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PubMed2003

Antiarrhythmic effects of JTV-519, a novel cardioprotective drug, on atrial fibrillation/flutter in a canine sterile pericarditis model.

UNLABELLED: Effect of JTV-519 on AF. INTRODUCTION: A new cardioprotective drug, JTV-519, blocks Na+ current and inwardly rectifying K+ current and inhibits Ca2+ current. However, its role in atrial electrophysiology is unknown. We investigated the antiarrhythmic effects of JTV-519 on atrial fibrillation/flutter in the canine sterile pericarditis model. METHODS AND RESULTS: In nine dogs with sterile pericarditis, 38 episodes of sustained (>30 sec) atrial fibrillation (8 dogs) and 24 episodes of sustained atrial flutter (7 dogs) were induced by rapid atrial pacing. When atrial fibrillation or atrial flutter was sustained >15 minutes, it was cardioverted and reinduced. The inducibility of atrial fibrillation/flutter, the atrial effective refractory period, and the intra-atrial conduction time were compared before and after the continuous infusion of JTV-519 (0.03 mg/kg/min). JTV-519 significantly decreased the mean number of sustained atrial fibrillation episodes (from 4.2 +/- 2.9 to 0 +/- 0, P < 0.01). In contrast, atrial flutter was still inducible in 4 dogs after JTV-519 (from 2.7 +/- 2.5 to 1.6 +/- 2.1, P = NS). JTV-519 significantly prolonged effective refractory period (from 123 +/- 18 to 143 +/- 14 msec, from 127 +/- 18 to 151 +/- 12 msec, and from 132 +/- 13 to 159 +/- 9 msec at basic cycle lengths of 200, 300, and 400 msec, respectively, P < 0.01), but it did not affect the intra-atrial conduction time (from 47 +/- 11 msec to 48 +/- 11 msec, P = NS). CONCLUSION: JTV-519 had significant protective effects on atrial fibrillation in the canine sterile pericarditis model, mainly by increasing effective refractory period, suggesting that it may have potential as a novel antiarrhythmic agent for atrial fibrillation.

Animals↗
PubMed1989

The effect of atrial dilatation on the genesis of atrial arrhythmias.

The effect of atrial stretching on the genesis of atrial arrhythmias was studied in 26 dogs. Left atrial dilatation was produced by inflation of a balloon catheter. Electrophysiological studies were performed by programmed electrical stimulation of the atrium and ventricle. The irritability of the atrium markedly increased when it was distended and atrial arrhythmias (sustained or non-sustained atrial tachyarrhythmias) could regularly be induced by administration of an early extrastimulus or--more rarely--by atrial burst pacing. In 10 cases spontaneous atrial tachycardia appeared during atrial balloon dilatation. The atrial effective refractory period shortened and the atrial conduction time lengthened on atrial stretching, while other electrical variables (cycle length, sinus node recovery time, atrioventricular conduction time, intraventricular conduction, ventricular refractory period, QT interval) remained unchanged. Atrial balloon dilatation was not accompanied by marked haemodynamic changes, and the left ventricular pressure curve, the contractility of the left ventricle and the central venous pressure did not change significantly on atrial stretching. The experimental data suggest that the atrial dilatation plays an important part in the pathogenesis of atrial arrhythmias.

Animals↗
PubMed1987

Methodological aspects of the use of heart rate stratified RR interval histograms in the analysis of atrioventricular conduction during atrial fibrillation.

A new computer assisted method for analysing RR interval histograms was devised in 32 patients with sustained atrial fibrillation. Twenty four hour ECG recordings were divided consecutively into periods with 64 heart beats and mean heart rates calculated for each period. Using increments of 10 beats.min-1 serial heart rate stratified histograms with 5120 RR intervals were constructed according to the calculated heart rate. In all histograms the RR intervals were sorted into 20 ms wide subgroups between 180 and 2100 ms. The analysis showed a bimodal RR distribution in 26 patients. Several indices were chosen to characterise a given RR interval peak in the histogram analysis. The rate dependence of peak was calculated for each individual peak. In the presence of two or more peaks a peak dominance change value was defined. Furthermore, differences and ratios between peak values at peak dominance change value (peak gap and peak value ratio) were calculated. A contour index was used to describe the smoothness of the appearance of the histogram. Comparisons were made between the histograms with periods composed of different numbers of heart beats (8, 16, 32, 64) for the mean heart rate calculation and between the histograms constructed with different numbers of RR intervals (512, 1024, 2560, 5120, 10,240, pooled data) in six patients. A significant finding was that greater than 5000 RR intervals should be used for the construction of a heart rate stratified histogram. Comparison was also made between the repeated histograms with a mean time interval of 137 days (7-413 days) in eight patients. The findings showed a high reproducibility of the heart rate stratified histogram.

