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

The effectiveness and electrophysiologic mechanisms of antiarrhythmic effect of digoxin were examined in 27 patients with paroxysmal atrioventricular nodal reciprocal tachycardia (PAVNRT) and supraventricular tachycardia (SVT) due to latent complementary conductive pathways, i. e. latent Wolff-Parkinson-White (WPW) syndrome. To assess antiarrhythmic action of digoxin, transesophageal pacing and plasma digoxin radioimmonoassays were used. Preventive antiarrhythmic efficiency of digoxin was 53% in PAVNRT patients, and 25% in SVT patients with latent WPW syndrome. Antegrade atrioventricular conduction block seems to be the mechanism of oral digoxin preventive effect. There was no relationship between antiarrhythmic efficiency of digoxin and its plasma level.
 ...
PMID:[Use of digoxin in patients with paroxysmal supraventricular tachycardia]. 266 9

In clinical arrhythmias, the main therapeutic role of calcium channel entry blockers is related to their effect on the sinus and atrioventricular (AV) node. Consequently, in cardiac arrhythmias where the AV node is part of the reentry circuit, a beneficial effect of diltiazem and verapamil can be demonstrated. These include AV nodal reentry and orthodromic tachycardia in patients with Wolff-Parkinson-White syndrome. In addition, the ventricular response by the AV node during atrial tachycardias can also be controlled with these agents. A specific type of ventricular tachycardia seen in the absence of structural heart disease has also been reported to respond to intravenous and oral verapamil. Calcium channel blockers have no proven depressant effect on accessory pathway conduction. Similarly, the value of these agents in the treatment of ventricular tachycardia in association with chronic coronary artery disease and idiopathic dilated cardiomyopathy is rather limited. The use of calcium entry blockers in patients with wide QRS tachycardia, therefore, is to be discouraged unless it can be proved that supraventricular tachycardia with aberrant conduction is the underlying basis.
 ...
PMID:Use of calcium channel entry blockers in the treatment of cardiac arrhythmias. 268 83

The term "enhanced atrioventricular nodal conduction" (EAVN) is used to indicate an electrophysiologic condition characterized by subnormal conduction delay with reduced decremental properties in the AV node, which can be responsible for rapid ventricular rates in the event of fast atrial rhythms. Although identification of such an entity usually requires definition of the AV conduction intervals, some authors have suggested that EAVN can be diagnosed, by means of atrial pacing only, when 1:1 conduction with narrow QRS complexes occurs during atrial pacing at rate higher than 200 bpm. The use of incremental transesophageal atrial pacing (TAP) as a noninvasive tool for identification of EAVN was investigated in 19 patients. Fifteen had a history of supraventricular tachyarrhythmias (11 Wolff-Parkinson-White syndrome; 2 Lown-Ganong-Levine syndrome; 1 intranodal AV reentry tachycardia; 1 sick sinus syndrome); 4 patients exhibited an electrocardiographic pattern of preexcitation without a history of tachyarrhythmias. Analysis of AV conduction at fast induced rates was hampered in 5 patients because of the easy occurrence of reciprocating tachycardia and/or atrial fibrillation during TAP, as well as because of the persistence of delta wave at cycle lengths (CL) shorter than 300 ms. Among the remaining patients, in 7 (50%, Group A), 1:1 AV conduction was present at pacing CL shorter than 300 ms. In 7 patients (50%, Group B), AV block occurred at pacing CL longer than 300 ms.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Transesophageal pacing in the diagnosis of accelerated atrioventricular conduction]. 272 Jul 18

Twenty-nine patients with paroxysmal supraventricular tachycardias of different origins and clinical pattern were investigated to detect latent thyroid disorders; hyperthyroidism was diagnosed in 2 of those, and hypothyroidism, in 4. Functional thyroid disorders were more common in patients with mitral prolapse and supraventricular tachycardias due to additional conductive pathways (the Wolff-Parkinson-White syndrome) and paroxysmal nodal reciprocal tachycardia, particularly if they were resistant to antiarrhythmic treatment and/or had aggravated thyroid history. It is suggested that thyroid dysfunction is just a triggering factor of arrhythmia since thyrostatic and replacement therapy eliminate paroxysms of tachycardia, while organic pathology of the heart and its conductive network remains unaffected.
 ...
PMID:[Study of thyroid function in patients with paroxysmal supraventricular tachycardia]. 273 16

