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PubMed1990

Pharmacological characterization of the adenylate cyclase-coupled adenosine receptor in isolated guinea pig atrial myocytes.

Although adenosine is known to activate K+ conduction in atrial tissue, there is still debate as to the involvement of cAMP-dependent mechanisms. In isolated adult guinea pig atrial myocytes, we demonstrate that the highly A1-selective adenosine receptor agonist 2-chloro-N6-cyclopentyladenosine reduced basal cAMP levels by 30-40% in the absence and presence of the nonxanthine phosphodiesterase inhibitor Ro 20-1724. Isoprenaline caused a concentration-dependent increase in cAMP levels, which was more pronounced in the presence of the phosphodiesterase inhibitor. Several adenosine derivatives suppressed the isoprenaline-induced cAMP increase by approximately 80%. The rank order of potency was 2-chloro-N6-cyclopentyladenosine (IC50, 93 nM) greater than (R)-N6-phenylisopropyladenosine (IC50, 309 nM) greater than 5'-N-ethylcarboxamidoadenosine (IC50, 813 nM) much greater than (S)-N6-phenylisopropyladenosine (IC50, 26,300 nM). A similar but complete suppression of the isoprenaline-induced cAMP increase was produced by the muscarinic receptor agonist carbachol (IC50, 398 nM), which like adenosine is known to activate atrial K+ channels. The A1-adenosine receptor-selective antagonist 8-cyclopentyl-1,3-dipropylxanthine antagonized the effect of 2-chloro-N6-cyclopentyladenosine concentration-dependently, with a KB value of 9.6 nM. In atrial myocytes isolated from guinea pigs pretreated with pertussis toxin, the inhibitory effects of adenosine analogs on basal and isoprenaline-stimulated cAMP accumulation were markedly attenuated. It is concluded that the adenosine receptor in guinea pig atrial myocytes, which is known to be linked to K+ channels, is also coupled to adenylate cyclase via a pertussis toxin-sensitive guanine nucleotide-binding protein and shows the characteristics of the A1-adenosine receptor subtype.

4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone↗
PubMed2006

Novel point mutation in the NKX2-5 gene in a Moroccan family with atrioventricular conduction disturbance and an atrial septal defect in the oval fossa.

Defects of the oval fossa usually occur as isolated malformations, but can show an autosomal dominant pedigree in familial cases. Several mutations have been described for the transcription factor NKX2-5, and co-segregate with varied cardiac anomalies. We have identified by sequence analysis a novel missense heterozygous mutation in the NKX2-5 gene, specifically a substitution of glutamine for proline at codon 160, in a Moroccan family, the affected members having a deficiency of the floor of the oval fossa and atrioventricular block.

Adolescent↗
PubMed1990

Characterization of slow conduction in the common type of atrial flutter--using transient entrainment.

To characterize slow conduction of the common type of atrial flutter (common AF), in which excitation wave propagated in a counterclockwise fashion, transient entrainment during the distal high lateral right atrium (HRAd) pacing and during the proximal coronary sinus (CSp) pacing was studied in 7 patients with common AF. In transient entrainment of common AF, conduction time from stimulus to CSp during HRAd pacing was always longer than that from stimulus to HRAd during CSp pacing. It was also longer than that from stimulus to CSp during HRAd pacing in 5 control patients without common AF in sinus rhythm. Return cycles at HRA and CS after cessation of rapid pacing during transient entrainment were studied. In HRAd pacing, return cycle at the proximal high lateral right atrium was almost equal to the pacing cycle length, or almost equal to or slightly shorter than the flutter cycle length (AFCL). Return cycle at CSp was almost equal to AFCL. In CSp pacing, return cycle at the distal coronary sinus was much longer than AFCL and increased at progressively shorter pacing cycle lengths. In conclusion, slow conduction was demonstrated in the lateral limb (from HRA laterally to CS) of the reentrant circuit in common AF, but it did not exhibit decremental conduction property. Return cycle at an endocardial recording site after transient entrainment in common AF does not always exhibit an uniform pattern, affected by the relative location of and the distance between the recording site, the pacing site, the reentrant circuit and the area of slow conduction.