Atrial Fibrillation↗
PubMed1994

[Mechanisms of atrial fibrillation: recent advances].

Atrial fibrillation (AF) is due to the presence of multiple reentry pathways. Although this mechanism has been known for some time, new information has recently been acquired about the factors of atrial vulnerability and the conditions of myocardial alteration. There are two main factors of atrial vulnerability: intra-atrial conduction defects and abnormalities of the refractory periods. In addition, the concept of critical mass and the influence of the autonomic nervous system have to be taken into consideration. The abnormalities of the refractory periods liable to increase atrial vulnerability are their shortening, spatial dispersion and poor adaptation to the heart rate. All these changes may be demonstrated at cellular level. The product of the intra-atrial conduction velocity and the duration of the refractory period defines the wave length. The risk of developing reentry pathways increases as the wave length shortens. Moreover, the more the atrium fibrillates, the greater will be the decrease of the refractory periods, atrial fibrillation giving rise to atrial fibrillation. Histological lesions of the atrial tissue may be demonstrated, even in the absence of underlying cardiac disease. They mainly consist of fibrosis, fatty degeneration and myocytic hypertrophy. In the long-term, atrial fibrillation leads to a number of structural abnormalities of the atrial, and sometimes ventricular tissues, progressing to cardiomyopathy in some cases.

Action Potentials↗
PubMed2003

Atrial ischemia promotes atrial fibrillation in dogs.

BACKGROUND: Coronary artery disease is a significant risk factor for atrial fibrillation (AF), but the basis for this association is incompletely understood. The present study evaluated the hypothesis that atrial ischemia can create a substrate for AF maintenance. METHODS AND RESULTS: Atrial ischemia was induced by occlusion of an atrial arterial branch that did not provide blood flow to the ventricles. Atrial-arterial occlusion increased the duration of AF induced by burst pacing from 57+/-32 seconds (control) to 803+/-214 seconds (P<0.001) after 0.5 hour of occlusion and to 887+/-209 seconds (P<0.001) after 3 hours of occlusion. Prolonged AF (>20 minutes) was induced in 0 of 16 dogs (0%) under control conditions, 7 of 16 (44%, P<0.01) at 0.5 to 3 hours, and 5 of 13 (38%, P<0.01) 3 to 5 hours after occlusion. Atrial conduction was slowed substantially within the ischemic zone: eg, conduction delay was 8+/-1 ms at a cycle length of 200 ms, control, versus 22+/-5 ms (P<0.01) after 0.5 hours and 27+/-5 ms (P<0.001) after 3 hours of ischemia. Refractoriness was initially unaffected but was prolonged 5 hours after occlusion. Phase-delay analysis and high-density mapping confirmed severe conduction slowing in the ischemic zone. Histological examination confirmed the location of ischemic regions and revealed extensive ischemia-induced necrosis at sites of conduction delay. CONCLUSIONS: Experimental atrial ischemia creates a substrate for AF maintenance, apparently by causing local conduction slowing that promotes reentry. These results suggest that atrial ischemia may significantly promote AF, and may be relevant to AF mechanisms in association with coronary artery disease.

Animals↗
PubMed1988

Electrophysiological effects of the antiarrhythmic agent GYKI-23107 in dogs.

Cardiac electrophysiological properties of GYKI-23107, a new membrane stabilizing antiarrhythmic agent were studied in anaesthetized open-chest dogs. Epi- end endocardial electrograms (for sinus potential and for His bundle recording) were obtained during sinus rhythm and following atrial and ventricular pacing. The registration were performed under control conditions as well as five minutes after drug administration of 8 mg/kg slow i.v. or 20 minutes after 20 mg/kg intraduodenal administration respectively. GYKI-23107 did not influence significantly either the sinus cycles, PA-intervals, sinus node potentials, or the classical electrophysiological parameters of sinoatrial function as the corrected recovery time of the sinus node, sino-atrial conduction time or the secondary post-stimulation sinus cycles before and after vegetative blockade. Neither the AH intervals, anterograde Wenckebach period, nor ventriculo-atrial conduction time changed significantly. QRS duration, configuration and HV-intervals remained also unchanged after drug administration in doses which used in this study, and which seemed to be in therapeutic range. The agent did not influence significantly the effective refractory periods of the atrium and ventricle during sinus rhythm. This study suggest that the GYKI-23107 is not depressive on the anterograde (AV), retrograde (VA), intraventricular conduction and is slightly depressive on the intrinsic pacemaker properties.

