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)

Electrophysiologic effects of intravenous (i.v.) cibenzoline were evaluated in 18 patients with accessory pathways or dual atrioventricular (AV) nodal pathways (12 men and 6 women with a mean age of 44 +/- 18 years). Twelve patients had accessory AV pathways, including 6 patients with a manifest accessory pathway. Six patients had AV nodal reentrant tachycardia (AVNRT). Electrophysiologic studies were performed before and after cibenzoline (1.4 mg/kg i.v.) infusion for 5 min. Sinus cycle length did not change significantly after cibenzoline administration. Cibenzoline increased both the AH (85 +/- 20 vs. 91 +/- 21 ms, p less than 0.05) and HV intervals (41 +/- 10 ms vs. 53 +/- 11 ms, p less than 0.001). Neither the atrial nor ventricular effective refractory period (ERP) was altered by cibenzoline. Complete block in the accessory pathway occurred antegradely in 4 patients and retrogradely in 1 patient. Cibenzoline prevented induction of AV reentrant tachycardia (AVRT) in 3 of 8 patients with sustained orthodromic AVRT by abolishing retrograde accessory pathway conduction or prolonging the retrograde accessory pathway ERP. Of 5 patients who continued to have inducible AVRT before and after cibenzoline administration, the tachycardia cycle length was increased in 3, mainly due to the increase in retrograde accessory pathway conduction time. Cibenzoline prevented induction of sustained AVNRT in 4 of 5 patients by prolonging the minimum pacing cycle length, maintaining 1:1 ventriculoatrial (VA) conduction through the retrograde fast AVN pathway or shortening the antegrade fast AVN pathway ERP equal to the slow AVN pathway. In one patient who had an uncommon type of AVNRT, sustained tachycardia was induced by cibenzoline.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Electrophysiologic effects and efficacy of cibenzoline in patients with supraventricular tachycardia. 127 81

Cycle length alternation (CLA) is commonly observed during supraventricular tachycardia (SVT) onset and termination. The present study was designed to gain insights into the mechanism and potential clinical relevance of CLA by comparing computer simulations of tachycardia to directly observed behavior in a canine model of AV reentrant tachycardia (AVRT). The computer model was based on the hypothesis that CLA is secondary to feedback between AV nodal output during SVT and subsequent AV nodal input, and used the measured anterograde AV nodal recovery curve (AV vs A1A2) to predict sequential AV and RR intervals during SVT. Orthodromic AVRT was created experimentally in 11 open-chested, autonomically-blocked (atropine plus nadolol) dogs using a sensing and pacing circuit that mimicked a retrograde-conducting accessory pathway. Steady-state cycle length and AV interval during experimental AVRT closely paralleled predictions made by the computer model. CLA appeared consistently at the onset of experimental AVRT at programmed VA intervals less than or equal to 100 msec (corresponding to VA less than or equal to 150 msec as measured clinically) in all dogs. The amplitude and duration of CLA increased as the VA interval decreased, and closely paralleled predictions based on the computer model. Abrupt accelerations in atrial pacing to the same rate as AVRT did not result in alternation of cycle length. In conclusion, alternation of cycle length results from feedback between AV nodal output and subsequent AV nodal input at the onset of reentrant supraventricular tachycardia, and does not require changes in autonomic tone or dual AV nodal pathways. CLA occurrence, amplitude, and duration are predictable based on AV node recovery properties, and depend on retrograde conduction properties of the reentrant circuit. The presence of CLA suggests that the AV node is an integral component of the SVT reentry circuit, and may be useful clinically to identify the mechanism of supraventricular tachycardias.
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PMID:Cycle length alternation during supraventricular tachycardia: occurrence and mechanism in a canine model of AV reentrant tachycardia. 169 Apr 4