The efficacy of amiodarone was evaluated in 85 patients with supraventricular tachycardia (SVT) refractory to several antiarrhythmic agents (mean 3.8 +/- 1.0). All but six patients had organic heart disease. Patients were followed for 19 months (range 2-60 months). Response to amiodarone treatment was considered excellent (no recurrence of SVT) in 22 of 52 patients with paroxysmal atrial fibrillation (PAF), in four of 13 patients with chronic atrial fibrillation (CAF), and in three of 15 patients with Wolff-Parkinson-White syndrome-related circus movement tachycardia (WPW-CMT). Response was improved (marked improvement in symptoms with partial suppression of SVT) in 22 patients with PAF, in seven patients with CAF, in 10 patients with WPW-CMT, and in four patients with atrioventricular nodal reentry tachycardia. Response was considered poor (insignificant or no suppression of SVT) in three patients with PAF, in one patient with CAF, and in one patient with WPW-CMT. Seven patients required discontinuation of amiodarone due to adverse effects. We conclude that amiodarone is efficacious and relatively safe for control of SVT refractory to conventional antiarrhythmic agents irrespective of the underlying electrophysiologic mechanism.
 ...
PMID:The usefulness of amiodarone in management of refractory supraventricular tachyarrhythmias. 274 45

The electrophysiology of antidromic reentry, a less common phenomenon than orthodromic reentry, remains a poorly understood aspect of the Wolff-Parkinson-White (WPW) syndrome. We used a pacing model of ventricular preexcitation in patients without WPW, so that electrophysiological events in the normal pathway during atrial extrastimulation (A1-A2 technique) could be precisely delineated without the obscuring effect of an actual accessory pathway. Ventricular preexcitation was simulated by an A1-V1 sequential basic drive with A2-V2 extrastimulation at progressively shorter A1-A2 (equal to V1-V2) coupling intervals. At each coupling interval tested within the zone of atrioventricular (A-V) nodal effective refractory period (since anterograde block of A2 was considered mandatory for manifestation of antidromic reentry), responses were assessed after A2 alone (method I), V2 alone (method II), and A2 plus V2 (method III, the complete preexcitation model). The entire pacing protocol was performed at two A-V intervals, short (50 msec) and long (150-180 msec), thereby simulating different proximities between the A pacing site and "accessory pathway" location. Of 47 consecutive unmedicated patients screened for the study protocol, 38 failed to meet minimal prerequisites for possible initiation of antidromic reentry because of failure in 18 (38% of total) to achieve anterograde A-V nodal block of A2, even though 1:1 ventriculoatrial conduction to cycle lengths less than or equal to 500 msec (less than or equal to 400 msec in 12) was present; and poor or absent ventriculoatrial conduction in the others. The nine remaining candidates underwent the full pacing protocol. Antidromic reentry (retrograde atrial response following V2 in method III) was observed in only two cases (4% of total), and both were associated with retrograde His-Purkinje system delays (documented by method II) occurring in tandem with a long A-V interval, thereby allowing for completion of retrograde A-V nodal recovery after penetration by A2. Indeed, such a prolonged recovery time prevented initiation of antidromic reentry in six of the nine patients (proven by intact ventriculoatrial conduction in method II). Retrograde A-V nodal block of V2, independent of A2, prevented an antidromic echo in one case. Findings in our model help to clarify the various factors, including specific anterograde and retrograde A-V nodal properties; anatomic relation between the accessory and normal pathways; and the retrograde His-Purkinje system delays, that must prevail in a concerted fashion to permit the initiation of antidromic reentry during the A1-A2 technique in patients with the WPW syndrome.
 ...
PMID:Electrophysiological determinants of antidromic reentry induced during atrial extrastimulation. Insights from a pacing model of Wolff-Parkinson-White syndrome. 275 41

The slow inward current contributes to the normal electrical and contractile activity of several cardiac and vascular tissues and also may mediate the electrical abnormalities responsible for certain cardiac arrhythmias. The slow inward current differs from the fast inward sodium current in that it is carried primarily by calcium rather than sodium, requires a more positive level of membrane potential to be activated, has slower activation and inactivation kinetics, is responsible for normal depolarization in sinus and atrioventricular (AV) nodal cells and is blocked by a rather specific group of agents that includes verapamil, diltiazem and nifedipine. Recent data suggest that slow-channel openings occur in bursts, separated by silent periods, and that less negative membrane potentials and beta-adrenergic stimulation increase the probability that the channels will open. Inactivation of the channels is associated with a lower probability of channel opening. Slow-channel blocking agents such as verapamil, diltiazem and nifedipine appear to bind to activated, rather than rested, slow channels. Therefore, their effects are more prominent at faster pacing rates and at less negative membrane potentials. Clinically occurring cardiac arrhythmias dependent on the slow inward current include primarily sinus and AV nodal reentry and reciprocating tachycardia in the Wolff-Parkinson-White syndrome when one of the pathways incorporates the AV node. Damaged atrial, ventricular and specialized tissue also can generate slow response-mediated reentry or forms of automaticity that may be clinically important under certain circumstances.
 ...
PMID:Slow inward current and cardiac arrhythmias. 285 19

