Interatrial Conduction Time Research Articles

Value of interatrial conduction time and P wave dispersion in prediction of atrial fibrillation following coronary bypass surgery

This prospective observational study investigated predictive power of interatrial conduction time (IACT) and P wave dispersion (PWD), in addition to other atrial fibrillation (AF) predictors, in patients undergoing coronary artery bypass surgery (CABG). Eighty-one patients undergoing CABG were enrolled. Before surgery, IACT and PWD were measured. Time interval from electrocardiographic P wave to echocardiographic transmitral a wave was defined as IACT. Rhythm monitorization was used for AF detection. Continuous and categorical data were compared with independent samples t test and Chi-square statistics. Multiple logistic regression analysis was used to identify independent AF predictors. During a follow-up period of 6.4 ± 2.1 days, AF developed in 14 patients (17%). There were no significant differences between patients with or without AF according to age, gender, number of bypass grafts, cross-clamp duration, systolic function, and left atrial diameter. Significantly increased PWD and IACT were found in AF group (PWD: 37 ± 9 ms vs 24 ± 8 ms, p=0.005 and IACT: 129 ± 11 ms vs 117 ± 11 ms, p=0.01) as compared to group without AF. Increased PWD (OR 1.17; 95% CI 1.04-1.31; p=0.02), absence of beta-blocker treatment (OR 8.88; 95% CI 1.62-48.45; p=0.01), diabetes (DM) and hypertension (HT) combination (OR 1.45; 95% CI 1.15-4.22; p=0.01) were independent AF predictors. However, IACT predictive power had borderline significance (OR 1.03; 95% CI 0.95-1.12; p=0.06). Increased PWD, absence of beta-blocker therapy, HT-DM combination were independent AF predictors following CABG. There was significant difference between groups according to IACT, however predictive value of IACT was nonsignificant. Other studies are needed to establish predictive power of IACT.

Assessment of atrial conduction time by tissue Doppler echocardiography and P-wave dispersion in patients with mitral annulus calcification

The aim of our study was to investigate atrial conduction time in patients with mitral annulus calcification (MAC) using P-wave dispersion (PWD) and electromechanical coupling measured with the surface electrocardiogram and the tissue Doppler echocardiography. Fifty-nine patients with MAC and 43 control subjects underwent resting the surface electrocardiogram and tissue Doppler echocardiography. The difference between the maximum (Pmax) and minimum P-wave durations was calculated and defined as PWD. Interatrial and intraatrial electromechanical delays were measured with tissue Doppler echocardiography. Both Pmax and PWD were higher in patients with MAC compared with controls (111.4 ± 15.8 vs 97.3 ± 18.8 milliseconds; P < .0001 and 46.4 ± 14.6 vs 31.4 ± 13.1 milliseconds; P < .0001, respectively). Both interatrial and intraatrial conduction time were also delayed in patients with MAC compared with controls (29.8 ± 13.3 vs 17.6 ± 12.5 milliseconds; P < .0001; 9.4 ± 5.1 vs 6.8 ± 4.0 milliseconds; P < .008, respectively). Left atrial (LA) diameter was significantly higher in patients with MAC compared with controls (35.4 ± 5.0 mm vs 32.3 ± 4.2 mm; P < .001). The LA diameter correlated significantly with both interatrial conduction times and PWD ( r = 0.56; P < .0001 and r = 0.47; P < .0001, respectively). There is a delay in both intraatrial and interatrial electromechanical coupling intervals in patients with MAC.

