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A 72-year-old woman undergoing percutaneous intervention to a calcified proximal left anterior descending (LAD) coronary artery lesion using Shockwave Intravascular Lithotripsy (S-IVL) developed new atrial flutter. She then returned to sinus rhythm after treatment with amiodarone. S-IVL can cause cardiomyocyte depolarization. We hypothesize that pacing can occur during atrial repolarization, inducing supraventricular tachyarrhythmias and even triggering atrial macro re-entrant circuits. We recommend synchronizing shock wave delivery with R waves on the electrocardiogram to lower the risk of arrhythmias.

The standard 12-lead Electrocardiogram (ECG) system is the most commonly used technique for obtaining the electrocardiographic signal to evaluate the heart’s electrical activity. In the surface ECG, atrial repolarization (Ta wave) is not observed. However, during the exercise stress test, ST-segment depression validates the existence of Ta wave.To record the Ta wave and enhance atrial depolarization (P wave) in Sinus Rhythm (SR) ECG, Modified Limb Lead (MLL) system is used. PTa Interval (PTaI) represents the duration from the beginning of P wave to the end of Ta wave. This study aims to develop a corrected PTaI (PTac) formula to correct the PTaI from MLL ECGs for different heart rates. ECGs were recorded from 35 volunteers in SR and Sinus Tachycardia (ST) condition of mean age 24 ± 5 years using EDAN PC ECG system. Regression analysis was implemented on the recorded data to derive the slope for PP Interval (PPI) vs. PTaI plots in both groups. In SR group, PPI correlated well with PTaI (r = 0.48) compared to the ST group (r = 0.17). A new corrected PTaI (\({\text{PTa}}_{\text{c}} {\text{N}}\)) formula was developed from the slope values of SR and ST and compared with the previously developed PTac formula. The developed PTac formula of this study showed accurate results with the least slope in different heart rates. Implementation of new PTac formula in automatic algorithms further improves the clinical diagnosis related to atrial ECG components.

AVE0118, an inhibitor of IKur, Ito and IK,ACh, was in the drug pipeline for atrial fibrillation. To investigate the limitation of AVE0118 as an anti-atrial fibrillatory drug, we studied its electropharmacological effects particularly focusing on the anti-atrial fibrillatory action as reverse translational research. We adopted the chronic atrioventricular block beagle dogs (n = 4), having a pathophysiology of bradycardia-associated, volume overload-induced chronic heart failure, in which the atrial fibrillation was induced by 10 s of burst pacing on atrial septum. AVE0118 in doses of 0.24 and 1.2 mg/kg, i.v. over 10 min hardly altered electrophysiological variables. Meanwhile, AVE0118 in a dose of 6 mg/kg, i.v. over 10 min delayed the inter-atrial conduction in a frequency-dependent manner and prolonged the atrial effective refractory period in a reverse frequency-dependent manner, whereas it did not significantly alter the duration of atrial fibrillation or its cycle length. The increment of atrial effective refractory period was 3.3 times greater compared with that of ventricular one at a basic cycle length of 400 ms. Torsade de pointes was not induced during the experimental period. Thus, AVE0118 may possess a favorable cardiac safety pharmacological profile, but its weak anti-atrial fibrillatory effect would indicate the limitation of atrial repolarization-delaying agents for suppressing atrial fibrillation.

Comparative study between Standard limb lead system (SLL) and Modified limb lead system (MLL) was carried out in this paper. Electrocardiograms (ECG) of Forty-five female subjects were recorded in sinus rhythm with SLL and MLL for 60 s with the help of EDAN SE-1010 PC ECG system. In MLL system, the amplitudes of P wave increased and the amplitude of ventricular components reduced. In PR interval atrial repolarization wave (Ta) wave was noticed and it is opposite to direction of P wave. There were no changes observed in durations of ECG wave. The MLL system with observable Ta wave improves the diagnosis of arrhythmias and atrial related diseases. The developed MLL system provides significant information related to atrial components. This study shows that MLL system is an alternate lead system to provide detailed information about atrial components of ECG.