Two types of arrhythmias are associated with the Wolff-Parkinson-White syndrome: those in which the accessory pathway is a required part of the reentrant circuit, e.g., orthodromic atrioventricular reciprocating tachycardia, and those that conduct over the accessory pathway but do not require its activation for maintenance of tachycardia, e.g., atrial flutter/fibrillation. Increased sympathetic tone shortens the refractoriness of atrial and ventricular tissue; however, conduction in the atrium and ventricle is not considered the limiting factor for maintenance of atrioventricular reciprocating tachycardia or conduction over the accessory pathway in atrial arrhythmias. Intravenous beta-adrenergic blockers given to patients in the resting state have a minimal to moderate effect in depressing atrioventricular nodal conduction, but have little or no effect on accessory pathway refractoriness or conduction in most patients. In patients presenting with atrioventricular reentry, intravenous administration of beta-adrenergic blocking drugs often is not effective to terminate tachycardia. However, long-term oral therapy with these agents may be beneficial, especially in patients in whom enhanced sympathetic tone is responsible for the initiation or maintenance of tachycardia.
 ...
PMID:Beta-blocker therapy for the Wolff-Parkinson-White syndrome. 288

Paroxysmal supraventricular tachycardia most often results from atrioventricular (AV) reentry using an accessory AV pathway (Wolff-Parkinson-White syndrome) or reentry within the region of the AV node. In AV reentry, using an accessory pathway, suppression of the tachycardia may be achieved by depressing either anterograde AV nodal conduction or retrograde accessory pathway conduction. Intracardiac recordings and programmed electrical stimulation have established that beta-adrenergic antagonists and calcium channel blockers principally affect AV nodal conduction (anterograde limb of the reentrant circuit), whereas class IA and IC agents principally affect the accessory AV pathway (retrograde limb). Pharmacologic therapy has been more effective when directed at the limb in which conduction is most marginal at the tachycardia rate (weak limb). In individual patients, intracardiac recordings and programmed electrical stimulation can be used to identify the weak limb, indicating the class of agents most likely to be effective. Specialized techniques allowing direct recording of accessory pathway activation suggest that limitations in accessory pathway conduction may be explained by anatomic impediments. Conduction is most limited at the atrial interface of the accessory pathway in some patients, whereas in others the ventricular interface may be the limiting factor. Class IA and IC agents appear to have the greatest effect at sites where conduction is most tenuous, i.e., at the anatomic impediments. Similar considerations apply to AV nodal reentry. Anterograde slow AV nodal pathway conduction is most often depressed by digitalis preparations, beta-adrenergic antagonists, and calcium channel blockers, whereas retrograde fast AV nodal pathway conduction is more often depressed by class IA and IC agents. Intracardiac recordings and programmed electrical stimulation can also be used in these patients to identify the weak limb and direct pharmacologic therapy. Direct catheter recordings of AV nodal conduction remain elusive, limiting knowledge of the different conduction properties of the anterograde and retrograde limbs and the site(s) of drug action. Studies in progress, comparing the retrograde AV nodal conduction time during tachycardia with that during ventricular pacing at the same rate, suggest that the His bundle may be incorporated in the reentrant circuit in some patients. It appears that verapamil more readily depresses retrograde fast pathway conduction in these patients than in those in whom the His bundle does not form part of the reentrant circuit, but the reasons for this are unknown.
 ...
PMID:Use of intracardiac recordings to determine the site of drug action in paroxysmal supraventricular tachycardia. 305 92

Encainide has been used to treat 230 patients with supraventricular arrhythmias, including patients with reentry supraventricular tachycardia of the atrioventricular reentry (Wolff-Parkinson-White syndrome) and the atrioventricular nodal reentry types associated with atrial fibrillation, paroxysmal supraventricular tachycardia or both, as well as incessant supraventricular tachycardia. The available data are summarized in this review. The short- and long-term response to encainide for preventing recurrence or lessening symptoms was excellent in most cases. There was little arrhythmia aggravation, and side effects, which were mostly central nervous system and visual in nature, did not cause discontinuation of the drug. Anterograde accessory pathway block was clearly an important effect. Whether retrograde block or refractoriness in the accessory pathway is the most important mechanism remains to be resolved. Pediatric patients with tachycardia-related cardiomyopathy responded well to encainide. Oral encainide's absence of effect on blood pressure or myocardial contractility is an added benefit.
 ...
PMID:Treatment of supraventricular arrhythmias with encainide. 309 21


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>