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At least 775 records · Page 43Linked to original sources
PubMed2000

[Administration of adenosine for termination of atrioventricular nodal reentry tachycardia: induction of atrial fibrillation with rapid conduction over an accessory pathway and unmasking of concomitant Wolff-Parkinson-White syndrome].

The antiarrhythmic properties of adenosine, its ultra-short half-life and the absence of frequent serious side effects make it a front-line agent in arrhythmia management, especially in the treatment of atrioventricular nodal reentrant tachycardia. Due to a shortening of atrial refractoriness, adenosine can facilitate the induction of atrial fibrillation. Life threatening tachycardias may result from a potential rapid conduction of atrial fibrillation over an accessory pathway especially if the latter one has a short antegrade refractory period. We report a case of a 59 year old female patient in which intravenous administration of adenosine during typical atrioventricular nodal reentrant tachycardia was followed by atrial fibrillation with rapid conduction over a hitherto unknown accessory pathway. After intravenous administration of adenosine the tachycardia was terminated successfully within 38 s. After a short period of asystole, spontaneous atrial fibrillation developed unmasking an antegrade preexcitation with subsequent rapid ventricular response (210 b/min). The three-lead ECG showed a narrow QRS complex tachycardia. Because of spontaneous conversion to sinus rhythm and the absence of hemodynamic compromise there was no need for external cardioversion. During electrophysiological study an antidromic atrioventricular reentrant tachycardia was recorded over a left posteroseptal accessory pathway including antegrade conduction properties only. Because of its ultrashort half-life, serious side effects after adenosine administration are rare. The possibility of life threatening proarrhythmias after intravenous adenosine administration should be taken into consideration if the etiology of a paroxysmal supraventricular tachycardia is not clear and a concomitant Wolff-Parkinson-White syndrome cannot be excluded. As with application of all intravenous antiarrhythmic agents, the administration of adenosine should only be performed if continuous ECG monitoring and cardioversion facilities are available and possible.

Adenosine↗
PubMed2000

Using intracardiac catheter recordings from the His and proximal coronary sinus to distinguish isthmus conduction block during catheter ablation of type I atrial flutter.

Isthmus conduction block, demonstrated with the use of multipolar catheter recordings, is considered the preferred endpoint for ablation of type I atrial flutter. This study investigated the feasibility of using recordings from the His and coronary sinus (CS) to document isthmus conduction block. Isthmus conduction block was produced with linear radiofrequency (RF) ablation in 27 patients with type I atrial flutter. In 13 patients (group I), RF was delivered until bidirectional isthmus conduction block was demonstrated with multipolar Halo catheter recordings. In 14 patients (group II), RF was delivered during pacing from the lateral isthmus at 600 ms until a reversal in activation of the proximal CS and His occurred. At this point, data from the Halo recordings were reviewed to see if reversal correlated with conduction block; if not, further ablation was performed until block was demonstrated. The initial reversal in His and CS activation during RF energy delivery correlated with isthmus block in only 4 (28.6%) of 14 patients in group II. Additional RF delivery produced isthmus block in the other ten patients resulting in a further increase in the St-CS interval of 35 +/- 20 ms. A His-CS interval of at least -40 ms signified isthmus block with a sensitivity and specificity of 48% and 100%, respectively. Reversal in His-CS activation during pacing from the lateral margin of the isthmus is not specific for the creation of isthmus block. While activation of the proximal CS bipole > 40 ms after activation of the His appears specific for isthmus block, the low sensitivity of this finding limits its clinical use.

Atrial Flutter↗
PubMed2004

Synergistic action of atrial dilation and sodium channel blockade on conduction in rabbit atria.