Background This study estimates atrial repolarization activities (Ta waves), which are typically hidden most of the time from body surface electrocardiography when diagnosing cardiovascular diseases. The morphology of Ta waves has been proven to be an important marker for the early sign of inferior injury, such as acute atrial infarction, or arrhythmia, such as atrial fibrillation. However, Ta waves are usually unseen except during conduction system malfunction, such as long QT interval or atrioventricular block. Therefore, justifying heart diseases based on atrial repolarization becomes impossible in sinus rhythm. Methods We obtain TMPs in the atrial part of the myocardium which reflects the correct excitation sequence starting from the atrium to the end of the apex. Results The resulting TMP shows the hidden atrial part of ECG waves. Conclusions This extraction makes many diseases, such as acute atrial infarction or arrhythmia, become easily diagnosed.

International audience; The atrial-specific ultrarapid delayed rectifier K+ current (IKur) inactivates slowly but completely at depolarized voltages. The consequences for IKur rate-dependence have not been analyzed in detail and currently available mathematical action-potential (AP) models do not take into account experimentally observed IKur inactivation dynamics. Here, we developed an updated formulation of IKur inactivation that accurately reproduces time-, voltage-, and frequency-dependent inactivation. We then modified the human atrial cardiomyocyte Courtemanche AP model to incorporate realistic IKur inactivation properties. Despite markedly different inactivation dynamics, there was no difference in AP parameters across a wide range of stimulation frequencies between the original and updated models. Using the updated model, we showed that, under physiological stimulation conditions, IKur does not inactivate significantly even at high atrial rates because the transmembrane potential spends little time at voltages associated with inactivation. Thus, channel dynamics are determined principally by activation kinetics. IKur magnitude decreases at higher rates because of AP changes that reduce IKur activation. Nevertheless, the relative contribution of IKur to AP repolarization increases at higher frequencies because of reduced activation of the rapid delayed-rectifier current IKr. Consequently, IKur block produces dose-dependent termination of simulated atrial fibrillation (AF) in the absence of AF-induced electrical remodeling. The inclusion of AF-related ionic remodeling stabilizes simulated AF and greatly reduces the predicted antiarrhythmic efficacy of IKur block. Our results explain a range of experimental observations, including recently reported positive rate-dependent IKur-blocking effects on human atrial APs, and provide insights relevant to the potential value of IKur as an antiarrhythmic target for the treatment of AF.

Aim: Varicocele is abnormal dilation of testis veins without unclear pathophysiology. Morphological studies showed imbalance between vasoconstrictor and vasodilator mechanisms. We aimed to determine the relationship between varicocele and cardiovascular system disorders with electrocardiography (ECG) parameters. Methods: This is a prospective study which was conducted in a University Hospital between February and June 2018. Thirty patients (18-45 years old) with high grade varicocele from urology outpatient clinic and 32 healthy volunteers for the control group were recruited to the study. Results: P-min. value was significantly higher in control group than patients with high grade varicocele (p= 0.03). PR, QT and QTc intervals, PWD and P-max values were similar. Also, there were no significant differences in terms of the other ECG parametersbetween the groups. Conclusions: In this small prospective study we have found no association between high grade varicocele and potential electrocardiographic arrhythmia predictors namely OTd, QTc interval, PWD, Tp-e interval, Tp-e/QT ratio and Tp-e/QTc ratio. Long-term follow-up and large-scale prospective studies are needed to confirm our results.

Analysis of atrial repolarization dynamics in ECG using system identification techniquesThe ARX model is used for studying the PTaI and PPI dynamics.Analysis of atrial repolarization variability and heart rate variability in healthy and AT subjects BackgroundThe interaction between the PTa and PP interval dynamics from the surface ECG is seldom explained. Mathematical modeling of these intervals is of interest in finding the relationship between the heart rate and repolarization variability. ObjectiveThe goal of this paper is to assess the bounded input bounded output (BIBO) stability in PTa interval (PTaI) dynamics using autoregressive exogenous (ARX) model and to investigate the reason for causing instability in the atrial repolarization process. MethodsTwenty-five male subjects in normal sinus rhythm (NSR) and ten male subjects experiencing atrial tachycardia (AT) were included in this study. Five minute long, modified limb lead (MLL) ECGs were recorded with an EDAN SE-1010 PC ECG system. The number of minute ECGs with unstable segments (Nus) and the frequency of premature activation (PA) (i.e. atrial activation) were counted for each ECG recording and compared between AT and NSR subjects. ResultsThe instability in PTaI dynamics was quantified by measuring the numbers of unstable segments in ECG data for each subject. The unstable segments in the PTaI dynamics were associated with the frequency of PA. The presence of PA is not the only factor causing the instability in PTaI dynamics in NSR subjects, and it is found that the cause of instability is mainly due to the heart rate variability (HRV). ConclusionThe ARX model showed better prediction of PTa interval dynamics in both groups. The frequency of PA is significantly higher in AT patients than NSR subjects. A more complex model is needed to better identify and characterize healthy heart dynamics.

