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)

Effect of diazepam on the AV nodal conductivity was studied using a direct perfusion technique of the canine AV node artery in situ. As compared to acetylcholine which induced a rapid onset of third degree AV block with prompt recovery, diazepam injected into the AV node artery in doses from 300 micrograms to 3 mg elicited first to third degree AV blocks of longer duration following gradual prolongation of PR interval. The response was not affected by bilateral vagotomy and sympathectomy. Pretreatment of the AV node with hexamethonium or atropine also failed to modify the diazepam-induced AV blocks. Thus, diazepam seemed to suppress conductivity of the AV node by a direct action. The AV nodal tachycardia induced by infusion of norepinephrine was readily antagonized by a single injection of diazepam, but norepinephrine failed to reverse the AV block induced by diazepam infusion.
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PMID:Negative dromotropic effect of diazepam on the AV node of dog heart in situ. 52 67

Atrioventricular (AV) nodal reentrant tachycardia is a common cause of supraventricular tachycardia. The present study describes catheter ablation of this form of tachycardia in 23 patients using direct current shocks. The aim of ablation was to abolish conduction through the retrograde pathway while preserving the anterograde conduction. All patients had symptomatic, drug resistant, slow-fast variety of dual atrioventricular nodal reentrant tachycardia. Using the retrograde atrial activation in the His bundle catheter as the reference, the optimal ablation site was selected by positioning an electrode catheter to obtain atrial activation synchronous with or earlier than the atrial activation at the reference electrode. Shocks of 100-300 joules were delivered at this site resulting in blockade of retrograde conduction in all patients. Ventriculo-atrial conduction studied 24 hours after the procedure was still absent in 16, modified in 2 and resumed in 3 patients. Two patients developed permanent complete heart block and were given pacemakers. At repeat electrophysiologic study performed after 2-4 months in 10 patients, the supraventricular tachycardia could not be induced. The AH interval was 67 +/- 10 msec during control study and to 115 +/- 39 msec at restudy (p < 0.001). The ventriculo-atrial conduction was absent in 7 cases and had been modified in 1 case. Over a follow up period of 1-30 months (mean 10.8 +/- 7.1 mo) 17 patients (73%) remained free of the arrhythmia without medication or pacemaker. Three other patients were easily controlled with digoxin. Thus, catheter modification of AV node results in permanent cure of the AV nodal tachycardia in majority of patients.
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PMID:Catheter ablation of retrograde fast pathway in patients with atrioventricular nodal reentrant supraventricular tachycardia. 130 82

Twenty consecutive symptomatic patients of mitral valve prolapse (MVP) and 20 normal age, sex and symptom matched controls were studied. Ambulatory monitoring studies revealed the presence of atrial premature beats (APC) in 16 subjects in each group. Isolated ventricular premature beats (VPC) were observed in 12 patients with MVP and 15 subjects in control group (p = ns). Complex VPCs (Lown IVa, IVb) were recorded in 4 patients of MVP vs 3 controls (p = ns). There was no correlation between the occurrence of arrhythmias with the degree of MVP or the degree of mitral regurgitation. Likewise, MVP patients with prolonged QTc interval did not show higher incidence of spontaneous arrhythmias when compared to those with normal QTc interval. Nineteen patients underwent electrophysiological studies. Two patients showed evidence of abnormal sinus node function. Both these patients in addition had AV nodal abnormalities, manifested by prolonged AH interval. Programmed stimulation studies induced AV nodal tachycardia in one and non-sustained ventricular tachycardia in two (polymorphic in one and monomorphic in the other). Ambulatory monitoring in both these patients did not show any evidence of complex VPCs or VT, indicating poor correlation between inducibility and presence of spontaneous complex VPCs. Patients with MVP do not have a higher prevalence of spontaneous atrial or ventricular arrhythmias when compared to matched normal controls with similar symptomatology. The presence of mitral regurgitation, severity of MVP and associated prolonged QTc interval is not associated with higher prevalence of arrhythmias. The correlation between spontaneous and inducible arrhythmias is poor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Arrhythmias and conduction defects in patients with mitral valve prolapse: a study based on ambulatory monitoring and electrophysiologic studies. 145 58