Effects of acute autonomic modulation on atrial conduction delay and local electrograms duration in paroxysmal atrial fibrillation

Slowed atrial conduction may contribute to reentry circuits and vulnerability for atrial fibrillation (AF). The autonomic nervous system (ANS) has modulating effects on electrophysiological properties. However, complex interactions of the ANS with the arrhythmogenic substrate make it difficult to understand the mechanisms underlying induction and maintenance of AF. Aim To determine the effect of acute ANS modulation in atrial activation times in patients (P) with paroxysmal AF (PAF). Methods and results 16P (9 men; 59 ± 14 years) with PAF, who underwent electrophysiological study before AF ablation, and 15P (7 men; 58 ± 11 years) with atrioventricular nodal reentry tachycardia, without documentation or induction of AF (control group). Each group included 7P with arterial hypertension but without underlying structural heart disease. The study was performed while off drugs. Multipolar catheters were placed at the high right atrium (HRA), right atrial appendage (RAA), coronary sinus (CS) and His bundle area (His). At baseline and with HRA pacing (600 ms, shortest propagated S2) we measured: i) intra-atrial conduction time (IACT, between RAA and atrial deflection in the distal His), ii) inter-atrial conduction time (interACT, between RAA and distal CS), iii) left atrial activation time (LAAT, between atrial deflection in the distal His and distal CS), iv) bipolar electrogram duration at four atrial sites (RAA, His, proximal and distal CS). In the PAF group, measurements were also determined during handgrip and carotid sinus massage (CSM), and after pharmacological blockade of the ANS (ANSB). AF was induced by HRA programmed stimulation in 56% (self-limited — 6; sustained — 3), 68.8% (self-limited — 6; sustained — 5), and 50% (self-limited — 5; sustained — 3) of the P, in basal, during ANS maneuvers, and after ANSB, respectively ( p = NS). IACT, interACT and LAAT significantly lengthened during HRA pacing in both groups (600 ms, S2). P with PAF have longer IACT ( p < 0.05), a higher increase in both IACT, interACT ( p < 0.01) and electrograms duration ( p < 0.05) with S2, and more fragmented activity, compared with the control group. Atrial conduction times and electrograms duration were not significantly changed during ANS stimulation. Nevertheless, ANS maneuvers increased heterogeneity of the local electrograms duration. Also, P with sustained AF showed longer interACT and LAAT during CSM. Conclusion Atrial conduction times, electrograms duration and fractionated activity are increased in PAF, suggesting a role for conduction delays in the arrhythmogenic substrate. Acute vagal stimulation is associated with prolonged interACT and LAAT in P with inducible sustained AF and ANS modulation may influence the heterogeneity of atrial electrograms duration.

Abnormal Atrial Repolarization and Depolarization Contribute to the Inducibility of Atrial Fibrillation in Brugada Syndrome

Brugada syndrome is often accompanied by atrial tachyarrhythmia, such as atrial fibrillation (AF). The aim of this study was to examine atrial vulnerability in patients with Brugada syndrome. Two groups of patients were compared: 18 patients with Brugada syndrome (Brugada syndrome group) and 11 age-matched patients with neither organic heart disease nor AF episodes (control group). Programmed electrical stimulation was performed from the right atrium (RA), and the effective refractory period of the right atrium (ERP-RA), interatrial conduction time (IACT), monophasic action potentials (MAPs) at the high RA, and the inducibility of AF lasting > 30 seconds were studied. MAP duration at 80% repolarization (MAPD(80)) was calculated. AF was induced with a single extrastimulus or double extrastimuli in all patients with Brugada syndrome but in none of the control patients. The ERP-RA did not differ between the groups. IACT at the shortest diastolic interval was significantly increased in the Brugada syndrome group compared to that in the control group. The maximum slope of the MAPD(80) restitution curve was significantly steeper in the Brugada syndrome group than in the control group (2.4 + or - 2.0 versus 0.82 + or - 0.36, P < 0.02). Ventricular fibrillation was induced with ventricular programmed stimulation in all Brugada syndrome patients. Both abnormal interatrial conduction and steep restitution of action potential duration may contribute to the atrial arrhythmogenicity in Brugada syndrome.

