Atrial Premature Depolarizations Research Articles

Intracardiac ultrasound-guided transseptal puncture in horses: Outcome, follow-up, and perioperative anticoagulant treatment.

Cardiac catheterizations in horses are mainly performed in the right heart, as access to the left heart traditionally requires an arterial approach. Transseptal puncture (TSP) has been adapted for horses but data on follow-up and closure of the iatrogenic atrial septal defect (iASD) are lacking. To perform TSP and assess postoperative complications and iASD closure over a minimum of 4 weeks. Eleven healthy adult horses. Transseptal puncture was performed under general anesthesia. Serum cardiac troponin I concentrations were measured before and after puncture. Weekly, iASD closure was monitored using transthoracic and intracardiac echocardiography. Relationship between activated clotting time and anti-factor Xa activity during postoperative enoxaparin treatment was assessed in vitro and in vivo. Transseptal puncture was successfully achieved in all horses within a median duration of 22 (range, 10-104) minutes. Balloon dilatation of the puncture site for sheath advancement was needed in 4 horses. Atrial arrhythmias occurred in 9/11 horses, including atrial premature depolarizations (N = 1), atrial tachycardia (N = 5), and fibrillation (N = 3). Serum cardiac troponin I concentrations increased after TSP, but remained under the reference value in 10/11 horses. Median time to iASD closure was 14 (1-35) days. Activated clotting time correlated with anti-factor Xa activity in vitro but not in vivo. Transseptal puncture was successfully performed in all horses. The technique was safe and spontaneous iASD closure occurred in all horses. Clinical application of TSP will allow characterization and treatment of left-sided arrhythmias in horses.

Authors reply regarding "A-V-V-A response to single atrial premature depolarization in a narrow QRS tachycardia: What is the mechanism?"

We respond to a letter by Dr. A. Goyal. If the tachycardia were junctional ectopic tachycardia (JET), the occurrence of the ventriculoatrial block following an atrial premature depolarization could not be explained. Therefore, we conclude that atrioventricular nodal reentrant tachycardia was more likely than JET.

Yoshimura etal. A-V-V-A response to single atrial premature depolarization in a narrow QRS tachycardia: What is the mechanism?

Yoshimura etal. A-V-V-A response to single atrial premature depolarization in a narrow QRS tachycardia: What is the mechanism?

Upper common pathway analysis using late atrial premature depolarization in atrioventricular nodal reentry tachycardia

BackgroundAnatomic and electrophysiologic findings suggest that the actual circuit of atrioventricular nodal reentrant tachycardia (AVNRT) involves the perinodal atrium. However, occasional instances in which the atrium is dissociated from the AVNRT have led to the concept of an upper common pathway (UCP). ObjectiveWe aimed to assess the prevalence of UCP in AVNRT using a late atrial premature depolarization (LAPD) maneuver. MethodsPatients who were diagnosed with typical AVNRT by electrophysiologic studies were enrolled. For evaluation of the presence of UCP, an LAPD was given at the coronary sinus ostium (osCS) during AVNRT, and then pacing was repeated incrementally every 10 ms. Electrograms in the earliest retrograde atrial activation site (ERAS) near the proximal His were mapped and recorded during the pacing. Results were interpreted as follows: absence of UCP—an LAPD from the osCS can reset the tachycardia without depolarizing the ERAS; presence of UCP—an LAPD from the osCS can depolarize the ERAS without resetting the tachycardia; and indeterminate—an LAPD from the osCS either resets the ERAS and tachycardia simultaneously or does not reset both. ResultsThe LAPD maneuver was performed in 126 patients with AVNRT. It demonstrated an absence of UCP in 121 (96.0%) patients and the presence of UCP in 3 (2.4%) patients; the result was indeterminate in 2 (1.6%) patients. ConclusionThe LAPD maneuver revealed that the presence of UCP is indicated in only rare cases of AVNRT. In most AVNRT cases, the atrium is involved in the reentry circuit.