INTRODUCTION: The aim of this study was to investigate the interaction of atrial dilation and blockade of the rapid sodium channel on atrial conduction and degree of anisotropy. METHODS AND RESULTS: The right atrium was acutely dilated by increasing intra-atrial pressure from 2 to 9 cm H2O in 14 isolated rabbit hearts. A rectangular mapping array of 240 electrodes (spatial resolution 0.5 mm) was positioned on the free wall of the right atrium during pacing from four different directions at intervals of 240 and 140 msec. In nondilated atria, 0.5 and 1.0 mg/L of the use-dependent INa blocker flecainide prolonged the total conduction time under the mapping electrode by 15% to 75%. In dilated atria, flecainide depressed conduction by 24% to 89% (P < 0.05). The incidence of intra-atrial conduction block increased from 0.6%-0.8% to 3.3%-7.2% in nondilated atria and from 3.9%-4.6% to 13%-21% in dilated atria (P < 0.05). The direction of activation relative to the crista terminalis and major pectinate muscles was of major importance for occurrence of conduction block. During rapid pacing, the degree of anisotropy in conduction increased by the combination of atrial dilation and flecainide (1.0 mg/L) from 1.7 +/- 0.1 to 2.2 +/- 0.4 (P < 0.05). The effects of dilation and flecainide on conduction were clearly synergistic. The effect of flecainide on the atrial refractory period also was enhanced by atrial dilation. CONCLUSION: In dilated atria, blockade of the rapid sodium channels caused a higher degree of local conduction delay and intra-atrial conduction block than in nondilated atria.

Analysis of Variance↗
PubMed2003

In vivo canine cardiac electrophysiologic profile of 1,4-benzodiazepine IKs blockers.

Previous cardiac electrophysiologic studies of blockers of the slowly activating delayed rectifier (IKs) current have focused primarily on ventricular repolarization. This report summarizes an extensive in vivo cardiac electrophysiologic profile of four 1,4-benzodiazepine IKs blocker analogues (L-761334, L-763540, L-761710, and L-768673) in dogs. At 3.0 mg/kg intravenously, all four analogues elicited 14.5%-21.4% increases in ventricular refractoriness and 19.2%-22.6% increases in QTc interval. Concomitant 11.1%-13.5% increases in atrial refractoriness were noted with all four analogues. Decreases in sinus heart rate of 8.4%-17.3% were noted with all four compounds. No effects on atrial, His Purkinje, ventricular conduction or atrial and ventricular excitation were observed. One analogue, L-761710, significantly delayed atrioventricular (AV) nodal conduction (40.7+/-17.4% increase in atrial-to-His interval) and increased the AV conduction system functional refractory period 19.9+/-6.2%. The lack of effect of the other three 1,4-benzodiazepine IKs blockers on AV nodal function at dosages producing comparable effects on atrial and ventricular refractoriness suggest that the AV nodal effects of L-761710 were unrelated to IKs blockade. These findings indicate IKs plays important roles in both atrial and ventricular refractoriness as well as pacemaker function in the dog heart, suggesting potential utility for IKs blockers in the treatment of atrial and ventricular arrhythmias.

Action Potentials↗
PubMed1983

Indirectly estimated sinoatrial conduction time by the atrial premature stimulus technique: patterns of error and the degree of associated inaccuracy as assessed by direct sinus node electrography.

The atrial premature stimulus method for estimating sinoatrial conduction time (SACT) is commonly used. When the stimulated atrial premature depolarization (APD) does not appear to affect sinus node automaticity or conduction, the indirectly estimated SACT (SACT1) is quite accurate. That is, SACT1 correlates quite highly with SACT measured directly (SACTD) on sinus node electrograms (SNE). In this study we used direct SNE recordings in 17 patients to assess SACT1 when factors thought to produce inaccuracy in SACT1 were present. Three patients had sinoatrial entrance block, which might make some expect sinoatrial exit delay to be present. However, SACTD was normal in two (60 and 70 msec) and prolonged (130 msec) only in the one who had other evidence of sinus node dysfunction. Therefore, sinoatrial entrance block does not necessarily indicate sinoatrial exit delay. Thirteen patients had apparent depression of sinus node automaticity by the induced APD (A3A4 greater than A1A1). In all 13, SACT1 overestimated SACTD. One patient had apparent sinoatrial conduction delay induced by the APD and/or vagal transmitter release induced by the APD. In this patient, too, SACT1 exceeded SACTD. Thus when sinoatrial automaticity or conduction are depressed by the stimulated APD, SACT1 will overestimate SACTD. If SACT1 is normal, SACTD will be normal; however, if SACT1 is prolonged, SACTD may or may not be prolonged.