Evaluation of atrial vulnerability immediately after radiofrequency catheter ablation of accessory pathway in patients with Wolff–Parkinson–White syndrome

The intrinsic atrial vulnerability is proposed as one of the mechanisms of paroxysmal atrial fibrillation (PAF) in Wolff-Parkinson-White (WPW) syndrome. In this study, we examined the early changes in atrial refractoriness and intra- and inter-atrial conduction times after radiofrequency (RF) catheter ablation of accessory pathway (AP). Twenty-four consecutive patients with WPW syndrome and documented AV reciprocating tachycardia but without history of PAF (fourteen male, mean age 39 +/- 9.5 years) and 27 control subjects (six female, mean age 51.4 +/- 10.1 years) with AV nodal reentrant tachycardia (AVNRT) who underwent ablation of the slow AV nodal pathways were enrolled into the study. Regional atrial effective refractory periods (AERPs), AERP dispersion, and intra- and inter-atrial conduction times were obtained before and 30 min after ablation and were compared between two groups. In the study group, patients with and without inducible AF were also compared regarding these parameters. In the study group, AERPs in higher right atrium and right posterolateral atrium were significantly increased, and AERP dispersion, intra-atrial, and inter-atrial conduction times were significantly decreased after ablation; AERP in distal coronary sinus was unchanged. In control group, no significant difference was observed in these parameters. Inducibility of AF was significantly reduced following ablation of AP in the study group (from seven to zero of 24 patients, p = 0.016). Comparison between patients with (n = 7) and without (n = 17) AF revealed that left atrium diameter was larger, AERPs in the right posterolateral atrium before and after ablation, and ERP of AP were shorter in AF group. In WPW syndrome patients, RF catheter ablation of AP results in an 'immediate' decrease in atrial vulnerability. Since inducibility of AF becomes more difficult in this less vulnerable atrium, the AP itself may play an important role in the development of AF.

P wave and QT changes among inpatients with schizophrenia after parenteral ziprasidone administration

Objective Although ziprasidone has been reported to cause ventricular arrhythmias, there have been no studies regarding the influence of ziprasidone on atrial conduction. Intraatrial and interatrial conduction time prolongation and inhomogeneous propagation of sinus impulses are indicated by P wave changes on surface electrocardiography. We aimed to evaluate proneness to atrial fibrillation after intramuscular ziprasidone in drug-free inpatients with schizophrenia. Methods We evaluated 11 eligible inpatients who were drug free for at least 4 weeks with a primary diagnosis of schizophrenia disorder and 11 healthy controls who were hospital staff members. Electrocardiography was performed at baseline and 1.5–2 h after ziprasidone injection. A 12-lead surface electrocardiogram was obtained from each subject in the supine position at a paper speed of 50 mm/s and 2 mV/cm. Results The changes between baseline and the period after parenteral ziprasidone administration in P-wave duration, P-wave dispersion, QTc, QTc max, QTc min, and QT dispersion variables were significant ( p > 0.05). The initial P-wave dispersion was significantly longer in patients than in healthy controls ( p < 0.05). There were no correlations between electrocardiography parameters and clinical severity scores or demographic variables in either group. Conclusion Intramuscular ziprasidone administration does not seem to influence atrial and ventricular electrical conduction in drug-free inpatients with schizophrenia. However, schizophrenia might affect atrial conduction resulting in atrial fibrillation, which may be a cause of some complications in inpatients with this schizophrenia.

Interatrial Conduction Time and Left Atrial Function in Patients With Left Ventricular Systolic Dysfunction: Effects of Cardiac Resynchronization Therapy

