol (in 15). The drugs were tested for their ability to terminate episodes of PSVT as well as to inhibit their induction. Procainamide had an inhibitory effect on APRT in nine of 12 patients (75%) and terminated episodes of APRT in seven of 11 patients (63.6%); in all of them V-A block was responsible for the termination. In four of six patients (66.7%) with slow-fast AVNRT and in one patient with fast-slow AVNRT, inhibition of the induction of tachycardia attacks was noted after procainamide. Termination of AVNRT was seen in the same number of patients. Verapamil inhibited the induction of APRT in 12 of 18 patients (66.7%) and terminated episodes of APRT in 10 of 16 patients (62.5%), all by A-V block. In six of eight patients (75%) with slow-fast AVNRT, inhibition of the induction as well as termination of tachycardia were noted after verapamil. Disopyramide had an inhibitory effect on APRT in seven of 23 patients (30.4%) and terminated APRT in five of 21 patients (23.8%) by V-A block, while AVNRT (all slow-fast type) was terminated in only one of eight patients (12.5%) by disopyramide. Disopyramide was less effective than previously reported. This could be attributed to a relatively low dosage and slow infusion speed. Propranolol inhibited the induction of APRT and terminated episodes of APRT in only one of 10 patients (10%). In two of four patients (50%) with slow-fast AVNRT, an inhibitory effect by propranolol was noted, but termination was seen in only one patients.
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PMID:Effects of four antiarrhythmic drugs on the induction and termination of paroxysmal supraventricular tachycardia. 380 32

The effect of intravenous and oral disopyramide on the mechanisms of the arrhythmia were studied in 11 patients with the common type of atrioventricular (AV) nodal paroxysmal reentrant tachycardia. Programmed electric stimulation of the heart was used to initiate and terminate tachycardia and to evaluate the effect of disopyramide on mode of initiation and termination of tachycardia. Disopyramide was given intravenously to all patients during tachycardia. This resulted in termination of tachycardia, by block in the anterograde slow pathway in 1 and in the retrograde fast pathway in 3 patients. In all 4 patients, reinitiation of tachycardia was no longer possible. In these 4 patients, oral disopyramide prevented spontaneous and pacing-induced AV nodal tachycardia. In 4 of the remaining 7 patients in whom tachycardia was not terminated by intravenous disopyramide, reinitiation of the arrhythmia during programmed stimulation was prevented by the drug. In these 4 patients, oral disopyramide was also effective in preventing spontaneous occurrence of tachycardia. In 3 patients, tachycardia was not terminated and its reinitiation was not prevented by intravenous disopyramide. Only 1 of these 3 patients received disopyramide by mouth, and it failed to prevent reinitiation and spontaneous tachycardia. In conclusion, disopyramide is an effective drug in patients with AV nodal paroxysmal reentrant tachycardia. A good correlation was found between intravenous and oral effect of disopyramide on the mechanisms of the arrhythmia. The study of the effect of intravenous disopyramide predicted the outcome of oral disopyramide therapy.
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PMID:Effects of intravenous and oral disopyramide on paroxysmal atrioventricular nodal tachycardia. 636 89

The effects of the intravenous administration of three drugs, i.e., verapamil, disopyramide, and procainamide, on paroxysmal supraventricular tachycardia (PSVT), atrial fibrillation (Af) and atrial flutter (AF) were evaluated electrophysiologically. Efficacy on PSVT was 94.7% (36/38) with verapamil, 61.5% (13/18) with disopyramide and 100% (4/4) with procainamide. Efficacy on Af and AF was 9.1% (1/11) with verapamil and 80.0% (12/15) with disopyramide. PSVT termination mechanisms were as follows: 1) Verapamil: A-H block in 5 cases and H-A block in 5 cases with Type 1 A-V nodal reentrant tachycardia (AVNRT). H-A block in 6 cases with Type 2 and Type 3. A-H block in 17 of 18 cases with A-V reciprocating tachycardia (AVRT). Cycle length alternans were observed in 13 of 34 cases. 2) Disopyramide: H-A block in 2 cases with AVNRT and V-A block in 2 cases with AVRT. 3) Procainamide: V-A block in 4 cases with AVRT. These results suggest that verapamil and disopyramide are most effective on PSVT and Af, respectively.
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PMID:Electrophysiologic evaluation of antiarrhythmic drugs on supraventricular tachyarrhythmias. 682 76

Electrophysiological effects of 2 to 2.5 mg/kg iv disopyramide were studied in 10 patients with dual nodal pathways who used a slow pathway for anterograde and a fast pathway for retrograde conduction during paroxysmal supraventricular tachycardia (mean cycle length 308.5 +/- 37 ms; range 260-370 ms). Disopyramide terminated the tachycardia in six cases by production of ventriculoatrial block in five and by sinus overdrive in one. In the remaining four patients cycle length of the paroxysmal supraventricular tachycardia increased significantly from 270 +/- 8 ms to 377.5 +/- 28 ms. In all 10 patients disopyramide depressed retrograde fast pathway conduction manifest by an increase in mean ventricular paced cycle length producing ventriculoatrial block from less than or equal to 296.5 +/- 25 ms to 358 +/- 60 ms, and increase in retrograde fast pathway effective refractory period from less than or equal to 246 +/- 34 ms to 325 +/- 36 ms; the drug abolished ventriculoatrial conduction in two cases. Anterograde slow pathway and fast pathway conduction properties were unchanged after disopyramide (atrial paced cycle length producing AH block 292 +/- 30 to 306.5 +/- 30 ms; effective refractory period of anterograde fast pathway less than or equal to 274 +/- 56 to 284 +/- 44 ms, before and after the drug, respectively) suggesting that anterograde conduction was not crucial either for sustainment or for failure to initiate paroxysmal supraventricular tachycardia after the drug. Paroxysmal supraventricular tachycardia could not be reinduced in six cases after disopyramide. In the other four the ventricular paced cycle lengths producing ventriculoatrial block (318 +/- 41 ms) and effective refractory period of retrograde fast pathway (320 +/- 28 ms) were shorter than the cycle length of reinduced paroxysmal supraventricular tachycardia (367.5 +/- 35 ms) allowing perpetuation of the tachycardia. We conclude that disopyramide breaks atrioventricular nodal re-entrant tachycardia by specific blockade of the retrograde fast pathway though the effect on anterograde atrioventricular nodal conduction is variable.
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PMID:Selective blockade of retrograde fast pathway by intravenous disopyramide in paroxysmal supraventricular tachycardia mediated by dual atrioventricular nodal pathways. 684 16


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