Aged↗
PubMed1982

A second zone of compensation during atrial premature stimulation: evidence for decremental conduction in the sinoatrial junction.

125 consecutive patients with premature atrial stimulation were studied. Three demonstrated sinus node return cycles that were fully compensatory following premature atrial stimuli delivered early in diastole. This second zone of compensation was unaccompanied by significant alterations in the post-return cycle lengths or in P-wave morphology of the return cycle. To account for the occurrence of a complete compensatory pause following very early premature atrial depolarizations, we consider the possibility that retrograde conduction of the early atrial premature depolarization (APD) in the sinoatrial junction was delayed for a sufficient length of time to allow the sinus node to depolarize spontaneously on schedule. Collision between the APD and sinus beat would then occur despite the marked prematurity of the APD. Thus, the early APD had encountered the relative refractory period of the sinoatrial junction, suggesting that decremental conduction takes place within the sinoatrial region in man. These findings imply that there is the potential for reentry in the region of the human sinoatrial junction.

Aged↗
PubMed1995

Intravenous adenosine during atrioventricular reentrant tachycardia: induction of atrial fibrillation with rapid conduction over an accessory pathway.

Adenosine is considered to be a safe agent for termination of orthodromic atrioventricular reentrant tachycardia in patients with accessory pathways. A case with initially successful accessory pathway ablation and without preexcitation during sinus rhythm is presented, in which intravenous adenosine (6 mg) during orthodromic tachycardia was followed by atrial fibrillation and sudden onset of preexcitation with subsequent rapid ventricular response with moderate hemodynamic compromise.

Adenosine↗
PubMed2004

Deterioration of interatrial conduction in patients with paroxysmal atrial fibrillation: electroanatomic mapping of the right atrium and coronary sinus.

OBJECTIVES: The purpose of this study was to analyze the velocities across the coronary sinus ostium (cross-CSo) and within the coronary sinus (intra-CS) in patients with and without paroxysmal atrial (AF) fibrillation and to estimate the interatrial conduction deterioration area in AF patients. BACKGROUND: Interatrial conduction delay in AF patients has been reported. However, localization of the interatrial conduction delay still is not clear. METHODS: Thirteen patients with paroxysmal AF and 10 control patients with AV nodal reentrant tachycardia or ectopic atrial tachycardia were enrolled in the study. Right atrial and CS mapping were performed using the CARTO electroanatomic mapping system during sinus rhythm and during distal CS pacing. The activation times and spatial distances of cross-CSo and intra-CS were measured between paired sites, from which the activation velocities of cross-CSo and intra-CS were obtained. RESULTS: During sinus rhythm, the activation velocities of cross-CSo in the AF group (1.2 +/- 0.2 m/s) were significantly slower than those in the control group (2.9 +/- 1.6 m/s, P < .05). During distal CS pacing, the cross-CSo velocities of the AF group (1.0 +/- 0.5 m/s) also appeared slower than those in the control group (1.4 +/- 0.2 m/s, P = .07). However, no difference was found in intra-CS activation velocities between the two groups (2.8 +/- 1.9 vs 3.2 +/- 2.2 m/s and 1.5 +/- 0.3 vs 1.4 +/- 0.3 m/s, P > .05 during sinus rhythm and distal CS pacing, respectively). CONCLUSIONS: Interatrial conduction at the posteroparaseptal region across the CS ostium was significantly slower in patients with paroxysmal AF than in control patients, further supporting the link between interatrial conduction deterioration and paroxysmal AF.

Atrial Fibrillation↗
PubMed1991

Effects of atrial impulse timing on AV concealed conduction in the rabbit heart.