A-V-V-A response to single atrial premature depolarization in a narrow QRS tachycardia: What is the mechanism?

We present an atypical response to single atrial premature depolarization (APD) in a long RP' tachycardia. APD advanced the His-bundle potential immediately after it and resulted in a VA block; however, tachycardia persisted and consequently exhibited an A-V-V-A response. We propose the mechanism for an A-V-V-A response to APD in a long RP' tachycardia.

Utility of intracardiac echocardiography during ablation of atrial premature depolarizations with a prominent Chiari network

Utility of intracardiac echocardiography during ablation of atrial premature depolarizations with a prominent Chiari network

Delayed termination and transformation of a supraventricular tachycardia—What is the mechanism?

A 75-year-old woman underwent a diagnostic electrophysiology study because of a recurrent, symptomatic, drug-refractory supraventricular tachycardia (SVT). The 12-lead electrocardiogram showed only mild PR prolongation. Atrio-His and His-ventricular intervals measured 140 and 45 ms, respectively. She demonstrated retrograde ventriculoatrial activation that was earliest at the anteroseptum and decremental. Single atrial extrastimulation and spontaneous atrial premature depolarizations (APDs) repeatedly induced a short RP SVT.

An Exploratory Study on Vectorcardiographic Identification of the Site of Origin of Focally Induced Premature Depolarizations in Horses, Part I: The Atria.

Simple SummaryArrhythmias are common in horses, but in order to offer adequate treatment, the anatomical location from where the arrhythmia originates must first be known. The objective of this study was to differentiate between the various anatomical origins of atrial premature depolarizations and to further differentiate these from normal sinus rhythm based upon the vectorcardiography characteristics of seven horses without cardiovascular disease. With vectorcardiography, the magnitude and direction of the cardiac electrical forces were derived from an electrocardiographic recording and were plotted in three dimensions. The three directions were represented by the right–left axis, head–tail axis, and dorsoventral axis. Under general anaesthesia, atrial premature depolarizations were induced by pacing inside the heart, guided by a 3D mapping system that allowed us to see the 3D position of the pacing catheter inside the heart in real-time. An adapted statistical test optimized for spherical data was used to demonstrate that the maximal directions of the first and second half of the P wave showed significant differences between the paced locations and between the paced complexes and sinus rhythm. The current study provides a practical approach to identifying the approximate site of origin of an atrial arrhythmia using a custom 12-lead ECG.In human cardiology, the anatomical origin of atrial premature depolarizations (APDs) is derived from P wave characteristics on a 12-lead electrocardiogram (ECG) and from vectorcardiography (VCG). The objective of this study is to differentiate between anatomical locations of APDs and to differentiate APDs from sinus rhythm (SR) based upon VCG characteristics in seven horses without cardiovascular disease. A 12-lead ECG was recorded under general anaesthesia while endomyocardial atrial pacing was performed (800–1000 ms cycle length) at the left atrial free wall and septum, right atrial free wall, intervenous tubercle, as well as at the junction with the cranial and caudal vena cava. Catheter positioning was guided by 3D electro-anatomical mapping and transthoracic ultrasound. The VCG was calculated from the 12-lead ECG using custom-made algorithms and was used to determine the mean electrical axis of the first and second half of the P wave. An ANOVA for spherical data was used to test if the maximal directions between each paced location and the maximal directions between every paced location and SR were significantly (p < 0.05) different. Atrial pacing data were not available from the LA septum in three horses, the intervenous tubercle in two horses, and from the LA free wall in one horse. The directions of the maximal electrical axes showed significant differences between all paced locations and between the paced locations and SR. The current results suggest that VCG is useful for identifying the anatomical origin of an atrial ectopy.

An unusual incessant long RP tachycardia—What is the mechanism?