Atrial fibrillation (AF) is associated with increased morbidity and mortality. Atrial-selective potassium (K(+)) channel blockers may represent a novel therapeutic target. The best validated atrial-specific ion currents are the acetylcholine-activated inward-rectifier K(+) current IK,ACh and ultrarapidly activating delayed-rectifier K(+) current IKur. Two-pore domain and small-conductance Ca(2+)-activated K(+) channels and Kv1.1 channels may also contribute to the atrial repolarization. We review the molecular and electrophysiologic characteristics of atrial-selective K(+) channels and their potential pathophysiologic role in AF. We summarize currently available K(+) channel blockers focusing on the most important compounds.

Electrocardiography represents a relevant diagnostic tool for detecting cardiac disease in animals. Elephants can present various congenital and acquired cardiovascular diseases. However, few electrophysiologic studies have been reported in captive elephants, mainly due to challenging technical difficulties in obtaining good-quality electrocardiogram (ECG) tracings, and no data are currently available for free-ranging Asian elephants (Elephas maximus). The purpose of this pilot prospective study was to evaluate the feasibility of using a simple method for recording ECG tracings in wild, apparently healthy, unsedated Asian elephants (n = 7) in the standing position. Successful six-lead recordings (I, II, III, aVR, aVL, and aVF) were obtained, with the aVL lead providing the best-quality tracings in most animals. Variables measured in the aVL lead included heart rate, amplitudes and duration of the P waves, QRS complexes, T and U waves, and duration of the PR, QT, and QU intervals. A negative deflection following positive P waves, representative of an atrial repolarization wave (Ta wave), was observed for five out of the seven elephants.

We present a case of atrial repolarization waves from an ectopic atrial rhythm mimicking inferior ST segment elevation myocardial infarction in a 78-year-old male patient who presented with left sided chest wall and shoulder pain. His ischemic workup was negative, and the ST elevations completely resolved upon the resumption of sinus rhythm before discharge.

The aim of this study is to characterize the observable segment of the atrial repolarization (Ta wave) of the standard ECG during sinus rhythm in paroxysmal atrial fibrillation (PAF) patients and controls.Ta and P waves were measured from signal-averaged recordings of a standard 12-lead ECG in 40 patients, 20 with PAF, but in SR at the time of recording, and 20 healthy controls. Wave amplitudes and morphologies were measured.There were no significant differences in Ta amplitude between the PAF patients and controls. A subgroup analysis of patients on and off anti-arrhythmic drugs also showed no significant differences in Ta amplitudes. For both groups Ta wave had opposite polarity to the monophasic P wave. Biphasic P waves had Ta polarity opposite to the initial phase of the P wave. Ta wave amplitudes were largest in leads II (mean ± SD, –25 ± 16 μV), V2 (–22 ± 10 μV), V3 (–21 ± 10 μV) and V4 (–20 ± 8 μV). A significant correlation was found between Ta and P wave amplitudes, leads recording larger P waves also had larger Ta waves (PAF group: r = 0.15 (P = 0.02) PAF vs r = 0.33 (P = 0.002) HC).No differences in the amplitude of the observable section of the atrial repolarization phase of the ECG could be observed between patients with PAF and controls. Ta wave correlates with the corresponding P wave in both amplitude and polarity.

Objective—To characterize the electrocardiographic features of the atrial repolarization (Ta) wave in dogs with third-degree atrioventricular (AV) block. Sample—ECGs of 36 dogs with third-degree AV block and no identifiable structural heart diseases. Procedures—Standard 12-lead ECGs were acquired with a digital system, and measurements were manually edited. Results—A Ta wave was detectable in all dogs for at least 1 ECG lead. The Ta wave had negative polarity in leads I, II, III, and aVF and positive polarity in leads aVL and aVR, with a mean electrical axis of −114.26°. Mean duration and mean amplitude of the Ta wave in lead II were 140.2 milliseconds and −0.09 mV, respectively, with the ratio for the Ta-to-P wave duration of 2.3 and the ratio of Ta-to-P wave amplitude of −0.35. Significant correlations were found between the Ta wave duration and duration of the P-Ta interval, Ta wave amplitude and the ECG lead, Ta wave duration and body weight, and duration of the P-Ta interval and atrial rate. Measurements of the Ta wave were repeatable. Conclusions and Clinical Relevance—Measurements of the Ta wave in dogs with third-degree AV block were repeatable. The values for the Ta wave reported here can be used as reference values for dogs with AV conduction disturbances and an echocardiographically normal atrial size. Further studies are needed to validate these results in dogs with structural heart diseases.

