Paced P-wave morphology templates to guide atrial tachycardia localization: A derivation and validation study.

BACKGROUND: Surface ECG is a useful tool to guide mapping of focal atrial tachycardia (AT). OBJECTIVES: We aimed to construct 12-lead ECG templates for P-wave morphology (PWM) during endocardial pacing from different sites in both atria in patients with no apparent structural heart disease (derivation cohort), with the goal of creating a localization algorithm, which could subsequently be validated in a cohort of patients undergoing catheter ablation of focal AT (validation cohort). METHODS: We prospectively enrolled consecutive patients who underwent electrophysiology study, had no structural heart disease and no atrial enlargement. Atrial pacing, at twice diastolic threshold, was carried out at different anatomical sites in both atria. Paced PWM and duration were assessed. An algorithm was generated from the constructed templates of each pacing site. The algorithm was applied on a retrospective series of successfully ablated AT patients. Overall and site-specific accuracy were determined. RESULTS: Derivation cohort included 65 patients (25 men, age 37 ± 13 years). Atrial pacing was performed in 1025 sites in 61 patients (95%) in RA and in 15 patients (23%) in LA. The validation cohort included 71 patients (28 men, age 52 ± 19 years). AT were right atrial in 66.2%. The algorithm successfully predicted AT origin in 91.5% of patients (100% in LA and 87.2% in RA). It was off by one adjacent segment in the remaining 8.5%. CONCLUSIONS: A simple ECG algorithm based on paced PWM templates was highly accurate in localizing site of origin of focal AT in patients with structurally normal hearts.

Successful treatment of the focal ectopic atrial tachycardia in an infant with a single dose of ivabradin.

We report on a 12-month-old boy with an ectopic atrial tachycardia successfully treated with the ivabradine that acts on cardiac pacemaker cells by selectively inhibiting the If channel. The patient was diagnosed with supraventricular tachycardia in another centre, and multi-drug therapy was unsuccessful to restore sinus ryhthm, so he was sent to our hospital for catheter ablation. We stopped the medications the patient was taking and started using ivabradine. Sinus rhythm was restored 2 hours after ivabradine treatment was started.

Ripple mapping-guided atrial tachycardia ablation following open-heart surgery.

Ripple mapping can make the visualization of activation conduction on a 3-dimensional voltage map and is useful tool for scar-related organized atrial tachycardia (AT). This study sought to assess the efficacy of ripple mapping for interpreting reentrant circuits and critical isthmus in postoperative ATs. 34 consecutive patients with a history of mitral valve surgery (mean age, 54.5 ± 12.4 years) underwent high density (HD) RM during ATs with CARTO3v4 CONFIDENSE system. The voltage activation threshold was determined by RM over a bipolar voltage map. The identification of underlying mechanisms and ablation setting was based on RM without reviewing activation mapping. A total of 41 ATs (35 spontaneous, 6 induced) were characterized. 39 reentry circuits were successfully mapped (cycle length, 256 ± 43 ms). Of the 41 ATs, 28 were confirmed by ripple mapping alone (68%), and 12 (29%) by ripple mapping and entrainment mapping. Of 12 ATs in the left atrium, 9 (75%) needed entrainment to confirm, compared with 5 (17.8%) in the right atrium. Primary endpoint after initial ablation set was achieved in 32 of the 34 patients (94.1%). Freedom from atrial arrhythmias was 79.4% after the follow-up of 12 ± 5 months. Of the seven patients with recurrence, three underwent the repeated catheter ablation. Ripple mapping precisely delineated reentrant circuits in post-cardiac surgery AT resulting in a high success rate of ablation. Entrainment maneuvers remain useful for elucidation of complex AT circuits.

Ivabradine as a stabilising anti-arrhythmic agent for multifocal atrial tachycardia.

Multifocal atrial tachycardia has certain electrocardiographic similarities to atrial fibrillation. The mechanism of atrial fibrillation is heterogenous but in some cases may arise from a single ectopic driver with fibrillatory conduction to the rest of the atria. This has led to the speculation that multifocal atrial tachycardia may have a similar mechanistic unifocal site that disperses through the atrium in a fibrillatory pattern. Ivabradine has been reported to be efficacious in an adult with paroxysmal atrial fibrillation as well as in children with junctional or ectopic atrial tachycardias. This is the first report of successfully using ivabradine, a novel anti-arrhythmic If blocking agent, to convert multifocal atrial tachycardia in a 5-month-old critically ill infant to a pattern indicating a single ectopic atrial focus. This allowed the patient's single atrial focus to be ablated with return to sinus rhythm and decannulation from ventriculoarterial extracorporeal membrane oxygenation. This case suggests that multifocal atrial tachycardia may arise from a single automatic focus with downstream fibrillatory conduction to the atria.