Aged↗
PubMed2000

Radiofrequency ablation of focal atrial tachycardia and atrioatrial conduction from recipient to donor after orthotopic heart transplantation.

After cardiac transplantation, atrial arrhythmias may develop in the residual recipient atrium and conduct to the donor heart. Radiofrequency (RF) ablation of the atrioatrial conduction may be effective in arrhythmia control, although the recipient atrium continues its tachycardia. We hypothesize that in patients with posttransplant atrial tachycardia, it is possible to ablate both the arrhythmogenic focus in the recipient atrium and the atrioatrial conduction. A 47-year-old patient who had orthotopic heart transplantation 9 months earlier underwent RF ablation procedure because of medically uncontrolled atrial arrhythmia. By conventional electrophysiologic mapping, we localized the focus of the atrial tachycardia in the recipient atrium and the electrical atrioatrial connection across the anastomotic suture line. Selective applications of RF energy eliminated both targets successfully. RF ablation of recipient atrial tachycardia and atrioatrial conduction from recipient to donor may lead to long-term success of arrhythmia control.

Catheter Ablation↗
PubMed2000

Electrophysiological determinants of atrial fibrillation in sinus node dysfunction despite atrial pacing.

AIMS: The effectiveness of atrial pacing in reducing the incidence of atrial fibrillation in patients with sinus node dysfunction is incomplete, and the correlation between electrophysiological atrial properties and the effect of permanent atrial pacing has been poorly investigated. Accordingly, the aim of the present study was to correlate electrophysiological data, in terms of atrial refractoriness, conduction parameters, and propensity to atrial fibrillation induction, and the likelihood of atrial fibrillation after DDD device implantation. METHODS AND RESULTS: The authors reviewed electrophysiological data of 41 patients with sinus node dysfunction (mean age 70 +/- 8 years, who were investigated free of anti-arrhythmic treatments before pacemaker implantation. At a drive cycle length of 600 ms, effective and functional refractory periods, S1-A1 and S2-A2 latency, A1 and A2 width, and latent vulnerability index (effective refractory period [ERP] A2), were measured. Atrial fibrillation induction was tested with up to three extrastimuli in 34 patients. Induction of sustained atrial fibrillation (> 1 min) was considered as the end-point. P-wave duration on the surface ECG in lead II/V1 was also measured. Minimal atrial rate was programmed between 60 and 75 bpm (mean: 64 +/- 4 bpm). After implantation, the patients were followed-up for 28 +/- 17 months, and ECG-documented occurrence of atrial fibrillation was determined. Electrophysiological characteristics of patients with (n = 12) or without (n = 29) paroxysmal atrial fibrillation before implantation were similar. When comparing patients with (n = 11) or without (n = 30) post-pacing atrial fibrillation occurrence, no differences were found in age, underlying heart disease, left atrial size, minimal pacing rate, and follow-up duration. Additionally, between the two former groups, there was no significant difference in terms of effective refractory periods (233 +/- 47 ms vs 239 +/- 25 ms), functional refractory periods (280 +/- 48 ms vs 272 +/- 21 ms), S1-A1 (44 +/- 20 ms vs 37 +/- 13 ms) and S2-A2 latency (77 +/- 28 ms vs 66 +/- 22 ms), and A1 duration (60 +/- 23 ms vs 53 +/- 16 ms). In contrast, in patients with post-pacing atrial fibrillation occurrence, the P wave was more prolonged (116 +/- 22 ms vs 98 +/- 13 ms; P < 0.01), A2 was longer (116 +/- 41 ms vs 87 +/- 27 ms; P < 0.01), effective refractory periods/A2 was lower (2.1 +/- 0.4 cm vs 3.1 +/- 1.4 cm; P < 0.05), and rate of atrial fibrillation induction was higher (8/11 patients vs 8/23 patients; P < 0.05). Electrophysiological characteristics of patients free of post-pacing atrial fibrillation with associated (n = 6) or unassociated (n = 24) paroxysmal atrial fibrillation history before implantation were quite similar. In patients with post-pacing atrial fibrillation with associated (n = 6) or unassociated atrial fibrillation history (n = 5) before implantation, effective refractory periods was statistically different (207 +/- 23 ms vs 264 +/- 46 ms; P < 0.05). Values of effective refractory periods < 220 ms were significantly more frequent in patients with post-pacing atrial fibrillation than in patients without (4/11 patients vs 2/30 patients; P < 0.05). When comparing patients with post-pacing atrial fibrillation with effective refractory periods > or = 220 ms (n = 7) and < 220 ms (n = 4), A2 duration was remarkably prolonged (145 +/- 42 ms vs 90 +/- 11 ms; P < 0.05) in those with effective refractory periods > or = 220 ms. By contrast, between the two groups, effective refractory periods/A2 were identical (2.08 +/- 0.6 cm vs 2.15 +/- 0.3 cm; P = n.s.). CONCLUSION: Prolonged atrial refractoriness, lesser degrees of conduction disturbance and a lower rate of atrial fibrillation induction seem to be predictive of stable sinus rhythm. In contrast, patients with persistence of atrial fibrillation despite pacing have a more abnormal and inhomogeneous atrial substrate, as well as a higher rate of atrial fibrillation induction. Prolonged P wave, shortened refractoriness, or remarkably abnormal conduction disturbances in the presence of prolonged refractoriness limit the effectiveness of standard atrial pacing in atrial fibrillation prevention. Identification of predictive criteria of failure of single-site atrial pacing may be used to consider dual-site atrial pacing in such patients with sinus node dysfunction.

