Increase In Atrial Fibrillation Cycle Length Research Articles

Influence of detomidine on atrial fibrillation cycle length measured by intracardiac electrogram recording and by colour tissue Doppler imaging in horses

Shortening of atrial fibrillation cycle length (AFCL) is a marker of atrial electrical remodelling due to atrial fibrillation (AF). To investigate the effect of administration of detomidine on AFCL measured invasively from an intra-atrial electrogram (AFCLEGM) and noninvasively by tissue Doppler imaging (AFCLTDI). We hypothesised that detomidine would have no effect on AFCL but would improve the ease of TDI measurements and facilitate noninvasive AFCL determination. Prospective clinical study. Measurements were performed before and after i.v. administration of 7.5 μg/kg bwt detomidine in 33 episodes of AF in 32 horses (582 ± 64 kg bwt, 10 ± 3 years old) referred for electrical cardioversion. The AFCLEGM was measured from a right atrial intracardiac electrogram. The AFCLTDI was measured from atrial colour tissue velocity curves in 5 atrial wall regions. Mean AFCLEGM and AFCLTDI without and with sedation were compared using a repeated-measures linear mixed model with Bonferroni correction for multiple comparisons and calculation of the Bland-Altman mean bias and limits of agreement between AFCLEGM and AFCLTDI. The mean AFCL was significantly increased after sedation, but this increase was very small (mean difference +4 ms). For AFCLTDI measurements, sedation significantly improved the quality of the atrial myocardial velocity curves and the number of AF cycles that could be measured per cardiac cycle. The Bland-Altman bias between AFCLEGM without sedation and AFCLTDI with sedation ranged from -18 to +15 ms depending on wall region. Bland-Altman limits of agreement were similar between AFCLEGM without sedation and AFCLTDI without and with sedation. Therefore, noninvasive AFCLTDI measurements with sedation can be used to estimate the atrial fibrillatory rate. Sedation facilitates noninvasive AFCL measurements but causes a slight increase in AFCL. Noninvasive AFCL measurements can be used as an indicator of atrial electrical remodelling, to study AF pathophysiology and to investigate the effect of anti-arrhythmic drugs.

Catheter Ablation for Persistent Atrial Fibrillation

A new era of atrial fibrillation (AF) treatment began in 1997–1998 with the discovery that triggers within the pulmonary veins initiate AF and reports that elimination of these triggers is successful in treating AF in its paroxysmal form.1–3 However, in patients with persistent AF, the success rate of exclusive pulmonary vein isolation is substantially lower.4,5 To improve the outcome of persistent AF ablation, different ablation strategies have been explored, but to date the optimal strategy has not been defined. Although some groups argue that limited ablation, including pulmonary vein isolation and, if present, ablation of nonpulmonary vein triggers, is sufficient for persistent AF ablation, other groups, including ours, favor more extensive, substrate-based ablation in addition to pulmonary vein isolation. In this review, we will discuss the rationale for a substrate-based ablation strategy to treat persistent AF and show why elimination of triggers is not sufficient in most patients with persistent AF. Response by Roten et al on p 1232 In a simple model, an electric impulse in AF can form because of abnormalities in impulse generation (triggers) or can result from abnormal impulse propagation (reentry). By a strict definition, a trigger is a focal source of new impulse generation. The mechanism by which a new impulse can form is either abnormal automaticity or triggered activity. Trigger-ablation protocols target these sources of new impulse generation. Abnormal impulse propagation, on the other hand, depends on altered substrate properties causing nonuniform or slowed conduction. This in turn causes multiple forms of wave reentry thought to be responsible for AF perpetuation: random reentry (multiple wavelets), macro- and microreentry, or functional reentry (rotors). Substrate-based ablation strategies aim to abate abnormal impulse propagation and interrupt any form of atrial reentry. Triggers of paroxysmal AF are mainly located in the pulmonary …

Characterization of Electrograms Associated With Termination of Chronic Atrial Fibrillation by Catheter Ablation