Atrial fibrillation (AF) is one of the most common arrhythmia encountered in clinical practice. Although AF is due to the structural and electrophysiological alterations in the atria, its sustainability is multifactorial, and the actual mechanisms are still not clear. Despite the recent advances in catheter ablation technology and techniques, pharmacotherapy still remains the first-line therapy for the management of AF. Current pharmacotherapy targets ion channel alterations that in fact represent only one aspect of the management of this complex arrhythmia. Successful pharmacological treatment of AF and restoration of sinus rhythm is limited and is in part due to its potential deleterious side effects. Newer agents having diverse mechanisms acting on the recently uncovered pathophysiological processes are on the horizon. These include atrial repolarization delaying agents, newer class III agents, Na(+)-Ca(2+) channel blockers, stretch receptor blockers, I(KACH) blockers, gap junction modifiers, upstream therapies, and agents targeting ischemia-induced AF. Gene- and cell-specific therapies including 'tailored nanopharmacy,' newer rate control medications with minimal side effects and the emergence of novel drugs targeting multiple areas of AF arrhythmogenesis in tandem with electrical therapy may be the future direction in the management of AF.

Right atrial effective refractory periods (AERP) and monophasic action potentials (MAP) have been determined in 29 healthy males in four different age groups between 25 and 64 years. One age group (45-54 years) showed a significantly longer AERP than the others, with a mean of 283 msec compared with 230-238 msec in the other groups. However, no age trend was found in the total material. The AERP decreased at higher paced heart rates, the decrease between paced cycle lengths of 800 and 600 msec amounting to 13 msec. When the MAP and the AERP were determined in the same position of the atrium, they showed no statistically significant correlation. A possible explanation is that the cells contributing to the AERP and the MAP are not altogether the same. The MAP and the AERP determinations have a similar degree of reproducibility but possibly mirror different kinds of repolarization phenomenon.

Antiarrhythmic drugs are an essential tool in the management of atrial fibrillation (AF). Although we are already on the threshold of a large expansion in the use of ablation therapies, these will not, however, be appropriate for all patients, and pharmacological therapies will continue to have an important place in the management of atrial fibrillation. The plethora of antiarrhythmic drugs currently available for the treatment of atrial fibrillation is a reflection that none is wholly satisfactory, each having limited efficacy combined with poor safety and tolerability. Improved class III antiarrhythmic drugs, such as dronedarone, new classes of antiarrhythmic agents, such as atrial repolarization delaying agents, and upstream therapies dealing with substrate, represent potential sources of new pharmacological therapies. Copyright © 2008 Wiley Periodicals, Inc.

The aim of the study was to explore the global sequence of atrial repolarization and its correlation to that of activation. Endocardial monophasic action potentials (MAPs) were sequentially recorded from 51 +/- 14 sites in the right atrium of ten healthy pigs using the CARTO electroanatomic mapping system. Local activation time (AT), MAP duration, and 90% repolarization time (RT) were obtained, and from these data, color coded three-dimensional maps of AT and RT sequences and spatial distribution of MAP duration were reconstructed. The results of the study were: (1) An activation sequence was recognizable in all maps, starting from the posterosuperior wall and ending in the posteroinferior wall near the tricuspid annulus. (2) The repolarization sequence was also recognizable in all maps, and mainly followed the sequence of activation. (3) A significant positive correlation between the RT and AT was observed in all maps with an average r value being 0.571 +/- 0.159 (P < 0.01 - 0.0001), suggesting that progressively later AT associates with progressively longer RT. (4) No consistent correlation between the MAP duration and AT was found. In conclusion, repolarization gradients exist over the atrial endocardium in healthy pigs. The repolarization sequence follows the same sequence as the activation, suggesting that the spatiotemporal pattern of activation is an important determinant of the characteristics of the repolarization sequence.