Surgical and catheter based techniques for atrioventricular (AV) nodal modification have recently been described. Similarly, transcoronary embolization for the treatment of arrhythmias has recently emerged as a potentially useful approach. This report reviews our experience of a novel technique using embolization of the AV node with an inert agent, cross-linked collagen, for the treatment of AV nodal reentrant tachycardia. Three patients with refractory nodal tachycardia received 0.1-0.5 mL cross-linked collagen (2 mg/mL) delivered via a catheter placed within the nodal artery. All developed transient complete AV block with subsequent recovery of conduction. Two patients have had no further tachycardia and were noninducible at restudy. One patient required electrical modification because of recurrent symptoms. One patient sustained a limited posterior infarct due to back-spill of collagen into the distal right coronary artery. This novel technique provides an alternative approach to a cure for AV nodal tachycardia without producing long-term heart block.
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PMID:Transcoronary atrioventricular nodal modification using microvascular collagen. 172 Dec 10

Patients with dual AV nodal physiology have been demonstrated to have earliest retrograde activation sequence of the fast pathway in the lower septal right atrium and slow pathway in the proximal coronary sinus, and the posterior atrial septum. This case report describes a patient with dual AV nodal physiology demonstrating a dual sequence of retrograde activation with 2:1 block occurring in the fast pathway causing the conduction to proceed alternately via fast then slow pathway. This sequence was abolished by atropine allowing conduction to proceed via fast pathway. Surgical cure of patients with reentrant AV nodal tachycardia suggests the presence of two anatomically distinct AV nodal-like pathways. This case report confirms this observation and further suggests preferential autonomic modulation of the fast pathway.
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PMID:Alternating sequence of retrograde atrial activation in patients with dual AV nodal physiology. 246 14

Twenty patients with recurrent symptomatic supraventricular tachycardia were studied to estimate the efficacy of flecainide in the long-term treatment of these arrhythmias and to evaluate the prognostic value of programmed electrophysiologic stimulation. All patients had their arrhythmia inducible at baseline evaluation. Nine patients had a Wolff-Parkinson-White (WPW) syndrome, five had a concealed bypass tract, and two had dual atrioventricular (AV) nodal pathways. In the remaining patients there was an intraatrial reentry circuit. Previous medication was no to five antiarrhythmic drugs (mean 2.4 drugs). At baseline, a circus movement tachycardia was induced in 12, AV nodal tachycardia was induced in two, atrial tachycardia was induced in three, atrial fibrillation was induced in five, and a flutter was induced in two patients. After flecainide, 2 mg/kg intravenously in 10 minutes, six patients no longer had their arrhythmia inducible. In the WPW patients, atrial fibrillation was no more inducible. In 65% of the patients there was no recurrence during a follow-up period of 11 +/- 10 months. None of the six patients who no longer had their arrhythmia inducible had a recurrence of the tachycardia over a period of up to 3 years. Seven of the other 14 patients (who still had their arrhythmia inducible) had a recurrence of the tachycardia. Positive and negative predictive values are 50% and 100%, respectively. We conclude that flecainide prevents recurrences of supraventricular tachycardias in 65% of patients with inducible supraventricular tachycardias during a mean follow-up of 11 months. Programmed electrical stimulation has a high negative predictive value in this setting. Flecainide is especially effective in preventing atrial fibrillation in patients with WPW syndrome.
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PMID:Flecainide acetate in the treatment of supraventricular tachycardias: value of programmed electrical stimulation for long-term prognosis. 249 38

The effects of amiodarone and sotalol were studied with programmed electrical stimulation of the heart in 19 patients with inducible tachycardia (AV nodal tachycardia: 10 cases, circus movement tachycardia: 9 cases). Amiodarone was administered intravenously at a dose of 300 mg over 2 min and sotalol at a dose of 1.5 mg kg-1 over 10 min. Both i.v. amiodarone and sotalol lengthened the transnodal conduction time, the effective refractory period of the AV node and the AV nodal Wenckebach cycle length. Only sotalol significantly lengthened the effective refractory periods of the right atrium and the right ventricle. Infused intravenously during tachycardia, amiodarone interrupted arrhythmia in five of six patients and sotalol in seven of ten cases. Tachycardia was stopped by blockade of the impulse into the AV node in three amiodarone patients and in five sotalol patients. In the remaining four cases, the weak link of the circuit was the accessory pathway. Thus i.v. sotalol exhibits electrophysiologic effects consistent with both class II and III activity, whereas the effects of i.v. amiodarone are the result of different activities throughout all areas of the cardiac tissue.
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PMID:Mechanisms of termination of supraventricular tachycardias by intravenous class III antiarrhythmic agents. A comparison of amiodarone and sotalol. 260 17