The preexcitation index has been shown to be useful in determining the mechanism of paroxysmal supraventricular tachycardia (SVT) and the site of the accessory pathway in atrioventricular (AV) reentrant tachycardia. To test whether a preexcitation index could be computed analytically instead of by scanning the whole SVT cycle with extrastimuli, 19 patients with SVT were studied. The new index was computed using the following formula: (AV conduction time during SVT) + (ventriculoatrial conduction time during ventricular pacing at the SVT cycle length) - (SVT cycle length). There was a strong correlation between the preexcitation index determined by the extrastimulus technique and the new index in 15 patients in whom the preexcitation index could be determined (r = 0.99, p less than 0.01). The value on the new index was greater than 90 ms only in patients with dual AV nodal pathways. In the 4 patients in whom the preexcitation index could not be determined by the extrastimulus technique, the new index could differentiate AV reentrant tachycardia (index for 2 patients, 60 and 60 ms, respectively) from AV nodal reentrant tachycardia (index for 2 patients, 100 and 105 ms, respectively). In conclusion, the new index provided help in determining the mechanism of SVT, even when retrograde atrial preexcitation by a ventricular extrastimulus did not occur.
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PMID:A new method for estimating preexcitation index without extrastimulus technique and its usefulness in determining the mechanism of supraventricular tachycardia. 170 19

Since the first successful surgical intervention for Wolff-Parkinson-White syndrome by W. C. Sealy, a surgical electrophysiological intervention has been developed for every single supraventricular arrhythmia. The surgical rationale is based on the site of the mechanism of the arrhythmia and associated pathology which characterizes the "arrhythmogenic substrate". Wolff-Parkinson-White syndrome is a congenital heart disease characterized by an accessory atrioventricular connection distinct from the AV node-His bundle system. It is associated with AV reentrant tachycardia and/or atrial fibrillation with fast ventricular responses via the accessory pathway. The current surgical management is ablation of the accessory pathway using either an endocardial dissection or epicardial approach. Surgical ablation is associated with high efficacy and low morbidity. Epicardial dissection of the accessory pathway on the beating heart has helped to localize variant accessory pathways associated with Coumel's tachycardia or Mahaim's fiber electrophysiological entity. AV nodal reentrant tachycardia can be cured using direct AV nodal dissection (or perinodal cryoablation). Atrial flutter can be interrupted by cryoablation of the arrhythmogenic substrate located in the coronary sinus orifice of the region modifying atrial inputs. Chronotropic atrial function abolished by chronic or paroxysmal idiopathic atrial fibrillation can be restored using the corridor operation (sinus node-AV node insulation). Surgery is an alternative in patients with resistant atrial tachycardias. Currently surgery is indicated only after other non-invasive EP interventions have been either attempted or rejected.
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PMID:Surgery for supraventricular tachyarrhythmias. 176 6

Fifty patients with supraventricular tachycardia (SVT) underwent clinical electrophysiological studies (EPS), endomyocardial biopsies and cardiac catheterizations. EPS revealed AV nodal reentrant tachycardia (AVNRT) in seven patients, AV reentrant tachycardia utilizing concealed AV bypass tracts (AVR-CBT) in nine patients, AV reentrant tachycardia utilizing AV bypass tracts with ventricular preexcitation (manifest WPW) in 13 patients, sinus nodal or intra-atrial reentrant tachycardia (SNRT or IART) in three patients, atrial flutter (AF) in nine patients, automatic atrial tachycardia (AAT) in five patients, and multifocal atrial tachycardia (MAT) in four patients. According to the clinical observations, three patients with AVNRT (43%), six with AVR-CBT (67%), six with manifest WPW (46%), two with SNRT or IART (67%), eight with AF (89%), two with AAT (40%), and two with MAT (50%) showed other accompanying clinical abnormalities. In all patients who were studied histologically, changes in the myocardium were seen; myocarditic changes, postmyocarditic changes and nonspecific abnormalities were present in six (12%), 15 (30%), and nine (18%) respectively. Myocardial changes were observed in four out of seven cases with AVNRT (57%), in six out of nine with AVR-CBT (67%), in five out of 13 with manifest WPW (38%), in two out of three with SNRT or IART (67%), in six out of nine with AF (67%), in all five cases of AAT (100%), and in two out of four with MAT (50%). Nineteen out of 32 without clinical abnormalities except for arrhythmias (59%) had myocardial changes (six had myocarditic changes, ten had postmyocarditic changes, and three had nonspecific abnormalities). On the other hand, nine out of 21 with myocarditic or postmyocarditic changes were accompanied with various arrhythmias other than SVT (two had SSS, five had AV block or rBBB, and two had VT). Elevated LVEDP was present in 36% of the group with normal myocardium and in 53% of the group with myocardial changes. However, the low EF was shown in no patients with normal myocardium but in 21% of the group with myocardial changes. The low CI was also shown in only 9% of the group with normal myocardium but in 28% of the group with myocardial changes. These results suggest that patients with SVT may exhibit several histopathological changes in the myocardium, even in the absence of any clinical organic heart disease.
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PMID:Clinical, electrophysiological, and histopathological observations in supraventricular tachycardia. 245 68

