Intra-atrial Conduction Research Articles

Synergistic Action of Atrial Dilation and Sodium Channel Blockade on Conduction in Rabbit Atria

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. 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. 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.

Effects of Acute Systemic Endothelin Receptor Blockade on Cardiac Electrophysiology In Vivo

BQ-123, a selective endothelin-A receptor antagonist, has been demonstrated to suppress arrhythmias. However, the role of physiologic levels of endogenous endothelin-1 (ET-1) with respect to electrophysiologic properties of the heart is unknown. BQ-123 (0.45, 0.9, 1.8, 3.6, 7.2, and 14.4 microg/kg/min; n = 10) or saline (control, n = 5) was administered IV for 15 minutes of continuous-rate infusion at incremental doses to anesthetized normal pigs. BQ-123 had no effect on PR and QT interval, QRS duration, intraatrial and AV nodal conduction time as well as the atrial, AV nodal, and ventricular effective refractory periods. As compared with baseline, BQ-123 at 7.2 and 14.4 microg/kg/min caused an increase in heart rate (99 +/- 17 versus 110 +/- 14 and 118 +/- 14 bpm, respectively; P < 0.05), shortened sinus node recovery time (818 +/- 165 versus 641 +/- 69 and 609 +/- 74 milliseconds, respectively; P < 0.05) and decreased mean arterial pressure at 14.4 microg/kg/min (95 +/- 18 versus 80 +/- 11 mm Hg; P < 0.05). We conclude that in the normal pig, physiologic levels of ET-1 have no effect on conduction properties of atrial, AV nodal, or Purkinje fibers. However, antagonism of ET-1 by BQ-123 unmasks the effect of ET-1 on maintenance of vasomotor tone, which in turn may affect heart rate and sinus node automaticity in the intact pig.

Clinical Assessment of Antiarrhythmic Agents for Paroxysmal Atrial Fibrillation Guided by Modification of Electrophysiologic Arrhythmogenicity

Rapid atrial pacing alters atrial electrophysiology, promoting initiation and maintenance of atrial fibrillation (AF). The aim of this study was to assess differences in the electrophysiologic properties of atrial tissue between patients with and without AF episodes and to determine whether electrophysiologic properties can predict the clinical efficacy of antiarrhythmic agents. Sixty patients were studied, 33 with documented episodes of paroxysmal atrial fibrillation (PAF) and 27 control patients. Atrial effective refractory period (AERP), atrial vulnerability, and intra-atrial conduction time were measured at baseline and after rapid constant atrial pacing for 5 minutes at rates of 130, 150, 170, and 190 beats/min. The clinical efficacy of antiarrhythmic agents for PAF prophylaxis was assessed over 14 months with an antiarrhythmic agent identical to that administered intravenously, and the antiarrhythmic agent effects on AERP, atrial vulnerability, and intra-atrial conduction time were assessed. AERP shortening and atrial vulnerability increase were significantly larger in the PAF group. Antiarrhythmic agents that were clinically effective in suppressing PAF significantly attenuated AERP shortening, but antiarrhythmic agents that were clinically ineffective did not. Changes in AERP and atrial vulnerability observed after rapid atrial pacing are considered indicative of the electrophysiologic substrate of PAF. Attenuation of AERP and atrial vulnerability by antiarrhythmic agents might be useful in predicting their clinical efficacy.

Clinical prediction rule for atrial fibrillation after coronary artery bypass grafting