Prolonged interatrial conduction time (IACT) can be associated with abnormal left atrial (LA) function but has not been characterized in patients with left ventricular (LV) systolic dysfunction (LVSD) and QRS intervals >130 ms. Two-dimensional Doppler echocardiography and Doppler tissue imaging (DTI) were performed in 41 patients with LVSD (mean LV ejection fraction, 26 +/- 5%) and 41 similarly aged normal controls. Two-dimensional measurements included LV volume and ejection fraction and LA volume for the determination of LA emptying fraction and LA ejection fraction. IACT was defined as the time from the onset of the P wave to the onset of the DTI-derived late diastolic (A') velocity at the lateral mitral annulus. Two-dimensional Doppler measurements were reassessed in patients with LVSD 4 +/- 2 months after cardiac resynchronization therapy (CRT). IACT was longer in patients with compared to controls (105 +/- 25 vs 74 +/- 12 ms, P < .001); none of the controls had an IACT > 100 ms. In patients with LVSD, IACT was correlated modestly with measurements of LA volume (r = .41-.48, all P values < .009) but not with measurements of LA function. Patients with LVSD with IACTs > 100 ms (n = 20) prior to CRT had larger LA volumes and lower indices of LA function after CRT compared to those with IACTs < or = 100 ms. Significant reductions in LV end-systolic volumes and increases in LV ejection fractions occurred in both groups after CRT. DTI-derived IACT can be prolonged in patients with severe LVSD and wide QRS intervals. An IACT > 100 ms can affect LA remodeling and function at early follow-up after CRT but does not influence the response in LV end-systolic volume or ejection fraction.

Simultaneous Assessment of Pharmacokinetics of Pilsicainide Transdermal Patch and Its Electropharmacological Effects on Atria of Chronic Atrioventricular Block Dogs

Pharmacokinetics of pilsicainide transdermal patch and its electropharmacological effects were simultaneously assessed using chronic atrioventricular block dogs. After application of the patch (9.8 mg/kg), pilsicainide was continuously absorbed through the skin with a C(max) of 0.49 +/- 0.13 microg/ml, while its plasma concentration was kept above the clinically reported minimum effective plasma concentration for 2 - 8 h. Inter-atrial conduction time was significantly prolonged, whereas statistically significant prolongation was not detected in the atrial effective refractory period. Prolongation of the cycle length of atrial fibrillation and anti-fibrillatory action were confirmed. Thus, pilsicainide can be absorbed transdermally to exert long-lasting electropharmacological effects leading to anti-atrial fibrillatory action.

Usefulness of Interatrial Conduction Time to Distinguish Between Focal Atrial Tachyarrhythmias Originating from the Superior Vena Cava and the Right Superior Pulmonary Vein

Differentiation of the tachycardia originating from the superior vena cava (SVC) or the right superior pulmonary vein (RSPV) is limited by the similar surface P-wave morphology and intraatrial activation pattern during tachycardia. We sought to find a simple method to distinguish between the two tachycardias by analyzing the interatrial conduction time. Sixteen consecutive patients consisting of 8 with SVC tachycardia and the other 8 with RSPV tachycardia were studied. The interatrial conduction time from the high right atrium (HRA) to the distal coronary sinus (DCS) and the intraatrial conduction time from the HRA to the atrial electrogram at the His bundle region (HIS) were measured during the sinus beat (SR) and during the tachycardia-triggering ectopic atrial premature beat (APB). The differences of interatrial (Delta[HRA-DCS](SR-APB)) and intraatrial (Delta[HRA-HIS](SR-APB)) conduction time between SR and APB were then obtained. The mean Delta[HRA-DCS](SR-APB) was 1.0 +/- 5.2 ms (95% confident interval [CI]-3.3-5.3 ms) in SVC tachycardia and 38.5 +/- 8.8 ms (95% CI 31.1-45.9 ms) in RSPV tachycardia. The mean Delta[HRA-HIS](SR-APB) was 1.5 +/- 5.3 ms (95% CI -2.9-5.9 ms) in SVC tachycardia and 19.9 +/- 12.0 ms (95% CI 9.9-29.9 ms) in RSPV tachycardia. The difference of Delta[HRA-DCS](SR-APB) between SVC and RSPV tachycardias was wider than that of Delta[HRA-HIS](SR-APB) (37.5 +/- 9.3 ms vs. 18.4 +/- 15.4 ms, P < 0.01). The wide difference of the interatrial conduction time Delta[HRA-DCS](SR-APB) between SVC and RSPV tachycardias is a useful parameter to distinguish the two tachycardias and may avoid unnecessary atrial transseptal puncture.

Echocardiographic Predictors of Symptomatic Atrial Fibrillation In Patients with Rheumatic Mitral Stenosis and Normal Sinus Rhythm.