The influence of the timing of a nontransmitted or transmitted atrial impulse on the atrioventricular (AV) conduction time of the subsequent impulse was studied in nine isolated rabbit hearts. AV conduction curves were determined by applying the atrial extrastimulus test. The extrastimulus was delivered preceded or not by an interposed atrial impulse whose coupling interval with respect to the last atrial beat of a basic train was kept constant at 100, 120, 140, 160, 175, 200, 225, 250, and 300 msec. In all experiments, there was a "concealment interval," i.e., the AV effective refractory period was longer than the atrial functional refractory period, and in seven experiments was comprised between 100 and 160 msec. For any given extrastimulus coupling interval in the presence of an interposed nontransmitted atrial impulse, AV conduction time was significantly greater than in its absence; the increase was greater than the longer the nontransmitted atrial impulse coupling interval, i.e., the shorter the subsequent transmitted impulse coupling interval with respect to the previous interposed nontransmitted impulse. The AV conduction curves relating the extrastimulus AV conduction time to its coupling interval with respect to the last atrial impulse of the basic train fitted to a hyperbolic model both in the absence of the interposed atrial impulse and in its presence (mean square residual 31 +/- 23 msec2), and the interposed atrial impulse modified the constants of the functions; the slope of the linear transformations was progressively more negative as the interposed atrial impulse was delayed. Furthermore, the effects of the interposed atrial impulse--transmitted or not--on AV conduction time of the subsequent impulse were qualitatively similar, their magnitude depending on the time elapsed were qualitatively similar, their magnitude depending on the time elapsed between the two.

Animals↗
PubMed1989

[Transvenous high frequency current ablation of atrioventricular conduction in therapy refractory tachycardic atrial fibrillation].

We present a case of radiofrequency ablation of the atrioventricular conduction system by means of intravenous catheter technique in a patient with drug-refractory paroxysmal atrial fibrillation. Total AV block was produced. Since the ablation and implantation of a pacemaker this female has had no recurrences. The advantages of this method compared with electrical fulguration are better control of delivered energy and reduction of complications (catheter perforation, thromboembolism). The disadvantage of radiofrequency ablation is the difficulty in positioning the catheter so as to give the most precise contact with the tissue, which is a very time-consuming procedure.

Aged↗
PubMed2003

[Wolff-Parkinson-White syndrome in the child. A case report with associated atrial fibrillation].

UNLABELLED: In children, Wolff-Parkinson-White (WPW) syndrome is often revealed by reentrant tachycardia episodes. Rarely, this syndrome can be the cause of syncope or of sudden death, resulting from rapid conduction of atrial fibrillation to the ventricles through the accessory pathway. CASE REPORT: The authors report the case of a child, who had a WPW syndrome diagnosed after birth because of a supraventricular tachycardia and who was later asymptomatic. At ten years of age, he was admitted because of palpitations due to atrial fibrillation and rapid conduction through the accessory pathway. CONCLUSION: In a child with WPW syndrome, tachycardia with wide and irregular QRS complexes should evoke the involvement of atrial fibrillation, with rapid conduction to the ventricle. Drugs blocking conduction through the atrio-ventricular node are contra-indicated and the condition is an indication for radiofrequency ablation.

Atrial Fibrillation↗
PubMed1978

Determinants of antegrade echo zone in the Wolff-Parkinson-White syndrome.

Forty-five patients with the Wolff-Parkinson-White syndrome and reciprocating tachycardia which utilized the atrioventricular (A-V) node for antegrade conduction and an accessory pathway for ventriculo-atrial (retrograde) conduction were studied. The extrastimulus technique in the right atrium and coronary sinus at multiple pacing cycle lengths was used. Three types of "echo zones" were defined by the relationship of the antegrade effective refractory period (ERP) of the accessory pathway, the longest coupling interval accompanied by an atrial echo, the ERP of the A-V node, and the functional refractory period of the atrium. Eighteen of 45 patients (40%) had more than one type of echo zone demonstrated by changing either pacing site or pacing cycle length or both. Pacing site and intraventricular conduction delay were found to have important effects on the longest coupling interval accompanied by an atrial echo in those echo zones in which the longest coupling interval accompanied by an atrial echo was less than the antegrade ERP of the accessory pathway. The echo zone is a useful concept to explain the physiology of the common reciprocating tachycardia in patients with the Wolff-Parkinson-White syndrome. However, the echo zone is profoundly affected by pacing site and pacing cycle length. When these variables are changed, many patients can be shown to have more than one type of echo zone. Studies of the echo zone have limited value as therapeutic guides.

Cardiac Pacing, Artificial↗
PubMed1992

Flecainide in quinidine-resistant atrial fibrillation.