This study was designed to devise and validate a practical prediction rule for atrial fibrillation/atrial flutter (AF) after coronary artery bypass grafting (CABG) using easily available clinical and standard electrocardiographic (ECG) criteria. Reported prediction rules for postoperative AF have suffered from inconsistent results and controversy surrounding the added predictive value of a prolonged P-wave duration. In 1,851 consecutive patients undergoing CABG with cardiopulmonary bypass, preoperative clinical characteristics and standard 12-lead ECG data were examined. Patients were continuously monitored for the occurrence of sustained postoperative AF while hospitalized. Multiple logistic regression was used to determine significant predictors of AF and to develop a prediction rule that was evaluated through jackknifing. Atrial fibrillation occurred in 508 of 1,553 patients (33%). Multivariate analysis showed that greater age (odds ratio [OR] 1.1 per year [95% confidence intervals (CI) 1.0 to 1.1], p < 0.0001), prior history of AF (OR 3.7 [95% CI 2.3 to 6.0], p < 0.0001), P-wave duration >110 ms (OR 1.3 [95% CI 1.1 to 1.7], p = 0.02), and postoperative low cardiac output (OR 3.0 [95% CI 1.7 to 5.2], p = 0.0001) were independently associated with AF risk. Using the prediction rule we defined three risk categories for AF: <60 points, 61 of 446 (14%); 60 to 79 points, 330 of 908 (36%); and >or=80 points, 117 of 199 (59%). The area under the receiver-operator characteristic curve for the model was 0.69. These data show that post-CABG AF can be predicted with moderate accuracy using easily available patient characteristics and may prove useful in prognostic and risk stratification of patients after CABG. The presence of intraatrial conduction delay on ECG contributed least to the prediction model.

Comparative effects of thiopental and propofol on atrial vulnerability: electrophysiological study in a porcine model including acute alcoholic intoxication

Atrial tachyarrhythmias (AT) frequently complicate the perioperative period. Alcohol intoxication is a recognized causative factor for dysrrhythmias. We studied the effects of propofol and thiopental on atrial electrophysiology and vulnerability to AT in a closed-chest porcine model in which AT are facilitated by ethanol. Thirty-eight pigs were randomly assigned to thiopental (T-group, n=19) or propofol (P-group n=19). All animals were assigned to undergo a right atrial electrical stimulation protocol (RASP) at baseline. Thirty pigs were assigned to undergo additional RASP during ethanol infusion, while the remaining eight were assigned to undergo additional RASP during saline infusion (control group). We analysed effective refractory period (ERP), and intra-atrial conduction interval (ICI) (between atrial sites 4 cm apart), at several cycle lengths (CL). There were no significant differences at baseline. During ethanol infusion, propofol produced a greater rate-dependent decrease in excitability, manifested by a longer minimum paced CL with 1:1 atrial capture: 145 (11) vs 164 (27) ms in the T- and P-group, respectively (P=0.01). Propofol was associated with a greater rate-related slowing in conduction: difference between ICI at CL of 300 ms and ICI at minimum CL: 30 ms in P-group and 22 ms in T-group (P<0.03). In the P-group we observed a longer duration of induced arrhythmias (145 (131) vs 74 (91) s, P<0.03) and a higher proportion with atrial flutter (AFl) (76 vs 19%, P<0.001). Propofol in this model was more arrhythmogenic than thiopental, as manifested by a longer duration of induced arrhythmias, particularly AFI.

IEGM based method for estimating optimal AV delay in cardiac resynchronization therapy

Background: Huge intra-atrial conduction delay is common in HF patients due to mitral valve regurgitation and dilated left atrium. Normal AV or PV delay setting can cause patients to suffer from a similar symptom of pacemaker syndrome. Some clinical experience taught us programming AV or PV delay 30 ms to 60 ms after the end of P wave (or paced atrial depolarization) relieved patient’s symptom instantly and in the further follow-up. We formulated a simple relation using IEGM to estimate optimal AV delay based on the clinical observations. This study is to compare an IEGM based method against echo measured optimal AV delays. Methods: Nine patients had NYHA class III, LBBB, EF 35% implanted with SJM EPIC HF ICD. The device IEGM channels recorded the end of atrial depolarization (EAD), intrinsic RV and LV depolarization conducted from atria denoted as ARRV and ARLV. The predicted optimal AV or PV delay is simply the sum of the end of atrial depolarization and an add-on interval (d) which is 60 ms if EAD is less than 100 ms or 30 ms if EAD is greater than 100 ms. AV (or PV delay) needs to be less than both ARRV and ARLV. The echo E and A wave method tested AV delay at 50 ms, 300 ms (intrinsic conduction) and several AV delays with 30 ms resolution. Results: All RA leads were at RA appendage, RV leads at RV apical position and LV leads at mid lateral wall. The EAD was 70.0 ms 16 ms. The echo determined optimal AV delay was 119 ms 29 ms and the IEGM predicted AV delay was 130 ms 16 ms. The difference between these two methods was 22 ms 11 ms which was smaller than the resolution in common clinical testing. Conclusions: The simple IEGM based method for predicting optimal AV delays were reasonably close toecho determined optimalAV delays. Automated AV delay in devices may provide better CRT performance daily and will reduce the usage of echo measurement in CRT and therefore the cost. 208