Since Sealy's pioneering surgical intervention for Wolff-Parkinson-White syndrome, surgical electrophysiologic interventions have been developed for all supraventricular arrhythmias. The surgical rationales are based on the site of origin of the arrhythmic mechanism and the associated pathology that characterizes the "arrhythmogenic substrate." The Wolff-Parkinson-White syndrome is characterized by an accessory atrioventricular (AV) connection distinct from the AV node-His bundle system. It is associated with AV reentrant tachycardia or atrial fibrillation, or both, with fast ventricular responses through the accessory pathway. The current surgical management involves ablation of the accessory pathway using either an endocardial or an epicardial approach. Surgical ablation is associated with high efficiency and low morbidity. Epicardial dissection of the accessory pathway on the beating heart has helped to localize variant accessory pathways associated with Coumel's tachycardia or the Mahaim fiber. AV nodal reentrant tachycardia can be cured using direct AV nodal dissection (or perinodal cryoablation). Atrial flutter can be interrupted by cryoablation of the arrhythmogenic substrate located in the coronary sinus orifice region. The chronotropic atrial function, abolished by incessant or paroxysmal idiopathic atrial fibrillation, can be restored using the corridor operation (sinus node-AV node insulation). The success of surgical intervention in atrial tachycardias is uncertain, but it may be an option in selected patients with resistant atrial tachycardias.
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PMID:Surgical alternatives for supraventricular tachycardias. 259 18

Propafenone is an investigational type Ic anti-arrhythmic agent that markedly slows conduction velocity in all cardiac tissues. Propafenone also possesses weak beta- and calcium-channel blocking properties. The bioavailability of propafenone is dose-dependent. Hepatic metabolism of this agent is polymorphic and appears to correlate with the ability of the liver to oxidize debrisoquin sulfate. Propafenone is effective in suppressing spontaneous ventricular ectopy; however, the drug may be less effective in patients with sustained ventricular tachycardia or ventricular fibrillation when evaluated using programmed stimulation. Propafenone is also useful in the treatment of supraventricular tachycardias including atrioventricular (AV) nodal reentrant tachycardia, AV reentrant tachycardia associated with the Wolff-Parkinson-White syndrome, and atrial fibrillation. Adverse reactions seen with propafenone affect the gastrointestinal, central nervous, and cardiovascular systems. Comparative studies with currently available type Ic agents are needed to better define propafenone's place in therapy.
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PMID:Propafenone: a novel type Ic antiarrhythmic agent. 265 98