Sixty-two patients (51 females) with mitral stenosis and normal sinus rhythm were included in the study. Seven patients (11.3%) developed symptomatic AF and the remaining 55 were free of AF during a followed-up of 22±5 months. The following echocardiographic parameters were significantly increased and predicted the development of AF; left atrial (LA) mediolateral diameter (5.5 ± 0.5 cm vs 4.7 ± 0.7 cm), right atrial mediolateral diameter (4,7 ± 1.0 cm vs 3.6 ± 1.3 cm), LA area in the apical two chamber view ( 31 ± 3.2 cm2 vs 25 ± 5.8 cm2), right atrial volume (52 ± 22 cm3 vs 34 ± 19 cm3), and interatrial conduction time (IACT) (142 ± 22 msec vs 115 ± 16 msec). Conclusions: This study revealed that echocardiography can be used to predict symptomatic AF in patients with RMS and sinus rhythm.

Optimal Atrio-Ventricular Delay in CRT Patients Can Be Approximated Using Surface ECG

Background: Optimization of the programmed atrio-ventricular (AV) delay (AVD) may result in an improvement in acute and chronic outcome of CRT. Previous studies have shown positive correlation between inter-atrial conduction time (measured invasively during the implant procedure) and optimal AVD determined post-implant using Doppler echocardiography. We hypothesized that the optimal AVD can be predicted non-invasively from surface ECG. Methods: Patients (n=34) implanted with CRT-D devices who had sinus rhythm and no AV block underwent echocardiographic optimization of AVDs with simultaneous digital recording of the surface ECG and device telemetry.

Atrial Fibrillation in Patients With Brugada Syndrome: Relationships of Gene Mutation, Electrophysiology, and Clinical Backgrounds

The goal of our work was to examine the relationships of atrial fibrillation (AF) with genetic, clinical, and electrophysiological backgrounds in Brugada syndrome (BrS). Atrial fibrillation is often observed in patients with BrS and indicates that electrical abnormality might exist in the atrium as well as in the ventricle. SCN5A, a gene encoding the cardiac sodium channel, has been reported to be causally related to BrS. However, little is known about the relationships of atrial arrhythmias with genetic, clinical, and electrophysiological backgrounds of BrS. Seventy-three BrS patients (49 +/- 12 years of age, men/women = 72/1) were studied. The existence of SCN5A mutation and clinical variables (syncopal episode, documented ventricular fibrillation [VF], and family history of sudden death) were compared with spontaneous AF episodes. Genetic and clinical variables were also compared with electrophysiologic (EP) parameters: atrial refractory period, interatrial conduction time (CT), repetitive atrial firing, and AF induction by atrial extra-stimulus testing. Spontaneous AF occurred in 10 (13.7%) of the BrS patients and SCN5A mutation was detected in 15 patients. Spontaneous AF was associated with higher incidence of syncopal episodes (60.0% vs. 22.2%, p < 0.03) and documented VF (40.0% vs. 14.3%, p < 0.05). SCN5A mutation was associated with prolonged CT (p < 0.03) and AF induction (p < 0.05) in EP study, but not related to the spontaneous AF episode and other clinical variables. In patients with documented VF, higher incidence of spontaneous AF (30.8% vs. 10.0%, p < 0.05), AF induction (53.8% vs. 20.0%, p < 0.03), and prolonged CT was observed. Spontaneous AF and VF are closely linked clinically and electrophysiologically in BrS patients. Patients with spontaneous AF have more severe clinical backgrounds in BrS. SCN5A mutation is associated with electrical abnormality but not disease severity.