Heterogeneity of action potential durations in isolated mouse left and right atria recorded using voltage-sensitive dye mapping.

An imaging system for di-4-ANEPPS (4-[beta-[2-(di-n-butylamino)-6-naphthylvinyl]pyridinium]) voltage-sensitive dye recordings has been adapted for recording from an in vitro mouse heart preparation that consists of both atria in isolation. This approach has been used to study inter- and intra-atrial activation and conduction and to monitor action potential durations (APDs) in the left and right atrium. The findings from this study confirm some of our previous findings in isolated mouse atrial myocytes and demonstrate that many electrophysiological properties of mouse atria closely resemble those of larger mammals. Specifically, we made the following observations: 1) Activation in mouse atria originates in the sinoatrial node and spreads into the right atrium and, after a delay, into the left atrium. 2) APD in the left atrium is shorter than in the right atrium. 3) Sites in the posterior walls have longer APDs than sites in the atrial appendages. 4) Superfusion of this preparation with 4-aminopyridine and tetraethylammonium resulted in increases in APD, consistent with their inhibitory effects on the K+ currents known to be expressed in mouse atria. 5) The muscarinic agonist carbachol shortened APD in all areas of the preparation, except the left atrial appendage, in which carbachol had no statistically significant effect on APD. These results validate a new approach for monitoring activation, conduction, and repolarization in mouse atria and demonstrate that the physiological and pharmacological properties of mouse atria are sufficiently similar to those of larger animals to warrant further studies using this preparation.

Novel use of postpacing interval mapping to guide radiofrequency ablation of focal atrial tachycardia with long intra-atrial conduction time

If the intra-atrial conduction time of a focal tachycardia is prolonged and exceeds the tachycardia cycle length, isochronal electroanatomical maps may be confusing by not showing the classical centrifugal pattern of focal activation. In addressing the hypothesis that by mapping post pacing intervals (PPI), the shortest PPI (ideally identical to tachycardia cycle length) would clearly display the site of origin of a focal tachycardia; this technique was used successfully to identify the origin and ablate the atrial tachycardia of a patient with previously corrected Tetralogy of Fallot.

Evaluation of atrial refractoriness immediately after percutaneous mitral balloon commissurotomy in patients with mitral stenosis and sinus rhythm

Background Chronic atrial stretch and rheumatic inflammatory activity leads to atrial dilatation and conduction slowing, and this increases the susceptibility to atrial fibrillation (AF). The aim of this study was to examine the effects of changes in the chronic atrial stretch on atrial refractoriness in the early period after percutaneous mitral balloon commissurotomy (PMBC) in patients with mitral stenosis and sinus rhythm. Methods Twenty-five patients undergoing PMBC were enrolled in this study. We evaluated the changes in pulmonary arterial pressure (PAP), left atrial (LA) pressure, mean mitral diastolic gradient, and mitral valve area in addition to the changes in atrial effective refractory periods (AERPs), AERP dispersion, and intra-atrial and interatrial conduction times after PMBC. Results There were significant decreases in mean diastolic gradient, PAP, mean LA pressure, and LA size after PMBC. Accompanying these acute hemodynamic changes after PMBC, AERPs in high right atrium (HRA), distal coronary sinus (DCS), and right posterolateral (RPL) were found to be increased ( P <.001), and AERP dispersion, PA HIS (an interval between P wave on the surface electrocardiogram and atrial electrogram at the His bundle site), and HRA-DCS intervals were significantly reduced after PMBC ( P <.001). It was revealed with linear regression and correlation analysis that only the changes in AERP dispersion were correlated with changes in LA pressure. Conclusions Relief of chronic atrial stretch results in an increase in AERPs and decrease in AERP dispersion, suggesting the potential reversibility of the electrophysiological features of chronic atrial dilatation. Our study emphasizes that an acute reduction of chronic atrial stretch in mitral stenosis resulted in favorable effects on atrial electrophysiological characteristics, and our results provide the first detailed insights into the electrophysiological changes after PMBC in patients with sinus rhythm.