A 40-year-old man underwent a diagnostic electrophysiology study because of a slow incessant long RP supraventricular tachycardia (SVT). Echocardiography revealed an ejection fraction of 35%. Upon presentation to the electrophysiology laboratory, he was in SVT. His refractory ventricular premature depolarizations (VPDs) delivered from the right ventricular (RV) apex failed to affect the tachycardia; the responses to earlier VPDs and coronary sinus (CS) atrial premature depolarizations (APDs) are shown in Figure 1, top and bottom, respectively.

Change in VA interval by a single atrial premature depolarization - What is the mechanism?

A long VA tachycardia during a typical atrioventricular nodal reentrant tachycardia (AVNRT) can be a concomitant atypical AVNRT, atrial tachycardia or rarely atrio-ventricular reentrant tachycardia (AVRT). There are reported associations of AVNRT with other tachycardia substrates. Maneuvers are useful for differentiating the mechanism of the second tachycardia. Atrial tachycardia (AT) is one common association. When the AT originates from the lower triangle of Koch/near coronary sinus ostium, it can mimic slow-slow/fast-slow AVNRT. We encountered an interesting case where a longer VA tachycardia got reproducibly induced when a critically timed atrial premature depolarisation was delivered on typical AVNRT. It was proved to be an AT. A slow pathway modification in the lower TOK was successful to eliminate both the tachycardia substrate.

Atrial fibrillation in horses part 1: Pathophysiology

Atrial fibrillation (AF) is the most common clinically relevant arrhythmia in horses, with a reported prevalence up to 2.5%. The pathophysiology has mainly been investigated in experimental animal models and human medicine, with limited studies in horses. Atrial fibrillation results from the interplay between electrical triggers and a susceptible substrate. Triggers consist of atrial premature depolarizations due to altered automaticity or triggered activity, or local (micro)reentry. The arrhythmia is promoted by atrial myocardial ion channel alterations, Ca2+ handling alterations, structural abnormalities, and autonomic nervous system imbalance. Predisposing factors include structural heart disease such as valvular regurgitation resulting in chronic atrial stretch, although many horses show so-called ‘lone AF’ or idiopathic AF in which no underlying cardiac abnormalities can be detected using routine diagnostic techniques. These horses may have underlying ion channel dysfunction or undiagnosed myocardial (micro)structural alterations. Atrial fibrillation itself results in electrical, contractile and structural remodelling, fostering AF maintenance. Electrical remodelling leads to shortening of the atrial effective refractory period, promoting reentry. Contractile remodelling consists of decreased myocardial contractility, while structural remodelling includes the development of interstitial fibrosis and atrial enlargement. Reverse remodelling occurs after cardioversion to sinus rhythm, but full recovery may take weeks to months depending on duration of AF. The clinical signs of AF depend on the aerobic demands during exercise, ventricular rhythm response and presence of underlying cardiac disease. In horses with so-called ‘lone AF’, clinical signs are usually absent at rest but during exercise poor performance, exercise-induced pulmonary hemorrhage, respiratory distress, weakness or rarely collapse may develop.

Incidence of Left Atrial Appendage Triggers in Patients With Atrial Fibrillation Undergoing Catheter Ablation

This study sought to investigate incidence of left atrial appendage (LAA) triggers of atrial fibrillation (AF) and/or organized atrial tachycardias (OAT) in patients undergoing AF ablation and to evaluate outcomes after ablation. Although LAA isolation is being increasingly performed during AF ablation, the true incidence of LAA triggers for AF remains unclear. All patients with LAA triggers of AF and/or OAT during AF ablation from 2001 to 2017 were included. LAA triggers were defined as atrial premature depolarizations from the LAA, which initiated sustained AF and/or OAT. Out of 7,129 patients undergoing AF ablation over 16 years, LAA triggers were observed in 21 (0.3%) subjects (age 60 ± 9 years; 57% males; 52% persistent AF). Twenty (95%) patients were undergoing repeat ablation. The LAA was the only nonpulmonary vein trigger in 3 patients; the remaining 18 patients had both LAA and other nonpulmonary vein triggers. LAA triggers were eliminated in all patients (focal ablation in 19 patients; LAA isolation in 2 patients). Twelve months after ablation, 47.6%remained free from recurrent arrhythmia. After overall follow-up of 5.0 ± 3.6 years (median: 3.7 years; interquartile range: 1.4 to 8.9 years), 38.1% were arrhythmia-free. All 3 patients with triggers limited to the LAA remained free of AF recurrence. One patient undergoing LAA isolation developed LAA thrombus during follow-up. The incidence of true LAA triggers is very low (0.3%). Most patients with LAA triggers have additional nonpulmonary vein triggers, and despite elimination of LAA triggers, long-term arrhythmia recurrence rates remain high. Potential risks of empiric LAA isolation during AF ablation (especially first-time AF ablation) may outweigh benefits.