Sinus node function in patients operated for mitral valve disease: indirect evaluation with epimyocardial electrodes

To study the interatrial conduction times and atrial node performance in patients submitted to mitral valve surgery with the aid of temporary atrial epicardic electrodes. The atriograms were carried out in the first postoperative day and before the hospital discharge of ten consecutive patients. Sixty percent of the patients could complete the post-operative study protocol. The main results were: a) Post-operative arrhythmias were detected in 50% of the patients; b) There were no statistical differences between the pre and post-operative 12 lead EKGs. c) The interatrial conduction time (IACT) ranged from 90 to 140ms in the first post-operative day, and from 110 to 130ms at hospital discharge; d) The sinus node recovery time (SNRT) ranged from 250 to 560ms in the first post-operative day and from 180 to 360ms at hospital discharge; e) The sinus atrial conduction time (SACT) remained between 70 and 140ms, both in the first post-operative day and at hospital discharge, and; f) The IACT was normal in patients whose left atrium (LA) was less than 50mm in diameter but supra normal in the remaining cases. Sinus node function and inter-atrial conduction are not altered by mitral valve operation. Post-operative programmed epicardic atrial stimulation is easy and safe.

Should we use the rate-adaptive AV delay in cardiac resynchronization therapy-pacing?

Recommendations for programming the rate-adaptive AV delay in CRT. In cases of continual biventricular pacing, the optimal AV delay in CRT (AVD(opt)) is the net effect of the pacemaker-related interatrial conduction time (IACT), duration of the left-atrial electromechanical action (LA-EAC(long)), and the duration of the left-ventricular latency period (S(V)-EAC(short)). It can be calculated by AVD(opt) = IACT+LA-EAC(long)-S(V)-EAC(short). We measured these three components in 20 CRT-ICD patients during rest and submaximal ergo metric exercise (71 +/- 9 W) resulting in a 22.5 +/- 9.6 bpm rate increase. IACT and S(V)-EAC(short) did not reveal significant differences. LA-EAC(long), however, varied significantly by -10.7 +/- 16.1 ms (P = 0.008) during exercise. In contrast to AVD(optVDD), there was a significant difference in AVD(optDDD) of -8.8 +/- 14.5 ms (P = 0.014) between the resting and submaximal exercise conditions. In DDD pacing, AVD(opt) was shortened by 2.6 ms/10 bpm. In consideration of the findings of the studies performed to date, the rate-adaptive AV delay should be deactivated.

A Multiple Ion Channel Blocker, NIP‐142, for the Treatment of Atrial Fibrillation

Atrial fibrillation (AF) is one of the most frequent cardiac arrhythmia and is associated with increased cardiovascular morbidity and mortality, and the risk of stroke. Although currently available antiarrhythmic drugs are moderately effective in restoring normal sinus rhythm in patients with AF, excessive delay of ventricular repolarization by these agents may be associated with increased risk of proarrhythmia. Therefore, selective blockers of cardiac ion channel(s) that are exclusively present in the atria are highly desirable. NIP-142 is a novel benzopyrane derivative, which blocks potassium, calcium, and sodium channels and shows atrial specific action potential duration prolongation. NIP-142 preferentially blocks the ultrarapid delayed rectifier potassium current (I Kur) and the acetylcholine-activated potassium current (I KACh). Since I Kur and I KACh have been shown to be expressed more abundantly in the atrial than in the ventricular myocardium, the atrial-specific repolarization prolonging effect of NIP-142 is considered to be due to the blockade of these potassium currents. In canine models, NIP-142 was shown to terminate the microreentry type AF induced by vagal nerve stimulation and the macroreentry type atrial flutter induced by an intercaval crush. These effects of NIP-142 have been attributed to the prolongation of atrial effective refractory period (ERP), because this compound prolonged atrial ERP without affecting intraatrial and interatrial conduction times in these models. The ERP prolongation by NIP-142 was greater in the atrium than in the ventricle. NIP-142 also terminated the focal activity type AF induced by aconitine. In addition, NIP-142 reversed the atrial ERP shortening and the loss of rate adaptation induced by short-term rapid atrial pacing in anesthetized dogs. Thus, although clinical trials are required to provide evidence for its efficacy and safety, the novel multiple ion channel blocker, NIP-142, appears to be a useful agent for the treatment of several types of AF with a low risk of proarrhythmic activity.