Role of surface electrocardiogram precordial leads in localizing different anatomic sites of ectopic atrial tachycardia arising from lower right atrium in pediatric population.

BACKGROUND: The study was designed to examine P wave morphology (PWM) in precordial leads (V1 -V6 ) during ectopic atrial tachycardia (EAT) originating from low right atrium (RA) to identify the anatomic sites of these foci in children. METHODS: Twenty-three consecutive pediatric patients (56% females, mean age 8.5 ± 2.5) with EAT originating from the low RA underwent detailed atrial endocardial activation mapping and radiofrequency ablation. PWM during EAT was analyzed using standard 12-lead ECG in relation to successful ablation sites in RA. RESULTS: Ectopic atrial tachycardia originated from coronary sinus ostium (CSo) in 12 patients, nonseptal tricuspid annulus (TA) in five, lower crista terminalis (CT) in three and lower free wall in three. In lead V1 , PWM showed a positive pattern during EAT originating from CSo (8/12) [91.7% sensitivity, 100% specificity, 100% positive predictive value (PPV), 100% negative predictive value (NPV)]. A negative pattern was observed in EAT originating from lower free wall (1/3) and nonseptal TA (5/5) [50% sensitivity, 100% specificity, 100% PPV, 75% NPV], while isoelectric pattern was in EAT originating from lower CT (3/3) [100% sensitivity, 100% specificity, 100% PPV, 100% NPV]. In leads V3 -V6 , PWM showed a negative pattern in at least two consecutive leads during EAT from CSo (12/12), nonseptal TA (5/5) and lower free wall (3/3) while it was positive in EAT originating from lower CT (3/3) [100% sensitivity, 95% specificity, 75% PPV and 100% NPV]. CONCLUSIONS: P wave morphology in precordial leads can help differentiate the anatomic sites of EAT from lower RA with high PPVs and NPVs.

Early Detection and Treatment of Atrial Arrhythmias Alleviates the Arrhythmic Burden in Paced Patients: The SETAM Study.

BACKGROUND: Remote monitoring (RM) can remotely detect atrial tachyarrhythmias (ATAs). The benefit of RM compared to conventional follow-up in the detection and management of ATA was assessed in recipients of dual-chamber pacemakers. METHODS: The multicenter randomized SETAM study enrolled 595 patients in sinus rhythm with a CHA2 DS2 -VASc score ≥2, without ATA history and untreated with antiarrhythmics and antithrombotics, randomly assigned to RM (RM-ON; n = 291) versus ambulatory follow-up (RM-OFF; n = 304) during 12.8 ± 3.3 months. ATA occurrence, burden, and management were analyzed together with adverse clinical events. RESULTS: Patients were 79 ± 8 years old, 63% men, with a CHA2 DS2 -VASc score of 3.7± 1.2. ATA were detected in 83 patients (28%) in the RM-ON versus 66 (22%) in the RM-OFF group (P = 0.06). The median time between the pacemaker implantation and the first treated ATA was 114 days [44; 241] in the RM-ON versus 224 days [67; 366] in the RM-OFF group (hazard ratio [HR] = 0.56; 95% confidence interval [CI]: 0.37-0.86; P = 0.01). Therapies for ATA were initiated in 92 patients and the time to treatment of ATA was shortened by 44% in the RM-ON group (HR = 0.565; 95% CI: 0.37-0.86; P = 0.01). Over the last 4 months of follow-up, the mean ATA burden was alleviated by 4 hours/day (18%) in the RM-ON group. The rate of adverse clinical events was similar in both groups. CONCLUSION: Remotely monitored patients were diagnosed and treated earlier for ATA, and subsequently had a lower ATA burden.

Yield of 48-hour Holter monitoring in children with unexplained palpitations and significance of associated symptoms.