A 12‐lead electrocardiogram interpretation algorithm to determine the anatomical site of origin of atrial premature depolarizations in horses: preliminary data

A 12‐lead electrocardiogram interpretation algorithm to determine the anatomical site of origin of atrial premature depolarizations in horses: preliminary data

Accuracy of smartphone-based ECG for the diagnosis of various cardiac arrhythmias

Diagnosis of cardiac arrhythmias can be challenging due to their frequent transient nature. Smartphone-based ECG has previously been studied for atrial fibrillation (AF) diagnosis. However, data is lacking regarding diagnostic accuracy of smartphone-based ECGs for other frequent arrhythmias. To assess the accuracy of Alivecor smartphone-based ECG (AECG) device for the diagnosis of various bradyarrhythmias or tachyarrhythmias. Hospitalized patients were eligible for inclusion if they had any of the following arrhythmias: AF, atrial tachycardia/flutter (AT), sinus rhythm with frequent atrial premature depolarizations (APD), sinus rhythm with frequent ventricular premature depolarizations (VPD), sinus tachycardia > 120 beats/min, sinus bradycardia < 40 beats/min, high-degree atrioventricular (AV) block, atrioventricular node reentrant tachycardia (AVNRT) and ventricular tachycardia (VT). Reference twelve-lead ECG were recorded, and the corresponding one-lead AECG was independently interpreted by four blinded electrophysiologists. Seventy-three patients (57 men; aged 72 ± 14 years) were included. For the diagnosis of bradyarrhythmias, AECG had a sensitivity and specificity of 75%–95% for sinus bradycardia, and 52%–98% for AV block. For atrial tachyarrhythmias, sensitivites and specificites were good for APD (83%–97%), AF (82%–87%), and sinus tachycardia (86%–98%), whereas sensitivity was poor for AT (49%–93%) and AVNRT (10%–99%), with very frequent confusion between them. For ventricular tachyarrhythmias, sensitivities and specificities were 70%–95% for VPD, and 89%–100% for VT ( Table 1 , Fig. 1 ). AECG is accurate for the diagnosis of sinus bradycardia, sinus tachycardia, APD, VPD, AF and VT. However, AV block, AT and AVNRT were poorly diagnosed by AECG, with a low sensitivity and very frequent confusion between AT and AVRNT.

Atrial Premature Depolarization-Induced Changes in QRS and T Wave Morphology on Resting Electrocardiograms in Horses.