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.

The HMG-CoA reductase inhibitor atorvastatin prevents atrial fibrillation by inhibiting inflammation in a canine sterile pericarditis model.

It has been recently reported that AF is associated with tissue inflammation. Statins reduce C-reactive protein (CRP) levels. However, the effect of statin on atrial fibrillation (AF) is unclear. The purpose of the present study was to evaluate the effect of statin on AF in a canine sterile pericarditis model. Sterile pericarditis was created in 20 dogs randomly assigned to two groups: a control group (10 dogs) and an atorvastatin treatment group (10 dogs). Atorvastatin was administered orally (2 mg/kg/day) beginning 1 week before the operation until the end of the study. Before and 2 days after the operation, CRP levels, the duration of induced AF, the atrial effective refractory period (AERP), and intra-atrial conduction time were determined. Before the operation, there were no significant differences in any of the parameters between the two groups. On the second postoperative day, the atorvastatin group had a lower CRP level (7.6+/-0.5 versus 11.7+/-1.3 mg/dl, P<0.0001), a shorter AF duration (177+/-57 versus 534+/-189 s, P<0.0001), a longer AERP (138+/-6 versus 130+/-6 ms, P<0.01), and a shorter intra-atrial conduction time (46+/-3 versus 51+/-5 ms, P<0.01) than the control group. Atorvastatin can prevent maintenance of AF by inhibiting inflammation in the canine sterile pericarditis model. Atorvastatin may thus be a novel therapeutic agent for AF.

Effects of intravenous nifekalant, a class III antiarrhythmic drug, on atrial vulnerability parameters in patients with paroxysmal atrial fibrillation.

Nifekalant, a class III antiarrhythmic drug, has been shown to suppress ventricular tachyarrhythmias, but its effects on AF are unclear. The aim of this study was to clarify the effects of nifekalant on the atrial vulnerability parameters in patients with paroxysmal AF. The study included 18 patients with paroxysmal AF who underwent electrophysiological study before and after intravenous infusion of nifekalant. The atrial electrophysiological parameters including the atrial effective refractory period (AERP), maximum intraatrial conduction delay, and wavelength index, calculated as the ratio of AERP to the maximum conduction delay, were quantitatively measured at baseline and during nifekalant infusion. The mean AERP was significantly prolonged from 214 +/- 27 ms at baseline to 242 +/- 39 ms after nifekalant (P < 0.001). Although earlier studies have shown that nifekalant does not affect the atrial conduction time, the mean maximum conduction delay of the study patients was significantly prolonged from 59 +/- 19 ms at baseline to 72 +/- 28 ms after nifekalant (P = 0.015). There was no significant difference in the wavelength index at baseline (4.1 +/- 1.7) and after nifekalant (4.1 +/- 2.5). However, when the differences of AERP and wavelength index were defined as each parameter during nifekalant infusion minus that at baseline, the difference of AERP showed a direct positive correlation with that of the wavelength index (P = 0.013). In conclusion, nifekalant may be effective in the prevention of AF due to prolongation of the AERP. However, in those patients who have a lesser degree of prolongation of the AERP by nifekalant, the wavelength index tended to be decreased, suggesting that the drug might augment the propensity for AF.

How to perform pulmonary vein isolation.