Objective - To investigate the feasibility of monophasic action potential ( MAP) mapping using an electro-anatomical mapping system ( CARTO) in obtaining information on global dispersion of atrial repolarization and to evaluate the role of dispersion of repolarization in the genesis of paroxysmal atrial fibrillation ( PAF). Methods and results - Right atrial MAPs were recorded from 53 +/- 18 sites in 10 healthy pigs and 33 +/- 21 sites in 6 patients with and 4 patients without history of PAF. In pigs, the global dispersions of activation time ( AT), MAP duration and end of repolarization time ( EOR), 70 +/- 8, 95 +/- 18 and 121 +/- 28 ms, respectively, were significantly greater than those among 10, 20 and 30 sites. In patients with PAF, the global dispersions of MAP duration and EOR ( 128 +/- 10 and 149 +/- 31 ms) were significantly greater than those in patients without PAF ( 84 +/- 10 and 91 +/- 17 ms). Conclusion - MAP mapping using the CARTO system was feasible in experimental and clinical settings in obtaining information on global dispersion of atrial repolarization. The number of recording sites could significantly affect repolarization parameters. The dispersions of atrial repolarization were significantly greater in patients with PAF than those without, suggesting the involvement of an increased dispersion of repolarization in the genesis of PAF.

To study the role of the dispersion of atrial repolarization (DAR) in the genesis of atrial fibrillation (AF), monophasic action potentials (MAP) were recorded simultaneously from a catheter at the high lateral right atrium (HLRA) and a catheter moving around the high, middle and low lateral right atrium (RA) the high, anterior and posterior septal RA and the RA appendage in 15 patients with paroxysmal AF and 15 patients with atrioventricular nodal re-entry tachycardia (AVNRT) or concealed Wolff-Parkinson-White syndrome (WPW) without history of AF. After recordings during sinus rhythm (SR), MAPs were recorded during programmed stimulation (PS) via the HLRA catheter at a drive cycle length (CL) of 500 ms. Thus, MAPs were recorded simultaneously from 2 sites at a time and sequentially from 4 to 12 sites during SR, drive pacing and PS. Taking the MAP at the HLRA as reference, the dispersion of repolarization time (dispersion of RT) and its two components, the dispersions of activation time (dispersion of AT) and MAP duration (dispersion of MAP duration) among the 4 to 12 sites were calculated and taken as parameters of DAR. RESULTS: During SR and PS, the maximal dispersion of RT was significantly greater in AF than in control patients, 113+/-49 ms vs 50+/-28 ms (P

Although the atrial free wall is a thin structure, atrial depolarization has been shown to have aspects of three-dimensionality. This study asks whether the same is true for atrial repolarization. By using a multi-element dual-surface probe, monophasic action potentials (MAPs) were recorded simultaneously at several opposing sites on the right atrial endocardial and epicardial surfaces in six open-chest pigs. The times of depolarization and repolarization were marked in recordings during sinus, paced rhythms, and during infusions of cold saline to the epicardial surface, which generated a temperature gradient across the atrial wall. Repolarization times were similar on endocardial and epicardial surfaces in some cites, but others showed significant differences during sinus and paced rhythms. Cold saline infusion produced a significant lengthening of MAP duration, and this was more pronouced on the atrial endocardial sites than on the epicardial sites. The observed differences in endocardial and epicardial repolarization times may be due to the presence of atrial pectinate muscles on the endocardial surface. These results suggest that in some regions atrial repolarization is a three-dimensional process. Possible limitations of this study include the fact that the depth of view of MAPs recorded from the atrial wall may extend to the opposing surface.