BackgroundThe electrocardiographic differentiation between atrial (APDs) and ventricular (VPDs) premature depolarizations is important. P wave prematurity and normal QRS and T wave morphology generally are used as discriminating criteria for APDs.Hypothesis/ObjectivesThe aim of this study was to determine whether P, Q, R, S, and T wave amplitude, PQ interval, QRS and P wave duration and P and T wave morphology differ between APDs and sinus beats. To determine the relationship between the RR coupling interval and the change in S wave amplitude between sinus beats and APDs.MethodsCase–control study. From a modified base‐apex configuration of 30 horses with APDs at rest, sinus beat and APD associated preceding RR interval, P, PQ and QRS duration and P, R, S, and T wave amplitudes were measured. Linear mixed models and logistic regression were used to determine the effect of APDs on the ECG variables studied.ResultsIn comparison to sinus beats, APDs were associated with a significant (P < .001) change in P amplitude (−0.03 ± 0.01 mV) and increase in S (0.20 ± 0.02 mV) and T (0.08 ± 0.03 mV) amplitude. PQ (−20.3 ± 5.2 ms) and RR (−519 ± 14 ms) interval and P duration (−21.1 ± 3.0 ms) decreased (P < .001). APDs were significantly associated with a singular positive P wave (OR: 11.0, P < .001) and were more likely to have a monophasic positive T wave (OR: 9.2, P < .001). A smaller RR coupling interval was associated with an increased relative difference in S amplitude (P < .01).ConclusionsAtrial premature depolarizations may lead to changes in QRS and T wave morphology. Knowledge of these changes is important to avoid interpreting certain APDs as VPDs.

Prevalence and distribution of focal triggers in persistent and long-standing persistent atrial fibrillation

The relevance of focal triggers in persistent atrial fibrillation (PerAF) and long-standing persistent atrial fibrillation (LSPAF) has not been previously investigated. We prospectively evaluated the prevalence and distribution of AF triggers in patients referred for catheter ablation of PerAF and LSPAF. We analyzed consecutive patients undergoing first time AF ablation who underwent a standardized trigger protocol including cardioversion of induced or spontaneous AF and infusion of up to 20 μg of isoproterenol for 15-20 minutes either before or after pulmonary vein (PV) isolation accomplished. Triggers were defined as AF/sustained atrial tachyarrhythmia or repetitive atrial premature depolarizations. A total of 2168 patients were included (mean age 57 ± 11 years; 1636 [75%] men), with 1531 patients having paroxysmal AF (PAF) (71%), 496 having PerAF (23%), and 141 having LSPAF (7%). PV triggers were found in 1398 patients with PAF (91%), 449 patients with PerAF (91%), and 129 patients with LSPAF (91%) (P = .856 for comparison across groups). Non-PV triggers were elicited in a total of 234 patients (11%), and the prevalence was similar across the different types of AF (PAF, 165 [11%]; PerAF, 54 [11%]; LSPAF, 15 [11%]; P = .996 for comparison across groups). PVs are the main AF trigger site in patients with PerAF and LSPAF, with an overall prevalence similar to that found in patients with PAF. These results support the current recommendations for PV isolation as the cornerstone of catheter ablation to eliminate AF triggers in PerAF and LSPAF.

Fast T Wave Detection Calibrated by Clinical Knowledge with Annotation of P and T Waves.

BackgroundThere are limited studies on the automatic detection of T waves in arrhythmic electrocardiogram (ECG) signals. This is perhaps because there is no available arrhythmia dataset with annotated T waves. There is a growing need to develop numerically-efficient algorithms that can accommodate the new trend of battery-driven ECG devices. Moreover, there is also a need to analyze long-term recorded signals in a reliable and time-efficient manner, therefore improving the diagnostic ability of mobile devices and point-of-care technologies.MethodsHere, the T wave annotation of the well-known MIT-BIH arrhythmia database is discussed and provided. Moreover, a simple fast method for detecting T waves is introduced. A typical T wave detection method has been reduced to a basic approach consisting of two moving averages and dynamic thresholds. The dynamic thresholds were calibrated using four clinically known types of sinus node response to atrial premature depolarization (compensation, reset, interpolation, and reentry).ResultsThe determination of T wave peaks is performed and the proposed algorithm is evaluated on two well-known databases, the QT and MIT-BIH Arrhythmia databases. The detector obtained a sensitivity of 97.14% and a positive predictivity of 99.29% over the first lead of the validation databases (total of 221,186 beats).ConclusionsWe present a simple yet very reliable T wave detection algorithm that can be potentially implemented on mobile battery-driven devices. In contrast to complex methods, it can be easily implemented in a digital filter design.