This study sought to determine the characteristics of atrial electrograms predictive of slowing or termination of atrial fibrillation (AF) during ablation of chronic AF. There is growing recognition of a role for electrogram-based ablation. Forty consecutive patients (34 male, 59 +/- 10 years) undergoing ablation for chronic AF persisting for a median of 12 months (range 1 to 84 months) were included. After pulmonary vein isolation and roof line ablation, electrogram-based ablation was performed in the left atrium and coronary sinus. Targeted electrograms were acquired in a 4-s window and characterized by: 1) percentage of continuous electrical activity; 2) bipolar voltage; 3) dominant frequency; 4) fractionation index; 5) mean absolute value of derivatives of electrograms; 6) local cycle length; and 7) presence of a temporal gradient of activation. Electrogram characteristics at favorable ablation regions, defined as those associated with slowing (a >or=6-ms increase in AF cycle length) or termination of AF were compared with those at unfavorable regions. The AF was terminated by electrogram-based ablation in 29 patients (73%) after targeting a total of 171 regions. Ablation at 37 (22%) of these regions was followed by AF slowing, and at 29 (17%) by AF termination. The percentage of continuous electrical activity and the presence of a temporal gradient of activation were independent predictors of favorable ablation regions (p = 0.016 and p = 0.038, respectively). Other electrogram characteristics at favorable ablation regions were not significantly different from those at unfavorable ablation regions. Catheter ablation at sites displaying a greater percentage of continuous activity or a temporal activation gradient is associated with slowing or termination of chronic AF.

Cardioversion of persistent atrial fibrillation by a combination of atrial specific and non-specific class III drugs in the goat

In electrically remodeled atria the effect of blockers of the delayed rectifier K+ current I(Kr) on repolarization is reduced, whereas the efficacy of 'early' class III drugs (I(Kur)/I(to)/I(Kach) blockers) is enhanced. We evaluated the electrophysiological and antifibrillatory effects of AVE0118, dofetilide, and ibutilide (alone and in combination) on persistent atrial fibrillation (AF) in the goat. The effects of separate and combined administration of AVE0118, dofetilide, and ibutilide were determined before and after 48 h of AF. AVE0118 alone markedly prolonged the atrial refractory period (400 ms cycle length) (AERP400) before and after 48 h of AF. The prolongation of AERP(400) by dofetilide and ibutilide, respectively, was reduced by AF from 22+/-2 to 7+/-2 ms (p<0.01) and 25+/-5 to 5+/-2 ms (p=0.01). Pre-treatment with AVE0118 restored the prolongation of AERP400 by dofetilide or ibutilide (to 20+/-3 and 30+/-6 ms; p<0.01). This effect was atrial specific since the QT-interval was not changed. The antifibrillatory action was evaluated in 10 goats that were in persistent AF for 57+/-7 days. Dofetilide (20 microg/kg/h) or ibutilide (4 mg/h) alone restored sinus rhythm in only 20% of the animals. AVE0118 (1, 3 and 10 mg/kg/h) [DOSAGE ERROR CORRECTED] terminated AF in 11, 30, and 60%, respectively. Additional infusion of I(Kr) blockers caused an additional number of cardioversions, resulting in a final cardioversion rate of 56, 80, and 100%, respectively. AVE0118 alone prolonged the AF cycle length (AFCL) while the conduction velocity during AF (CV(AF)) remained unchanged (70+/-1 vs. 68+/-2 cm/s; p=0.3). Addition of dofetilide or ibutilide caused a synergistic increase in AFCL and a slight increase in CV(AF) to 74+/-1 cm/s (p<0.001). The length of the reentrant trajectories increased from 7.6+/-0.3 (control) to 11.6+/-0.5 cm after AVE0118 alone (p<0.001) and 14.8+/-0.8 cm after addition of dofetilide or ibutilide (p<0.001). In electrically remodeled atria, blockade of I(Kur)/I(to)/I(KAch) restored the class III action of I(Kr) blockers. Persistent AF could be effectively cardioverted by infusion of a combination of AVE0118 and dofetilide or ibutilide. This antifibrillatory action was associated with an almost twofold lengthening of the intra-atrial pathways for reentry.

Electroanatomic Remodeling of the Left Atrium in Patients Undergoing Repeat Pulmonary Vein Ablation: Mechanistic Insights and Implications for Ablation