Animals↗
PubMed1988

[Usefulness of transesophageal stimulation in the evaluation of sinus node function in patients with sick sinus syndrome].

The purpose of this study was to find out whether transesophageal pacing could be utilized for assessment of sinus node function, besides Wenckebach point, in patients with sick sinus syndrome. In 17 patients with sino-atrial disease (group I) we compared the results of sinus node tests obtained both in the basal state and after pharmacological autonomic blockade by endocavitary stimulation and 24 hours later, by transesophageal pacing. In another group of 17 patients with sino-atrial disease (control group) we compared the results obtained from two endocavitary studies. In group I, sinus cycle length and corrected sinus recovery time did not show significant differences between the two studies either the basal state or after autonomic blockade, whereas sino-atrial conduction time was more prolonged during esophageal pacing (P less than 0.01). In the control group, sinus node measures did not show significant differences between the two studies. In group I, the following coefficients of correlation were obtained: A) in the basal state sinus cycle length, r = 0.65, corrected sinus recovery time, r = 0.57, sinoatrial conduction time, r = 0.52; B) after autonomic blockade sinus cycle length, r = 0.95, corrected sinus recovery time, r = 0.62 and sino-atrial conduction time, r = 0.53. In the basal state, the correlation for sinus cycle length and corrected sinus recovery time between the two studies was lower in the "study group" than in the "control group" (P less than 0.05). However, after autonomic blockade the correlation for sinus node measures did not show any significant differences between the two groups of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2000

Interatrial conduction of atrial tachycardia in heart transplant recipients: potential pathophysiology.

Surgical suture lines formed at the site of anastamosis have been considered to be electrically inert and thus present a line of block to conduction. However, a number of reports have suggested that conduction is occasionally possible across suture lines. Most of these cases have reported conduction between donor and recipient atria following cardiac transplantation. We report an illustrative case successfully treated with radiofrequency ablation, and present pathology findings that may give insight into the pathophysiology.

Adult↗
PubMed2004

Intra- and interatrial conduction delay: implications for cardiac pacing.

Atrial conduction disorders are frequent in elderly subjects and/or those with structural heart diseases, mainly mitral valve disease, hyperthrophic cardiomyopathies, and hypertension. The resultant electrophysiological and electromechanical abnormalities are associated with a higher risk of paroxysmal or persistent atrial tachyarrhythmias, either atrial fibrillation, typical or atypical flutter or other forms of atrial tachycardias. Such an association is not fortuitous because intra- and interatrial conduction abnormalities delays disrupt (spatial and temporal dispersion) electrical activation, thus promoting the initiation and perpetuation of reentrant circuits. Preventive therapeutic interventions induce variable, sometimes paradoxical effects as with the proarrhythmic effect of class I antiarrhythmic drugs. Similarly, atrial pacing may promote proarrhythmias or an antiarrhythmic effect according to the pacing site(s) and mode. Multisite atrial pacing was conceived to correct, as much as possible, abnormal activation induced by spontaneous intra- or interatrial conduction disorders or by single site atrial pacing, which are situations responsible for commonly refractory arrhythmias. Atrial electrical resynchronization can also be used to correct mechanical abnormalities like left heart AV dyssynchrony resulting from intraatrial conduction delays.

Atrial Fibrillation↗
PubMed1999

Atrioventricular nodal conduction during atrial fibrillation: role of atrial input modification.

BACKGROUND: Posteroseptal ablation of the atrioventricular node (AVN) has been proposed as a means to slow the ventricular rate during atrial fibrillation (AF). The suggested mechanism is elimination of the AVN "slow pathway." On the basis of the unpredictable success of the procedure, we hypothesize that, in fact, the slow pathway is preserved. Therefore, the slowing of the ventricular rate results from reduced bombardment of the AVN. METHODS AND RESULTS: In 8 rabbit heart atrial-AVN preparations, cooling of the posterior and/or the anterior AVN approaches revealed nonspecific effects on the slow and fast pathway portions of the AVN conduction curve. In 13 other preparations, simulated AF during posterior cooling (n=6) prolonged the His-His (H-H) intervals but did not reveal specific slow pathway injury. In the remaining 7 preparations, AF was applied before and after posteroseptal surgical cuts. During AF with posterior origin, the cuts resulted in longer mean H-H along with slowing of the AVN bombardment rate. However, there was no change in the minimum observed H-H, suggesting an intact slow pathway. During AF with anterior origin, the mean and the shortest H-H remained unchanged before and after the cuts in all preparations. This was associated with the maintenance of high-rate AVN bombardment. CONCLUSIONS: Posteroseptal ablation does not eliminate the slow pathway. Ventricular rate slowing can be obtained if the ablation procedure results in a posteroanterior intra-atrial block leading to a reduction of the rate of AV nodal bombardment.