Background: Although up to 30% of short QT syndrome (SQTS) patients suffer from atrial arrhythmias, less is known about atrial repolarization abnormalities. PQ segment depression (PQD) is a well defined ECG marker of acute pericarditis. PQD is related to atrial fibrillation and carries a poor prognosis in the setting of acute inferior myocardial infarction, and it has been rarely observed during ablation of the left upper pulmonary vein. Objective: The aim of this study was to evaluate the incidence of PQD in SQTS and to analyze the association between PQD and atrial arrhythmias. Methods: Digitalized resting 12-lead ECGs of SQTS patients were analyzed for PQD in all leads and for QT and Tpeak-Tend intervals in leads II and V5. PQD was defined as ≥ 0.05 mV (0.5 mm) depression from the isoelectric line. The QT and Tpeak-Tend intervals were measured by a standard tangential method in leads II and V5 and were corrected according to Bazett's formula. Results: 790 leads from 67 SQTS patients [mean age 36±18 years, 49 males (73%)] were analyzed (14 leads of three patients were missing). PQD was seen in 54 (80%) patients and in 276 (35%) leads and was more frequent in leads II, V3, V4, I, and aVF [n=45 (67%), n=31 (46%), n=26 (43%), n=26 (39%), n=28 (41%), respectively] and also more prominent in lead II. QTc (II), QTc (V5) and Tpeak-Tend (II), Tpeak-Tend (V5) intervals were not significanty different between patients with PQD in any lead and without PQD in any lead (321±34 ms, 324±29 ms, 70±11 ms, 70±14 ms; vs 323±25 ms, 320±28 ms, 64±11 ms, 66±12 ms; respectively, p=ns for all intervals). There was also no significant difference between patients with and without PQD in any inferior lead. Tpeak-Tend (II) intervals were significantly longer in patients with PQD in leads V1, V3, V4 and V5 (74±10 ms, 73±12 ms, 75±12 ms, 76±9 ms; vs 67±14 ms, 66±17 ms, 66±11 ms, 68±13 ms; respectively, p

Studies have confirmed that apamin sensitive SK channels express abundantly on cardiac myocytes and atrioventricular node cells, play an important role in human atrial repolarization, modulate human ventricular repolarization and participate in atrioventricular nodal function. So, the roles of

Atrial fibrillation (AF) is the most common cardiac arrhythmia, and the total number of AF patients is constantly increasing. The mechanisms leading to and sustaining AF are not completely understood yet. Heterogeneities in atrial electrophysiology seem to play an important role in this context. Although some heterogeneities have been used in in-silico human atrial modeling studies, they have not been thoroughly investigated. In this study, the original electrophysiological (EP) models of Courtemanche et al., Nygren et al. and Maleckar et al. were adjusted to reproduce action potentials in 13 atrial regions. The parameter sets were validated against experimental action potential duration data and ECG data from patients with AV block. The use of the heterogeneous EP model led to a more synchronized repolarization sequence in a variety of 3D atrial anatomical models. Combination of the heterogeneous EP model with a model of persistent AF-remodeled electrophysiology led to a drastic change in cell electrophysiology. Simulated Ta-waves were significantly shorter under the remodeling. The heterogeneities in cell electrophysiology explain the previously observed Ta-wave effects. The results mark an important step toward the reliable simulation of the atrial repolarization sequence, give a deeper understanding of the mechanism of atrial repolarization and enable further clinical investigations.

Kinetics of Atrial Repolarization Alternans. INTRODUCTION: Repolarization alternans (Re-ALT), a beat-to-beat alternation in action potential repolarization, promotes dispersion of repolarization, wavebreaks, and reentry. Recently, Re-ALT has been shown to play an important role in the transition from rapid pacing to atrial fibrillation (AF) in humans. The detailed kinetics of atrial Re-ALT, however, has not been reported so far. We developed a chronic free-behaving ovine pacing model to study the kinetics of atrial Re-ALT as a function of pacing rate. METHODS: Thirteen sheep were chronically implanted with 2 pacemakers for the recording of broadband right atrial unipolar electrograms and delivery of rapid pacing protocols. Beat-to-beat differences in the atrial T-wave apex amplitude as a measure of Re-ALT and activation time were analyzed at incremental pacing rates until the effective refractory period (ERP) defined as stable 2:1 capture. RESULTS: Atrial Re-ALT appeared intermittently but without periodicity, and increased in amplitude as a function of pacing rate until ERP. Intermittent 2:1 atrial capture was observed at pacing cycle lengths 40 ms above ERP, and increased in duration as a function of pacing rate. Episodes of rapid pacing-induced AF were rare, and were preceded by Re-ALT or complex oscillations of atrial repolarization, but without intermittent capture. CONCLUSION: We show in vivo that atrial Re-ALT developed and increased in magnitude with rate until stable 2:1 capture. In rare instances where capture failure did not occur, Re-ALT and complex oscillations of repolarization surged and preceded AF initiation. (J Cardiovasc Electrophysiol, Vol. 23, pp. 1003-1012, September 2012).