The advent of technology for the delivery of radiofrequency energy via electrode catheters, in the late 1980s, led to the perfection of techniques for the ablation of accessory pathways and classical flutter [1–4]. This has been so successful that these substrates for arrhythmia are rarely seen in the Western world. Two major arrhythmias, however, still remain to be conquered—atrial fibrillation and ventricular tachycardia/fibrillation. The occurrence of atrial fibrillation (AF) seems to be dependent on a number of factors [5]. In most situations there is some form of underlying atrial substrate, which is usually the presence of intra-atrial conduction delay. In addition, initiating factors for AF are required and the commonest of these appear to be atrial ectopic beats [6]. The major sources of these ectopic beats appear to be the pulmonary veins [7], although extrapulmonary vein sources are being increasingly reported [8,9]. Numerous recent studies suggest that AF may be treated by the techniques based on ablation within or around the pulmonary veins. Initial reports were based on the identification of pulmonary vein ectopic foci and the abolition of these sources [10]. The difficulties of making pulmonary foci fire and thereby identifying the culprit vein [11] led to the approach of attempting to achieve electrical isolation of all four pulmonary veins in the hope of abolishing the initiating triggers [12]. The recent results reported by Haissaguerre's group suggest that around 70% of patients with paroxysmal atrial fibrillation in normal hearts, can be made to hold long-term sinus rhythm by means of this technique [12,13]. Most patients have four pulmonary veins, two on the left and two on the right (Fig. 1). Many patients will have veins on the right or left side merging to a common ostium before entering …

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

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). We investigated whether a simple pacing approach via BB could reduce the induction of AF by extrastimuli (S2) from the right atrial appendage (RAA). 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. 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). Bachmann's bundle pacing reduces atrial conduction time caused by RAA-S2 and may be useful for preventing the induction of AF.

The standard maze-III procedure

The standard maze-III procedure

Impaired Longitudinal Conduction in Crista Terminalis is Necessary for Sustenance of Experimental Atrial Flutter

Sustained atrial flutter (AFL) can be induced by creating a lesion between the vena cava in dogs. In previous studies on this model, the crista terminalis (CT) was often injured, and thus, role of CT in sustained reentry was not well understood. We hypothesized that impaired longitudinal conduction in CT is necessary for sustained AFL. In 16 anesthetized, open-chest dogs, linear radiofrequency ablation of the intercaval region was performed without interrupting CT. Intra-atrial conduction times (IAT) along CT were measured using a plaque electrode (25x35 mm) containing 30 bipolar electrodes before and after additional ablation of CT (group A, n=10) or the pectinate muscle (PM) region (group B, n=6). In group A, IAT along CT was 27 +/- 5 ms at baseline and was increased to 43 +/- 3 ms after ablation of CT (P<0.001). In group B, IAT along CT was 28 +/- 4 ms at baseline and 27 +/- 3 ms after ablation of PM (P=NS). Sustained AFL lasting >20 minutes was induced in 10/10 dogs in group A only after additional ablation of CT, and in 0/6 dogs in group B (P<0.001). The cycle lengths of AFL after ablation of the intercaval region and additional ablation of CT were 119 +/- 14 and 140 +/- 14 ms, respectively (P<0.01). There was a significant positive correlation between the cycle length of AFL and IAT along CT (r2=0.63, P<0.001). These results indicate that longitudinal conduction property in CT and not in PM strongly affects sustenance of AFL in this model.

Occurrence of atrial fibrillation after flutter ablation: the significance of intra-atrial conduction and atrial vulnerability

Atrial vulnerability and intra-atrial conduction delay are important substrates for paroxysmal atrial fibrillation (AFib); however, their significance is unknown in patients undergoing atrial flutter ablation. Antegrade (high right atrium to coronary sinus: HRA-CS) and retrograde (CS-HRA) intra-atrial conduction times and AFib inducibility were assessed in 61 patients undergoing ablation for type I atrial flutter. Twenty-three patients had structural heart disease and 18 AFib before the procedure. After 16 ± 12 months of follow-up 17 patients experienced AFib, 5 of which progressed into chronic AFib. During the study, AFib was easily inducible in 14 patients, 7 of which developed AFib ( P = .03). Patients with post- ablation AFib were older (59 ± 11 vs. 44 ± 15 years, P = .001), had longer intra-atrial conduction times before (98 ± 17 ms vs. 68 ± 20 ms, P < .001) and after ablation (91 ± 19 ms vs. 73 ± 21 ms, P = .01) than those without AFib. Discriminant analysis revealed that only age, previous AFib and inta-atrial conduction delay (>90ms) were independent predictors of postablation AFib. Patients without a history of AFib and with normal intra-atrial conduction had a 3% risk of AFib, while patients with both factors had a 90% risk of AFib after ablation. Intra-atrial conduction delay is an important electrophysiological factor predicting atrial fibrillation after successful flutter ablation.