Animals↗
PubMed1997

Atrial fibrillation in patients with permanent VVI pacemakers: risk factors for atrial fibrillation.

OBJECTIVES: Atrial fibrillation (AF) does not only deteriorate the cardiac function and increases the thromboembolic risk but also triggers rapid and irregular ventricular rhythm in patients with atrial synchronous pacing. However, the risk factors for the development of AF in patients with pacemakers are not clearly determined yet. The present study was designed to determine the risk factors for AF in patients with VVI pacemakers. METHODS: This study included 80 patients (41 sick sinus syndrome, 39 AV block) who were followed for more than 6 months or developed AF regardless of the duration of follow-up after implantation of VVI pacemakers. Patients were divided into two groups according to whether or not AF developed during follow-up (mean: 25.7 +/- 2.5 months): group A developed AF and group B did not. The underlying arrhythmias, cardiovascular risk factors, left atrial size, characteristics of P wave were compared between the two groups. RESULTS: The mean age of the patients was 58.9 +/- 11.4 years and 28 (35%) were male. AF developed in 13 (16.3%) of 80 patients with VVI pacemakers. Sick sinus syndrome (SSS) as an underlying arrhythmia was significantly more frequent in group A than group B (84.6% vs. 44.8%, p < 0.01). P wave width was greater in group A (127.6 +/- 24.8 ms) than in group B (110.7 +/- 17 ms) (p < 0.05). There was, however, no significant difference in cardiovascular risk factors, left atrial size, P wave axis and amplitude between the two groups. CONCLUSION: These results suggest that sinus node dysfunction and intra-atrial conduction delay may be the risk factors for AF in patients with VVI pacemakers. Further studies are needed to determine how sick sinus syndrome and intra-atrial conduction delay increase the risk for AF in patients with VVI pacemakers.

Adult↗
PubMed1993

Areas of slow conduction in atrial re-entrant tachycardia: a case report and review of the literature.

An electrophysiologic study of atrial tachycardia is presented. During tachycardia, transient entrainment and sinus rhythm, two patterns of persistent double potentials in the high right atrium and fragmented activity in the low atrial septum were observed. No activity was recorded from multiple areas of the right atrium with endocardial mapping during sinus rhythm. The observations suggest that persistent fragmented activity represents slow conduction within the circuit which could be orthodromically entrained. Persistent double potentials probably represent slow conduction orthodromically and/or antidromically activated outside the circuit. However, a wave front from pacing impulses travelling through this area could entrain the circuit.

Aged↗
PubMed1982

Atrioventricular nodal conduction during atrial fibrillation in rabbit heart.

Atrial fibrillation was induced in 15 superfused rabbit atrial-atrioventricular nodal preparations in which surface bipolar electrograms were recorded simultaneously from the crista terminalis, interatrial septum, and His bundle along with microelectrode action potentials from cells in the atrionodal (AN), nodal (N), and nodal-His (NH) regions of the atrioventricular node. Effective engagement of the atrioventricular node with propagation to the His bundle was critically dependent on the relative timing of activation at the crista terminalis and interatrial septal input regions of the atrioventricular node. Conduction through the AN and N regions appeared dependent on the relative timing of activation wave fronts emerging from the two input regions. Asynchronous engagement of AN and N regions resulted in both distortion of action potentials and concealed conduction, with delayed conduction and block to the NH region and His bundle. Successful engagement of the NH region always produced a 1:1 NH-to-His bundle relationship. It is concluded that during atrial fibrillation 1) activation of the AN region occurs as a result of the variable interaction of inputs from the crista terminalis and interatrial septum; 2) predictably, effective synchronous engagement of the AN and consequently the N region is responsible for conduction to the NH and His bundle regions; 3) conversely, asynchronous activation inputs from the crista terminalis and interatrial septum result in fragmented, asynchronous as well as concealed conduction within the AN and N regions with block in the atrioventricular node and variable conduction to the His bundle.

Action Potentials↗
PubMed2004

Effect of Bachmann's bundle pacing on atrial fibrillation: electrophysiologic assessment.