We appreciate the insightful and clinically relevant comments of Dr Madias on our recent study.1 Dr Madias hypothesizes that prolongation of the P wave on the surface ECG, which has been epidemiologically linked with atrial fibrillation (AF),2 may complement our report1 that oscillations of atrial repolarization indicate a spectrum of AF vulnerability from control subjects without AF, through patients with paroxysmal AF to those with persistent AF. We have recently studied this issue3 by analyzing biatrial conduction in these patients to test the hypothesis that dynamic conduction slowing indicates vulnerability to AF, and may be most marked at the site of AF initiation. It is noteworthy that baseline ECG P-wave duration did not differ between control subjects and patients with …

Objectives. To establish a set of reference values for regional dispersion of repolarization of the right atrium in the in situ heart of pigs and to see if the global dispersion of repolarization could be estimated from regional mapping. Design. Monophasic action potential (MAP) were sequentially recorded from 28 ± 3 sites in seven different regional areas of the right atrium: lateral, anterior and posterior wall, septum, sinoatrial node (SAN), appendage, and near the tricuspid annulus (TA) in 10 healthy pigs using the CARTO mapping system. Results. The activation time (AT), MAP duration (MAPd) and end of repolarization time (EOR) of the whole right atrium were 68 ± 7, 239 ± 20 and 270 ± 23 ms, respectively. There were no significant differences on MAPd and EOR among the seven regional areas, nor between each of the regional and global values. The global dispersions of the MAPd and EOR were 75 ± 19 and 103 ± 13 ms, which were significantly greater than those obtained from any of the seven regional areas and those between two remote regions, SAN vs. TA and SAN vs. appendage regions. Conclusions. The data of regional and global dispersion of repolarization in healthy pigs can serve as reference values for evaluation of increased dispersion of repolarization. The global dispersions of MAPd and EOR in the right atrium were poorly estimated from regional mapping, suggesting the importance of global mapping in evaluating the dispersion of atrial repolarization.

Aims Patients with Brugada syndrome (BS) often experience atrial fibrillation (AF) and atrial vulnerability, as measured by increased atrial conduction time. To date, however, dispersion of atrial repolarization has not been reported in these patients. Methods and results Monophasic action potentials (MAPs) recorded from four sites of the right atrium were analysed in 11 patients (10 men, 1 woman; mean age, 40 ± 9 years) with BS and in 10 controls (8 men, 2 women; mean age, 35 ± 8 years). None of these patients had a history of AF. Monophasic action potentials were recorded during right atrial pacing at a drive cycle length of 600 ms after continuous pacing. Dispersion of MAP duration (D-MAPD90) was defined as the difference between the maximum and minimum MAP duration measured at 90% repolarization (MAPD90). Inducibility of AF and repetitive atrial firing were also determined. The MAPD90 did not differ significantly between the BS and control groups (245 ± 42 vs. 228 ± 24 ms, P = ns), but D-MAPD90 was significantly higher in the BS group (69.1 ± 35.0 vs. 41.4 ± 10.3 ms, P < 0.05). Atrial fibrillation was induced in six BS patients and repetitive atrial firing in four, but neither was induced in any of the control subjects. Conclusion The significantly increased dispersion of MAPD90 observed in patients with BS suggests that the heterogeneity of atrial repolarization may contribute to the development of atrial fibrillation in patients with BS.

The repolarizing T a wave of normal sinus rhythm is not fully visible unless there is a long P-R interval or complete atrioventicular block. Even with the latter, it is often of unseeably low voltage. It can powerfully influence inferior lead ST deviation in the stress test. The T a of inverted or retrograde P waves is of higher voltage than that of sinus rhythm and can simulate inferior injury. Evidence of specialized internodal tracts resides in 2 specific atrial action potential properties: resistance to gross hyperkalemia and supernormality. The T a wave figures essentially in the diagnosis of acute atrial infarction.

Small conductance Ca2+-activated K+ channels (SK channels) have been reported in excitable cells, where they aid in integrating changes in intracellular Ca2+ with membrane potential. We have recently reported the functional existence of SK2 channels in human and mouse cardiac myocytes. Moreover, we have found that the channel is predominantly expressed in atria compared to the ventricular myocytes. We hypothesize that knockout of SK2 channels may be sufficient to disrupt the intricate balance of the inward and outward currents during repolarization in atrial myocytes. We further predict that knockout of SK2 channels may predispose the atria to tachy-arrhythmias due to the fact that the late phase of the cardiac action potential is highly susceptible to aberrant excitation. We take advantage of a mouse model with genetic knockout of the SK2 channel gene. In vivo and in vitro electrophysiological studies were performed to probe the functional roles of SK2 channels in the heart. Whole-cell patch-clamp techniques show a significant prolongation of the action potential duration prominently in late cardiac repolarization in atrial myocytes from the heterozygous and homozygous null mutant animals. Morover, in vivo electrophysiological recordings show inducible atrial fibrillation in the null mutant mice but not wild-type animals. No ventricular arrhythmias are detected in the null mutant mice or wild-type animals. In summary, our data support the important functional roles of SK2 channels in cardiac repolarization in atrial myocytes. Genetic knockout of the SK2 channels results in the delay in cardiac repolarization and atrial arrhythmias.