Flecainide (100 mg twice daily) was used for prevention of paroxysmal atrial fibrillation (PAF) in 52 patients with frequent symptomatic attacks that were resistant or intolerant to quinidine (600-900 mg/day). Underlying heart disease was present in only 8 cases and left ventricular ejection fraction was always greater than 30%. No patient had had a myocardial infarction. Vagally induced PAF was clinically documented in 35 patients. Amiodarone, previously used and ineffective, was combined with flecainide in 33 patients. After 1-5.8 years of follow-up, complete disappearance of PAF was observed in 38 patients (73%). The success rate was slightly higher in patients with vagally induced PAF (p = 0.07). Extracardiac side effects necessitated withdrawal in only 3 cases. Permanent pacemaker was needed in 7 patients on amiodarone and flecainide because of excessive sinus bradycardia. Two patients, with previously documented atrial flutter, experienced presyncopal episodes of atrial flutter with 1:1 atrioventricular (AV) conduction and wide QRS complex. No death occurred during the follow-up. In this series, quinidine proved to be unsuccessful in 46 patients and it was withdrawn in 6. We concluded that flecainide is efficient and well tolerated for long-term prevention of PAF in patients resistant to quinidine. The possibility of 1:1 AV conduction during atrial flutter may suggest the use of verapamil or beta blockers in combination with flecainide in patients with previously documented atrial flutter.

Amiodarone↗
PubMed2003

A novel approach to the management of symptomatic junctional and ectopic atrial rhythms.

Chronic recurrent junctional and ectopic atrial rhythms are a challenge to manage as they are not responsive to pharmacologic therapy and will usually inhibit standard pacemakers. This report presents two patients with junctional and low atrial rhythms who were successfully managed with a recently introduced atrial overdrive suppression algorithm intended for the treatment of paroxysmal atrial fibrillation. In contrast with the standard AAI mode, the AF suppression algorithm paces progressively faster in response to sensed atrial events (or junctional rhythms with retrograde conduction). Maintaining atrial pacing produces a more normal A-V interval with relieve of symptoms.

Adult↗
PubMed1988

[Electrophysiologic effects of intravenous flecainide in intranodal junctional tachycardia in 30 patients].

The electrophysiological effects of flecainide acetate were studied in 30 patients (10 men, 20 women, mean age 48.3 +/- 18 years) suffering from sustained re-entrant intranodal tachycardia. A 2 mg/kg dose of flecainide administered over 10 minutes was given after the onset of sustained tachycardia within 3.8 +/- 2.3 min in 25 of the 30 patients; this was effected by a block in the retrograde leg of the circuit in 22 patients and by a block in the anterograde leg in 3 patients. In the remaining 5 patients the tachycardia was slowed down (367 +/- 27 ms vs 431 +/- 48 ms) chiefly by prolongation of the atrioventricular anterograde conduction. No significant side-effect was observed while the drug was being injected. Following treatment with flecainide, tachycardia was no longer inducible in 24 out of 30 patients (A) and it remained inducible in 6 patients (B, non-responders). The initial electrophysiological exploration revealed differences between these two groups in retrograde conduction: prolongation of the ventriculoatrial time during incremental ventricular stimulation (A: 41 +/- 32 ms vs B: 81 +/- 142 ms, p less than 0.05) and prolongation of the atrioventricular time above 100 ms (A: 2/24 patients, B: 3/6 patients, p less than 0.01). The following electrophysiological parameters were significantly (p less than 0.01) ,modified after intravenous flecainide: AH and HV conduction intervals, atrial refractory periods, anterograde and retrograde atrioventricular conduction. Complete retrograde block was observed in 12 patients of group A. Thus, in this study flecainide arrested a reciprocal intranodal rhythm in 25 out of 30 patients and prevented the reinduction of tachycardia in 24 of these.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Pharmacologic suppression of atrial flutter induced by atrial stimulation.