BACKGROUND: It has recently been reported that simultaneous multisite atrial pacing, Bachmann's bundle (BB) pacing, and coronary sinus (CS) pacing are useful for preventing the induction of atrial fibrillation (AF). HYPOTHESIS: We investigated whether a simple pacing approach via BB could reduce the induction of AF by extrastimuli (S2) from the right atrial appendage (RAA). METHODS: Programmed electrical stimulation was performed from the RAA and the area of BB at the superior aspect of the atrial septum, and bipolar recordings were obtained from the RAA, BB, and CS in 14 patients. RESULTS: In five patients, AF was induced with critically timed RAA-S2 delivered during RAA pacing. However, AF was not induced in any patient when RAA-S2 was delivered during BB pacing. The duration of the P wave during BB pacing was significantly shorter than that during RAA pacing and sinus rhythm (BB 80 +/- 16 ms vs. RAA 106 +/- 36 ms vs. sinus rhythm 100 +/- 24 ms, p < 0.05). The intra-atrial conduction time to the distal coronary sinus (CSd) caused by early S2 at the RAA was significantly reduced by BB pacing (BB 114 +/- 22 ms vs. RAA 157 +/- 35 ms, p < 0.001). CONCLUSION: Bachmann's bundle pacing reduces atrial conduction time caused by RAA-S2 and may be useful for preventing the induction of AF.

Adult↗
PubMed2001

Effects of verapamil on atrial fibrillation and its electrophysiological determinants in dogs.

BACKGROUND: Atrial tachycardia-induced remodeling promotes the occurrence and maintenance of atrial fibrillation (AF) and decreases L-type Ca(2+) current. There is also a clinical suggestion that acute L-type Ca(2) channel blockade can promote AF, consistent with an AF promoting effect of Ca(2+) channel inhibition. METHODS: To evaluate the potential mechanisms of AF promotion by Ca(2+) channel blockers, we administered verapamil to morphine-chloralose anesthetized dogs. Diltiazem was used as a comparison drug and autonomic blockade with atropine and nadolol was applied in some experiments. Epicardial mapping with 240 epicardial electrodes was used to evaluate activation during AF. RESULTS: Verapamil caused AF promotion in six dogs, increasing mean duration of AF induced by burst pacing, from 8+/-4 s (mean+/-S.E.) to 95+/-39 s (P<0.01 vs. control) at a loading dose of 0.1 mg/kg and 228+/-101 s (P<0.0005 vs. control) at a dose of 0.2 mg/kg. Underlying electrophysiological mechanisms were studied in detail in five additional dogs under control conditions and in the presence of the higher dose of verapamil. In these experiments, verapamil shortened mean effective refractory period (ERP) from 122+/-5 to 114+/-4 ms (P<0.02) at a cycle length of 300 ms, decreased ERP heterogeneity (from 15+/-1 to 10+/-1%, P<0.05), heterogeneously accelerated atrial conduction and decreased the cycle length of AF (94+/-4 to 84+/-3 ms, P<0.005). Diltiazem did not affect ERP, AF cycle length or AF duration, but produced conduction acceleration similar to that caused by verapamil (n=5). In the presence of autonomic blockade, verapamil failed to promote AF and increased, rather than decreasing, refractoriness. Neither verapamil nor diltiazem affected atrial conduction in the presence of autonomic blockade. Epicardial mapping suggested that verapamil promoted AF by increasing the number of simultaneous wavefronts reflected by separate zones of reactivation in each cycle. CONCLUSIONS: Verapamil promotes AF in normal dogs by promoting multiple circuit reentry, an effect dependent on intact autonomic tone and not shared by diltiazem.

Animals↗
PubMed2003

Electroanatomic mapping of right atrial activation in patients with and without paroxysmal atrial fibrillation.

Inter-atrial conduction delay in patients with atrial fibrillation (AF) has been reported. However, the area of this conduction delay has not been well identified. The activation time and conduction velocity over the right atrial endocardium were evaluated during sinus rhythm using the CARTO mapping technique in 6 patients with paroxysmal AF (AF group) and 11 patients without history of AF (control group). No significant differences were observed between the 2 groups in the mean activation times and conduction velocities from the earliest activation site to the superior septum, His bundle area and coronary sinus ostium, or in the total activation times of the right atrium. There was no significant difference between the two groups in the local conduction velocity between 2 adjacent sites in the free wall, septum and bottom of the right atrium. This study suggests the previously reported conduction delay in the posteroseptal region in patients with paroxysmal AF might locate within the posterior inter-atrial septum.

Atrial Fibrillation↗