Sequence of electrical activation, atrial remodelling and atrial fibrillation in patients with nodal re-entrant tachycardia

Objective — The objective of the study was to verify, if the particular sequence of electrical atrioventricular activation during tachycardia is associated with the development of atrial remodelling and predisposition to atrial fibrillation (AF) in patients with nodal reentry tachycardia (AVNRT).Methods and results — We assessed 117 consecutive patients with AVNRT identified during electrophysiological study.Two groups were identified: the AF group, n = 21 (17.9%, median age 46.0, 15 women), with clinically documented AF, and the control group, n = 96, without AF (median age 48.5, 69 women). Tachycardia cycle length (VV), anterograde AV, retrograde VA activation intervals and indexes (AV/VV, VA/VV) during AVNRT, atrial refractory period (AERP), intraatrial (IntraCT) and interatrial conduction time (InterCT) of the sinus beat and premature stimuli were analysed. The longer retrograde and shorter anterograde activation was found in AF patients with typical AVNRT, the opposite relations showed the subjects with atypical tachycardia. Intra and InterCT of sinus beat, and of paced extrastimuli were longer, AERP was borderline shorter in the AF-group than in the con-trols.The longest conduction times and shortest AERP were seen in the patients with VA/VV within 20-40% of the tachycardia cycle, this group comprised 71% of all AF-patients (P< 0.001).VA was predictive for AF in typical (OR/unit 1.04) and atypical AVNRT (OR/unit 0.93, P< 0.05).Conclusions — The particular sequence of electrical atrioventricular activation, seen in some patients during AVNRT, is associated with disturbances of atrial conduction, refractoriness and predisposes to atrial fibrillation.

Right atrial pacing and the risk of postimplant atrial fibrillation in cardiac resynchronization therapy recipients

In patients with cardiac resynchronization therapy (CRT) devices, right atrial (RA) pacing introduces a significant prolongation in interatrial conduction time, delaying left atrial mechanical systole and curtailing left ventricular filling. The resultant increase in left-sided filling pressures may facilitate atrial fibrillation (AF). We sought to determine whether the extent of RA pacing influences the incidence of AF after CRT. Consecutive CRT patients (n = 309) followed at our institution were retrospectively studied for percentage of RA pacing and incidence of high atrial rates, as determined by regular device interrogations. Additional clinical data were collected from the medical record. The mean follow-up was 18.1 +/- 13.3 months, during which 209 (67.6%) patients had at least 1 detected high atrial rate episode consistent with AF. Higher percentages of RA pacing were associated with a greater risk of postimplant AF, with its incidence increasing incrementally with quartiles of RA pacing: 44.6%, 64.3%, 79.7%, and 81.6%, respectively (P < .001). After controlling for all factors predictive of postimplant AF on univariate analysis (right atrial pacing quartile, follow-up duration, mitral regurgitation severity, and prior AF history), RA pacing quartile remained a significant predictor of post-CRT AF (hazard ratio 1.92, 95% CI 1.40-2.62, P < .001) upon multivariate analysis. In addition to predicting AF incidence, higher RA pacing quartiles were also associated with significantly greater AF burden. Compared to atrial sensing, atrial pacing is associated with a 2-fold increased risk of post-CRT AF. Prospective comparison of DDD and VDD pacing modes in CRT is warranted.

Characterization of the Acute Cardiac Electrophysiologic Effects of Ethanol in Dogs