To examine the electrophysiologic properties of human atrial flutter and its response to various classes of antiarrhythmic drugs, 39 patients were identified as having inducible sustained atrial flutter with atrial extra-stimulation techniques. Measurement of intra-atrial, interatrial, atrioventricular node and His-Purkinje-conduction intervals, atrial refractory periods, and atrial flutter-cycle length were made before and after intravenous administration of verapamil, ouabain, or cedilanid, propranolol, and procainamide in these 39 patients, as well as in seven control patients. Verapamil significantly shortened flutter-cycle length but suppressed atrial-flutter induction in only one of seven patients. Two of nine patients who received propranolol proved resistant to flutter provocation; the seven patients who remained nonsuppressible exhibited greater prolongation of interatrial-conduction time. Ouabain and cedilanid suppressed flutter inducibility in four of seven patients, and flutter-cycle length increased in those patients remaining inducible. Procainamide suppressed flutter induction in nine of 11 patients. These results suggest that procainamide is the most effective agent of those agents tested in suppressing atrial flutter induced by atrial extra-stimulation. Verapamil and propranolol proved quite ineffective in suppressing inducible atrial flutter.

Adult↗
PubMed1977

[Automatism of the sino-atrial node and sinoatrial conduction of excitation in hypoxia].

The effect of experimental hypoxia on the automatic activity of the sinus node and sinoauricular transmission of excitation was studied in 17 isolated preparations of rabbit hearts. A greater frequency of the shifts of sinoauricular delay was noted under hypoxia. Local electrophoretic applications of adrenalin demonstrated that the shifts of the delay occur because of the shifts of pacemakers. The mean frequency of the automatic activity recorded in the atria falls to zero between 6 and 20 min of hypoxia. Hypoxia causes the development of sinoauricular blocks and atrial arrhythmias in the form of individual extrasystoles, high-frequency discharges, or alternations of series of impulses with "mute" periods. The increased tendency towards arrhythmias in the sinoauricular zone is, according to the authors, due to the growing heterogeneity of the duration of action potentials that increases more than three-fold by the 10th minute of hypoxia. The possible reflection of the excitation wave ("echo") from the sinus node zone with an inhibited excitability was demonstrated.

Action Potentials↗
PubMed1992

Effects of flecainide on the rate dependence of atrial refractoriness, atrial repolarization and atrioventricular node conduction in anesthetized dogs.

UNLABELLED: Flecainide is effective against certain supraventricular arrhythmias (atrial fibrillation and atrioventricular [AV] node reentrant tachycardia), but its mechanisms of action are unknown. Previous in vitro work suggests that flecainide attenuates rate-dependent action potential duration shortening, producing tachycardia-dependent prolongation of the refractory period. This study was designed to assess whether similar changes occur in vivo and whether the effects of flecainide on AV node conduction depend on heart rate and on direction of propagation (anterograde vs. retrograde). The effects of flecainide at three clinically relevant concentrations were assessed in open chest, morphine-chloralose-anesthetized dogs. Flecainide increased atrial refractory period in a concentration- and rate-related fashion (e.g., dose 3 increased the atrial effective refractory period by 9 +/- 4% at a cycle length of 1,000 ms but by 36 +/- 5% and 55 +/- 10% at a basic cycle length of 400 and 300 ms, respectively; p less than 0.001 for each). Flecainide attenuated the action potential duration accommodation (measured by monophasic action potentials) to heart rate, causing tachycardia-dependent action potential duration prolongation and accounting for most of the rate-dependent atrial effective refractory period changes. Flecainide increased Wenckebach cycle length, but the concentration-response curve was much steeper in the retrograde (slope 41 +/- 7 ms/mumol.liter-1) than in the anterograde direction (17 +/- 4 ms/mumol.liter-1; p less than 0.01), indicating more potent effects on retrograde conduction. The depressant action of the drug on the AV node was also rate dependent, with an effect on the AH interval at a basic cycle length of 400 ms that averaged 1.8, 1.5 and 2 times that at a basic cycle length of 1,000 ms for doses 1 (p less than 0.05), 2 (p less than 0.01) and 3 (p less than 0.001), respectively. CONCLUSIONS: 1) Flecainide suppresses atrial action potential duration accommodation to heart rate changes in vivo, leading to rate-dependent atrial effective refractory period prolongation, which may be important in suppressing atrial fibrillation. 2) The drug has frequency- and direction-dependent effects on AV node conduction, which may lead to selective antiarrhythmic actions during AV node reentry.

Action Potentials↗