There is limited information describing late changes in the electroanatomic characteristics of the left atrium (LA) associated with recurrence after an anatomical circumferential pulmonary vein ablation (CPVA) for atrial fibrillation (AF). Forty-seven patients (57 +/- 8 years) undergoing a repeat ablation after CPVA were included. Using an electroanatomic mapping system, we measured the bipolar voltage by averaging points in the pulmonary vein (PV)-LA junction and four other LA sites. Conduction velocity and AF cycle length (AFCL) were also measured and the results are compared with the first procedure. After an initial decrease observed at the end of the first procedure, voltage and conduction velocity returned to intermediate values in all LA sites, with lower voltage at the LIPV antrum (P = 0.004), and lower conduction velocity across the LIPV and RSPV (P < 0.001). Conduction gaps were more prevalent at the septal aspect of the right PV encircling lines (85%), between the left atrial appendage (LAA) and the LSPV (70%) and lines at the posterior wall (71%). There was a nonsignificant increase in AFCL, with a more widespread distribution of organized electrograms (32.4% vs 46.6%). Recurrence after CPVA is associated with a reverse process of voltage and conduction velocity increase across ablated areas, especially the PV-LA junction, and is related to the presence of conduction gaps, which are distributed mostly at the septal aspect of the lines encircling the right PVs and at the LAA-LSPV area. Organization of atrial electrograms seen during AF ablation is maintained at a repeat procedure.

Altered electroanatomic patterns of right ventricle in myotonic dystrophy type 1 patients

Background: Prolongation of the atrial fibrillation cycle length (AFCL) and termination of AF during ablation have been reported. We investigate the significance of regions of maximal dominant frequency (DF) identified by spectral analysis, determining the effect of ablation at these sites located within the pulmonary veins (PV) on the fibrillatory process. Methods: Thirty-two patients undergoing AF ablation during ongoing arrhythmia were studied. Electroanatomic mapping was performed, acquiring 126 13 points/pt throughout both atria and coronary sinus (CS). At each point, 5s electrograms were obtained to determine the highest amplitude frequency on spectral analysis and construct 3D DF maps. Ablation was performed with the operator blinded to the DF maps. The effect of ablation at PVs with or without high-frequency DF sites (maximal frequencies surrounded by a decreasing frequency gradient 20%) was evaluated by determining the change in AFCL within the CS before and after isolation of each PV, and the termination of AF. Results: PV ablation was associated with an increase in AFCL (174 27 to 184 35ms; p 0.0001). While ablation at a PV harboring a DF site resulted in AFCL prolongation (180 30 to 198 40ms; p 0.0001), ablation at a PV without a DF site did not change the AFCL (169 22 to 170 22ms; p 0.4). Ablation at PVs harboring a DF site resulted in an increase in AFCL ( 5ms) within the CS in 89% with the mean increase in AFCL of 18 21ms (range 0-118ms) compared to 0.9 3.9ms (range -10 to 7ms; p 0.0001) after ablation at PVs without a DF site. The increase in AFCL with PV ablation demonstrated a strong concordance with ablation at a DF site (kappa-coefficient of 0.77). PV ablation resulted in AF termination in 14 pts; 11 at a DF site. In the remaining 3, 2 had frequent cessation of arrhythmia during mapping. Conclusion: High frequency PV activity identified by spectral analysis has an important role in maintaining AF. Ablation at these sites resulted in slowing of the fibrillatory process and termination of paroxysmal AF.

Reversal of atrial electrical remodeling after cardioversion of persistent atrial fibrillation in humans.

Although atrial electrical remodeling has been studied extensively in animal models, the reversibility of this phenomenon after termination of clinical atrial fibrillation (AF) has not been demonstrated. We aimed to examine this important question of reversibility by using AF cycle length (AFCL) and coupling intervals of atrial premature beats after cardioversion as measures of atrial refractoriness. We measured AFCL at the right atrial appendage and distal coronary sinus before attempting internal cardioversion in 39 patients with persistent AF. Patients were monitored by daily transtelephonic recordings after discharge and admitted rapidly for repeat internal cardioversion if there was spontaneous AF recurrence. Measurements of AFCL were repeated immediately before repeat cardioversions in the 17 patients who had recurrence of AF. There was an increase in AFCL from the initial cardioversion to that measured at the time of first AF recurrence at both the right atrial appendage (161+/-22 vs 167+/-26 ms, P=0.05) and distal coronary sinus (162+/-20 vs 168+/-22 ms, P=0.01) sites. The magnitude of increase in AFCL was positively correlated with duration of sinus rhythm before AF recurrence (r=0.524, P=0.001). Other measures of refractoriness (shortest coupling interval of atrial premature beats and directly measured refractory periods after cardioversion) also increased from initial to subsequent cardioversions. These findings demonstrate that changes in atrial electrophysiology associated with chronic AF in humans are reversible after cardioversion and that the extent of this reversal is dependent on the duration of sinus rhythm after cardioversion.