Holter monitoring, sinoatrial conduction time, prognosis

To evaluate the usefulness of the Holter method of sinoatrial conduction time (SACT) calculation in predicting the future occurrence of sinus node disease, and the emergence of indications for permanent pacing in patients with unexplained syncope. The study group included 218 patients (mean age 55 ± 17 years, 116 men) with syncope of unknown etiology in whom spontaneous atrial premature depolarizations (APDs) occurred during Holter monitoring and SACT could be calculated. A SACT value during daily activity > 150 ms was assumed as abnormal. The prospective observation time was 48 ± 11 months. During follow-up sinus node disease was diagnosed in 22 persons, including 18 patients with baseline SACT > 150 ms and 4 with SACT < 150 ms. Indications for pacemaker implantation were found in 16 patients, including 13 patients with baseline SACT > 150 ms and 3 with SACT < 150 ms. In subjects with and without sinus node disease diagnosed during the observation period, baseline SACTvalues were 175 ± 52 ms and 87 ± 34 ms, respectively (p < 0.01), and in patients qualified and not qualified for permanent pacing, the respective values were 178 ± 59 ms and 81 ± 38 ms(p < 0.01). Multivariate Cox analysis showed a significant relationship between baseline SACT > 150 ms and a future diagnosis of sinus node disease and pacemaker implantation. The results suggest that the Holter method of SACT calculation is useful in predicting sinus node disease and indications for permanent pacing in patients with unexplained syncope.

Superiorly directed atrial ectopy from the left inferior pulmonary vein

P wave morphology is often useful in planning and prognosticating invasive electrophysiology testing with an aim at ablation. It is generally believed that atrial ectopy of a pulmonary vein site of origin will be inferiorly directed. We report the case of superiorly directed P waves originating from the left inferior pulmonary vein, likely the result of a prior pulmonary vein isolation procedure. As demonstrated by our case, standard algorithms to identify the site of origin of atrial ectopy should be used with caution in patients with prior ablative procedures.

Catheter Ablation of an Unusual Decremental Accessory Pathway in the Left Coronary Cusp of the Aortic Valve Mimicking Outflow Tract Ventricular Tachycardia

The anatomic location of atrioventricular (AV) bypass tracts (or accessory pathways) is variable, but these generally traverse the tricuspid or mitral annulus and insert into the atrium and ventricle near the AV ring. There is only 1 case report of an accessory pathway ablated in the left coronary cusp (LCC),1 and this pathway had bidirectional conduction, was not decremental, and was associated with an orthodromic tachycardia. We report here the first case of an antegrade slowly conducting, decremental, accessory pathway that was also successfully ablated in the aortic LCC. This pathway generated antidromic tachycardia having a QRS morphology mimicking those seen in outflow tract ventricular tachycardia. A 42-year-old woman was evaluated for palpitations and presyncope for 2 years. These were commonly associated with shortness of breath and chest heaviness that would resolve spontaneously. Her baseline ECG was normal without ventricular preexcitation. Echocardiogram, coronary angiogram, and thyroid function were also unremarkable. On her third presentation to a hospital, a broad complex tachycardia was captured (representative 12-lead ECG shown in Figure 1). The cycle length was 480 ms, the QRS duration was 150 ms, and a left bundle branch morphology with a right inferior axis was noted. She was referred for ablation of suspected ventricular outflow tract tachycardia. Consent was obtained for mapping and ablation of this tachycardia. During placement of catheters, a spontaneous initiation of tachycardia occurred, which was noted to have 1:1 AV association. A quadripolar catheter was placed at the right ventricular apex and His bundle, with a decapolar catheter in the coronary sinus. During ventricular pacing, retrograde conduction occurred with a long ventriculoatrial interval. Tachycardia was readily initiated with ventricular premature beats showing retrograde decremental conduction (Figure 2). An antegradely conducting accessory pathway was noted during atrial pacing maneuvers. During delivery of premature atrial stimulations, shortening of …