Alcohol has been related to atrial fibrillation (holiday heart syndrome), but its electrophysiologic actions remain unclear. We evaluated the effects of alcohol in 23 anesthetized dogs at baseline and after 2 cumulative intravenous doses of ethanol: first dose 1.5 ml/kg (plasma level 200 mg/dl); second dose 1.0 ml/kg (279 mg/dl). In 13 closed-chest dogs (5 with intact autonomic nervous system, 5 under combined autonomic blockade and 3 sham controls), electrophysiologic evaluation and monophasic action potential (MAP) recordings were undertaken in the right atrium and ventricle. In 5 additional dogs, open-chest biatrial epicardial mapping with 8 bipoles on Bachmann's bundle was undertaken. In the remaining 5 dogs, 2D echocardiograms and ultrastructural analysis were performed. In closed-chest dogs with intact autonomic nervous system, ethanol had no effects on surface electrocardiogram and intracardiac variables. At a cycle length of 300 milliseconds, no effects were noted on atrial and ventricular refractoriness and on the right atrial MAP. These results were not altered by autonomic blockade. No changes occurred in sham controls. In open-chest dogs, ethanol did not affect inter-atrial conduction time, conduction velocity, and wavelength. Atrial arrhythmias were not induced in any dog, either at baseline or after ethanol. Histological and ultrastructural findings were normal but left ventricular (LV) ejection fraction decreased in treated dogs (77 vs. 73 vs. 66%; p = 0.04). Ethanol at medium and high doses depresses LV systolic function but has no effects on atrial electrophysiological parameters. These findings suggest that acute alcoholic intoxication does not directly promote atrial arrhythmias.

The Time Interval from the Initiation of the P‐Wave to the Start of Left Atrial Appendage Ejection Flow: Does It Reflect İnteratrial Conduction Time?

Recurrence of atrial fibrillation is more common in patients with atrial conduction delay. In the present study, we evaluated whether findings obtained from transesophageal echocardiography (TEE), a semi-invasive method, correlate with those from an invasive method, electrophysiologic study (EPS), in measuring interatrial conduction time. We compared two methods of calculating interatrial conduction time in a group of 33 patients. The origin of the P-wave on the surface electrocardiogram (ECG) was taken as the onset of atrial activation. The time interval from this point to the commencement of the left atrial appendage ejection flow (P-LAA) was measured by TEE. Meanwhile, simultaneous recordings of the left atrial appendage were obtained with a catheter positioned in the LAA, and an invasive interatrial conduction time was measured from the origin of the surface's earliest P-wave (I-IACT). The mean I-IACT (46.27 +/- 13.25 ms) correlated strongly with the mean P-LAA (49.91 +/- 12.72 ms; r = 0.839, P < 0.0001). The interatrial conduction time can be estimated with a relatively noninvasive method using P-LAA measurements. This technique can be applied widely in predicting AF recurrence, and appropriate therapy may be applied.

How can the rate-adaptive atrioventricular delay be programmed in atrioventricular block pacing?

To optimize recommendations for programming of the rate-adaptive atrioventricular (AV) delay. Optimal AV delay (AVD(opt)) is the net effect of the pacemaker-related interatrial conduction time (IACT), duration of the left-atrial electromechanical action (LA-EAC(long)) and duration of left-ventricular latency (S(V)-EAC(short)). It can be calculated by AVD(opt) = IACT + LA-EAC(long)-S(V)-EAC(short). We measured these three components in 20 DDD pacemaker patients (EF >45%) with the third degree AV block (AVB) at rest and submaximal ergometric exercise load of 71 +/- 9 W which resulted in a 31.5 +/- 9.9 bpm rate increase. Between exercise and rest, the components of and the final AVD(opt) showed no significant differences. Interatrial conduction time in VDD and DDD pacing varied by 2.3 +/- 8.4 ms and 1.4 +/- 8.8 ms, respectively, S(V)-EAC(short) changed by -2.6 +/- 21.8 ms and AVD(opt) by -3.5 +/- 33.3 ms and -4.3 +/- 37.8 ms in VDD and DDD operation, respectively. The greatest variation was of LA-EAC(long) by -8.4 +/- 32.7 ms. Linear regressions of the rate-dependent variations (Deltaf) in VDD operation yielded DeltaIACT(f) = 0.04Deltaf + 0.95 ms, DeltaLA-EAC(long) = -0.59Deltaf + 10.1 ms, and DeltaS(V) - EAC(short) = 0.14Deltaf -7.2 ms which resulted in DeltaAVD(opt) = -0.69Deltaf + 18.2 ms. A recommendation for programming of rate-adaptive AV delay in AV block patients cannot be given.