The usefulness of surface 12-lead electrocardiogram to predict intra-atrial conduction block after successful atrial flutter ablation

Intraatrial conduction block at the inferior vena cava-tricuspid annulus isthmus was shown to predict successful atrial flutter ablation. However, its demonstration requires the use of several electrode catheters. Thus, a simple approach using surface 12-lead ECG to prove the conduction block would be valuable. Twenty-two patients were prospectively studied during low septal and low lateral atrial pacing before and after successful atrial flutter ablation. Creation of the conduction block was confirmed by comparing the sequence of atrial activation using 3 multipolar catheters during atrial pacing before and after ablation. During low septal pacing, there was no significant difference before and after ablation in P-wave width, axis, or morphology. During low lateral atrial pacing, there was a significant P-wave axis rotation towards the right (from −67 ± 27° to +13 ± 35°, P < .001), and P-wave polarity in limb lead II changed from predominantly negative to predominantly positive in 21 of 22 patients. There was also an increase in P-wave width (from 136 ± 32 to 169 ± 36 ms, P < .001) and stimulus-to-QRS interval (from 268 ± 61 ms to 343 ± 95 ms, P < .001) during low lateral pacing that was not observed during low septal pacing. We conclude that creation of a conduction block in the inferior vena cava-tricuspid annulus isthmus modifies surface 12-lead ECG during low lateral atrial pacing only. We also suggest that P-wave polarity in limb lead II during low lateral pacing could be used as a noninvasive marker of unidirectional counter-clockwise conduction block during atrial flutter ablation.

Effects of angiotensin II type 1 receptor antagonist on electrical and structural remodeling in atrial fibrillation

ObjectivesThe purpose of the present study was to evaluate the effect of angiotensin II type 1 receptor (AT1R) antagonist on chronic structural remodeling in atrial fibrillation (AF). BackgroundWe previously reported that an AT1R antagonist, candesartan, prevents acute electrical remodeling in a rapid pacing model. However, the effect of candesartan on chronic structural remodeling in AF is unclear. MethodsSustained AF was induced in 20 dogs (10 in a control group and 10 in a candesartan group) by rapid pacing of the right atrium (RA) at 400 beats/min for five weeks. Candesartan was administered orally (10 mg/kg/day) for one week before rapid pacing and was continued for five weeks. The AF duration, atrial effective refractory period (AERP) at four sites in the RA, and intra-atrial conduction time (CT) from the RA appendage to the other three sites were measured every week. ResultsThe mean AF duration in the control group after five weeks was significantly longer than that with candesartan (1,333 ± 725 vs. 411 ± 301 s, p < 0.01). The degree of AERP shortening after five weeks was not significantly different between the two groups. The CT from the RA appendage to the low RA after five weeks with candesartan was significantly shorter than that in the control (43 ± 14 vs. 68 ± 10 ms, p < 0.05). The candesartan group had a significantly lower percentage of interstitial fibrosis than the control group (7 ± 2% vs. 16 ± 1% at the RA appendage, p < 0.001). ConclusionsCandesartan can prevent the promotion of AF by suppressing the development of structural remodeling.

Disorganized activating during chronic human atrial fibrillation is associated with a high incidence of epicardi breakthrough and intra-atrial conduction block

Disorganized activating during chronic human atrial fibrillation is associated with a high incidence of epicardi breakthrough and intra-atrial conduction block