Flestolol is an ultrashort-acting beta-blocking drug with a half-life of 6.9 minutes. Its antiarrhythmic efficacy was studied in 21 patients with spontaneous and inducible supraventricular tachycardia: atrioventricular (AV) nodal tachycardia in 6 patients and orthodromic AV reciprocating tachycardia in 15. It increased the effective refractory period of the AV node in all patients with AV nodal tachycardia (fast pathway, p less than 0.02; slow pathway, p less than 0.01), but did not alter the anterograde (n = 8) or retrograde (n = 9) refractory periods of accessory pathways. Flestolol prevented initiation of tachycardia by causing block in anterograde AV nodal conduction. It was more effective in patients with AV nodal tachycardia (5 of 6) than in those with AV reciprocating tachycardia (4 of 15, p less than 0.03). In patients in whom it was ineffective, the mean tachycardia cycle length increased by 54 ms because of an increase in AH interval (p less than 0.0001, n = 11). The cycle length of tachycardia induced 30 minutes after infusion was similar to the cycle length in the control state (354 vs 355 ms, n = 16). Flestolol's kinetics permitted clinically indicated electropharmacologic testing of a second antiarrhythmic drug in 8 patients and control of ventricular rate until arrhythmia surgery in 1 patient with incessant tachycardia. No hypotension or toxicity occurred. Our findings indicate that flestolol's principal antiarrhythmic effects are on the AV node, similar to the effects of other beta-blocking drugs. Its ultrashort duration of action is an advantage during electropharmacologic testing.
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PMID:Electropharmacology of flestolol for supraventricular tachycardia without associated structural heart disease. 289 Feb 90

The antiarrhythmic effects of flecainide acetate were evaluated in 9 patients with paroxysmal atrioventricular (AV) nodal tachycardia and 17 patients with AV tachycardia. An electrophysiologic study was performed before and after intravenous flecainide acetate, 2 mg/kg body weight, was infused over 15 minutes and was followed by a maintenance infusion of 1.6 mg/kg given over 1 hour to 26 patients and during oral treatment to 15. Treatment with oral flecainide acetate was continued for 14 +/- 5 months. Intravenous flecainide acetate terminated AV nodal tachycardia by blocking the retrograde fast pathway conduction in 7 of 7 patients and AV tachycardia by blocking retrograde conduction in the extranodal pathway in 10 of 10 patients. AV nodal tachycardia and AV tachycardia were noninducible in 8 of 9 patients (90%, p less than 0.001) and 11 of 17 patients (65%, p less than 0.001), respectively. Long-term treatment with oral flecainide acetate suppressed AV nodal tachycardia and AV tachycardia in 8 of 9 patients (90%, p less than 0.001) and 11 of 17 patients (65%, p less than 0.001), respectively. A favorable outcome was associated with block in the accessory pathway after intravenous flecainide acetate and noninducibility during oral treatment. Recurrences preferentially occurred in the younger patients. Flecainide acetate is effective in the acute and long-term management of paroxysmal supraventricular reentry tachycardia by suppressing conduction through the retrograde fast limb of the tachycardia circuit. The clinical effect can be predicted by electrophysiologic testing.
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PMID:Electrophysiologic and clinical effects of flecainide for recurrent paroxysmal supraventricular tachycardia. 313 98

The cardiac and coronary vasodilator effects of milrinone and amrinone were compared in isolated, blood-perfused papillary muscle and sinoatrial (SA) node and atrioventricular (AV) node preparations of dogs. Milrinone (0.3-100 nmol) and amrinone (0.01-3 mumol) were administered intra-arterially. Both drugs increased the force of contraction of paced and unpaced papillary muscles and the rate of automaticity of the latter; they increased sinus rate and accelerated AV nodal conduction. However, both drugs were not homogeneously effective on cardiac variables but affected them in the following order: The force of contraction of the ventricular muscle greater than SA nodal automaticity divided by AV nodal conduction greater than ventricular automaticity. In producing these cardiac effects, milrinone was 30-60 times more potent than amrinone. Both drugs increased (coronary) blood flow in all preparations. In this respect milrinone was about ten times more potent than amrinone. As a result, milrinone can be characterized as having almost equal cardiotonic and coronary vasodilatory effects, whereas amrinone is more coronary vasodilatory than cardiotonic. These differences in cardiovascular profile may contribute to their differential salutary mechanisms in the treatment of heart failure. Both drugs induced neither AV nodal tachycardia nor ventricular arrhythmia.
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PMID:Comparative study of cardiovascular profiles of milrinone and amrinone by use of isolated, blood-perfused dog heart preparations. 357 Nov 4


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