Aged↗
PubMed1979

[Current developments on the physiology of the cardiac atrial pacemaker an excitation conduction of the left atrium].

According to recent developments the atrial pacemaker area and the right atrium show a peculiar morpho-functional organization, i.e.: 1) The pacemaker area is formed of clusters of cells containing relatively few myofibrils and showing embryologic characteristics. Such cells are known as nodal cells and between these and the atrial muscles are in general situated transitional cells. Each cluster is separated from the other by collagenous boundaries. The resistance of the membranes to the current flow seems to be relatively low between the cells of the same cluster but the collagenous boundaries are, according to TRAUTWEIN e UCHIZONO (1963), very poor conductors. The pacemaker activity seems to originate inside the various clusters. 2) The functional relationships between the sinoatrial node and the atrioventricular node as well as the interatrial relationship would take place through preferential pathways. These pathways corresponding approximately to the tracts described by JAMES (1966) (anterior, posterior and middle internodal tracts) and to the interatrial or Bachmann bundle, seems to show a higher velocity conduction. In general the fibres of which the tracts are composed are neither morphologically nor functionally isolated from the atrial muscle. The functional consequences of the above mentioned nodal and atrial organization seems to be: a) The possible conditioning of the pacemaker functions by the various clusters activity i.e. the dominance of one cluster over another. b) The shifting of the pacemaker activity from one cluster to anothr due to the arrival of nervous stimuli or chemical substances, etc. According to some Authors as a consequence of the shift the pacemaker area can sometimes move out side the nodal tissue and settle inside an area belonging to the internodal pathways. c) Another consequence of the shift can be the different involvement of the conducting pathways which can lead to a change in the dynamics of the atrial invasion by the excitement.

Acetylcholine↗
PubMed1985

[Analysis of the structure of cardiac rhythm in atrial flutter].

Heart rhythm was studied by computer in 67 patients with atrial flutter of different etiology. It was discovered that respiratory activity has an influence on the conduction of atrial flutter waves to the ventricles. In the majority of cases, the conduction of atrial waves to the ventricles is multiple with a constant conduction ratio. However, in some cases the conduction of atrial flutter waves via the atrioventricular system occurs according to the Samoilov-Wenckebach periodicals. In the latter case and in atrial flutter with a conduction ratio of 4:1, one-third of patients manifest, after the recovery of the sinus rhythm, atrioventricular blockade, grade 1.

Adult↗