The electrophysiologic effects of the new class-1 antiarrhythmic drug cibenzoline (1.5 mg/kg within 10 min, followed by an infusion of 0.5 mg for 30 min) were investigated in six patients with atrioventricular (av) nodal reentrant tachycardia and nine patients with atrioventricular tachycardia. Sinus cycle length, sinus node recovery time, effective refractory period (ERP) of the atrium and the ventricle as well as the ERP of the av node were not significantly affected by cibenzoline. Retrograde conduction via the av node was prevented by cibenzoline in 6/15 patients, retrograde ERP was increased in 4/15 patients and in 5/15 patients determination of the retrograde ERP of the AV node was impossible. Intranodal conduction time (AH-interval) and infranodal conduction time (HV-interval) was increased from 96 +/- 27 ms to 117 +/- 40 ms (p less than 0.01) and 36 +/- 12 ms to 62 +/- 12 ms (p less than 0.01), respectively. In four patients with antegrade conduction along the accessory pathway no antegrade conduction was seen after the application of cibenzoline. Retrograde ERP of the accessory pathway was increased in two patients, it was unchanged in three patients, and no retrograde conduction along the accessory pathway was seen in four patients. AV nodal reentrant tachycardia was not inducible, after cibenzoline in 4/6 patients and in 5/9 patients with AV reentrant tachycardia. If tachycardia remained inducible, an increase in tachycardia cycle length from 333 +/- 46 ms to 402 +/- 24 ms was observed (p less than 0.01). In conclusion the electrophysiologic effects of cibenzoline make it a suitable drug for the treatment of av nodal reentrant tachycardia and atrioventricular tachycardia.
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PMID:[Electrophysiologic properties of cibenzoline in Wolff-Parkinson-White syndrome and atrioventricular nodal reentry tachycardia]. 268 51

The efficacy of intravenous flecainide acetate (maximum 2 mg/kg or 150 mg given at a rate of 15 mg/min) was assessed in patients with acute supraventricular tachycardia (SVT) (within 24 hours). Fifty patients were studied, 46 with spontaneous SVT and 4 with induced SVT at electrophysiologic assessment. Conversion to sinus rhythm was achieved within 45 minutes in 76%: in 25 patients with atrial fibrillation (76% conversion), 15 with atrioventricular (AV) nodal or AV reentrant tachycardia (100% conversion) and 10 with atrial flutter or atrial reentrant tachycardia (40% conversion). Adverse effects were noted in 21 patients (42%): paresthesia in 9, drowsiness in 8, nausea in 2, accelerated ventricular rate in 5, ventricular tachycardia in 1, sinus bradycardia in 1 and hypotension in 5. Adverse effects were associated with larger dosage and atrial flutter or atrial reentrant tachycardia. Thus, flecainide acetate is effective in converting to sinus rhythm acute atrial fibrillation and AV nodal and AV reentrant tachycardias, but not atrial flutter or atrial reentrant tachycardia.
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PMID:Flecainide acetate for conversion of acute supraventricular tachycardia to sinus rhythm. 310 10

This report provides an overview of the safety and efficacy of flecainide for supraventricular tachyarrhythmias (SVT) based on a review of the world literature. This review provided 107 entries, but 5 were review articles and 22 were articles not translated into English. The remaining 80 articles or published abstracts form the basis for this report. A total of 1,371 courses of therapy with intravenous or oral flecainide, or both, were represented. Efficacy was defined by each investigator. Intravenous flecainide was successful in terminating ongoing tachycardias in 81% of reported cases of atrioventricular (AV) nodal reentrant tachycardias, 88% of AV reentrant tachycardias and 100% of atrial tachycardias. Atrial fibrillation or flutter was terminated by intravenous flecainide in 62% of cases and arrhythmias associated with Wolff-Parkinson-White syndrome in 73%. Oral flecainide was successful in longer-term management of arrhythmia in 74 and 81% of patients with AV nodal and AV reentrant tachycardia, respectively, and in 83% with atrial tachycardia. Atrial flutter or fibrillation responded to oral drug in 61% of cases and arrhythmias related to Wolff-Parkinson-White syndrome in 61%. Adverse experiences were reported in studies totaling 695 patients (designated "at-risk patients"). They were not commented on in studies with the remaining 594 patients. Overall, a total of 6.9% of at-risk patients (3.7% of total patients) reported cardiac adverse experiences; 19% of at-risk patients (10% of total patients) reported at least 1 noncardiac adverse effect. Cardiac adverse events included worsened arrhythmias in 28, conduction disturbances in 15 and congestive heart failure in 5. The most frequent noncardiac adverse experiences were paresthesia and visual disturbance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Summary of efficacy and safety of flecainide for supraventricular arrhythmias. 313 38


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