Electrogram analysis is important in clinical and experimental settings. Activation recovery interval (ARI) has been used to measure ventricular action potential duration (APD) but its suitability for the atria has not been addressed. Mapping of atrial repolarization may be especially important during nerve stimulation since large heterogenous APD changes may manifest. This study assessed the utility of estimating APD in the atria using electrograms. A computer model of the atria was used to compute electrograms. Two different atrial waveforms were used, as well as two ventricular. APD was modulated with an acetylcholine- (ACh) dependent potassium channel and varying the spatial ACh distribution. ARI was computed, as well as the area under the repolarization wave (ATa). APD was measured by four methods. Atrial electrograms were also compared to monophasic action potentials recorded from a dog. ARI computed from atrial action potentials was not very precise, with errors ranging over 30 ms. Determining changes in APD induced by changing [ACh] yielded larger errors. Conversely, ventricular action potentials produced ARIs that very closely correlated with APD, and changes in APD . Positive ATa indicated regions of shortened APD, and islands of ACh release were clearly demarcated by ATa polarity. Experimentally, ARI was able to detect changes in APD, but did not measure APD well. The faster rate of ventricular repolarization produces larger currents that are less susceptible to electrotonic coupling effects, improving correlation with APD. ARI most closely correlated with APD measured as a fixed threshold above rest. Atrial APs produce electrograms that can be used to detect changes in APD. This may be improved by decreasing coupling. The ATa is a robust measure for precisely identifying spatial APD heterogeneities.

Atrial fibrillation is the most common cardiac arrhythmia in humans. The precise cellular mechanisms underlying atrial fibrillation are still poorly understood. Recent studies have identified several genetic defects as predisposing factors for this pathology. One of the identified genetic defects is the mutation N588K, which affects the cardiac IKr channel. Genetic variants in this channel have been identified to modify ventricular repolarization. The aim of this work is to investigate the effect of this mutation on atrial repolarization and the predisposition to atrial fibrillation.

Item does not contain fulltext OBJECTIVE: We aimed to study the involvement of atrial repolarization in body surface potentials. METHODS: Electrocardiograms of healthy subjects were recorded using a 64-lead system. The data analysis focused on the PQ intervals while devoting special attention to the low-amplitude signals during the PQ segment: the segment from the end of the P wave until onset QRS. The data were analyzed by inspecting body surface potential maps and the XYZ signals of the vectorcardiogram. RESULTS: Standard P-wave features exhibited normal values. The local potential extremes were found at positions not sampled by the standard leads. The PQ segment was found to be not isoelectric, the time course of the potential distribution being very similar to that during the P wave but for a reversed polarity and about 3-fold lower magnitudes. CONCLUSION: The results demonstrate a significant involvement of atrial repolarization during the PQ interval and essentially discordant "atrial T waves," suggesting a small dispersion of atrial action potential durations.

The timing diagram model could provide the cardiologist with the ways and means of quantifying interval/segment patterns. This analysis would be more exact than present use of electrocardiograms, which relies on subjective analyses of pathological events and the graph patterns they present. Improving the predictability of pathological events by filtering out overriding ventricular depolarization could identify sequential patterns of the atrial repolarization interval/segment. A healthy heart could provide a standard against which specific syndromes might be compared and contrasted for diagnostic purposes. The clinician would have yet another diagnostic tool which could identify patterns requiring aggressive preventive therapy much earlier in the clinical cycle of the patient with a family history of cardiovascular disease. Results of various treatments prescribed for the broad spectrum of cardiological pathologies could also be evaluated in relation to the manner in which these treatments bring the cardiac cycle into synchrony with normal patterns. This comparison would be accomplished by comparing the sequencing and length of time for specific interval/segment patterns demonstrated before, during, and after the treatment occurs. If successful, the proposed analysis of the ECG would ultimately contribute to more positive outcomes for patients who presently may have a poor prognosis. >