OBJECTIVE: To determine the yield of 48-hour Holter monitoring in children with unexplained palpitations and the significance of associated symptoms. METHODS: This descriptive study was conducted at the Children's Hospital and Institute of Child Health, Lahore, Pakistan, from January 1 to December 31, 2015. All children above 5 years of age with history of intermittent palpitations and normal basic cardiovascular workup were enrolled. A 48-hour Holter study was performed using Motara Holter Monitoring System. Frequency of various symptoms and abnormal Holter findings were analysed. SPSS 21 was used for data analysis. RESULTS: Of the 107 patients, 69(64.5%) were males and 38(34.5%) females. The median age was 10 years (interquartile range: 5-18 years). Most common concomitant symptoms with palpitation included syncope/pre-syncope in 35(32.7%) patients, chest pain 22(20.5%), shortness of breath 21(19.6%) and colour change/pallor 11(10.3%). Holter recording was positive in 40(37%) patients. Frequent premature ventricular contractions 12(11.2%) and atrial ectopic beats 9(8.4%) were the most common findings. Holter findings were significantly more common in patients with history of shortness of breath and colour change/pallor during palpitations (p=0.002). CONCLUSIONS: Extended 24-hour Holter monitoring in children with palpitations was an inexpensive, non-invasive investigation with a reasonably high diagnostic yield in detecting arrhythmias.

TNNI3K mutation in familial syndrome of conduction system disease, atrial tachyarrhythmia and dilated cardiomyopathy.

Locus mapping has uncovered diverse etiologies for familial atrial fibrillation (AF), dilated cardiomyopathy (DCM), and mixed cardiac phenotype syndromes, yet the molecular basis for these disorders remains idiopathic in most cases. Whole-exome sequencing (WES) provides a powerful new tool for familial disease gene discovery. Here, synergistic application of these genomic strategies identified the pathogenic mutation in a familial syndrome of atrial tachyarrhythmia, conduction system disease (CSD), and DCM vulnerability. Seven members of a three-generation family exhibited the variably expressed phenotype, three of whom manifested CSD and clinically significant arrhythmia in childhood. Genome-wide linkage analysis mapped two equally plausible loci to chromosomes 1p3 and 13q12. Variants from WES of two affected cousins were filtered for rare, predicted-deleterious, positional variants, revealing an unreported heterozygous missense mutation disrupting the highly conserved kinase domain in TNNI3K. The G526D substitution in troponin I interacting kinase, with the most deleterious SIFT and Polyphen2 scores possible, resulted in abnormal peptide aggregation in vitro and in silico docking models predicted altered yet energetically favorable wild-type mutant dimerization. Ventricular tissue from a mutation carrier displayed histopathological hallmarks of DCM and reduced TNNI3K protein staining with unique amorphous nuclear and sarcoplasmic inclusions. In conclusion, mutation of TNNI3K, encoding a heart-specific kinase previously shown to modulate cardiac conduction and myocardial function in mice, underlies a familial syndrome of electrical and myopathic heart disease. The identified substitution causes a TNNI3K aggregation defect and protein deficiency, implicating a dominant-negative loss of function disease mechanism.

[Perinatal Presentation and Complicated Course of a Multifocal Atrial Tachycardia]. / Polymorphes und komplexes klinisches Bild einer multifokal-ektopen Vorhoftachykardie mit perinataler Manifestation.

We report a male newborn who became symptomatic with supraventricular tachycardia on the first day of life. Neither adenosine nor electric cardioversion could terminate the tachycardia, therefore intravenous esmolol (ß-receptor blocker) was initiated. Inspite of subsequent administration of various antiarrhythmic medications in increasingly higher doses, repeated supraventricular tachycardic episodes occurred. The electrocardiogram showed typical findings of a multifocal atrial tachycardia as the underlying cause. When tachycardic episodes occurred, they also presented as atrial flutter at 460 bpm and a 2:1 block. Finally, high dosage of amiodarone (10 mg/kgbw/d) led to continuous control of the heart rate without tachycardic episodes. To date our patient is mostly in sinus rhythm but without tachycardic episodes and doing well.

Overdrive pacing from downstream sites on multielectrode catheters to rapidly detect fusion and to diagnose macroreentrant atrial arrhythmias.

BACKGROUND: Entrainment criteria for macroreentrant arrhythmias are based on detecting fusion between tachycardia and paced wavefronts, but this is often difficult for atrial tachycardias (AT) after ablation of atrial fibrillation. METHODS AND RESULTS: With the use of a multipolar catheter, pacing was performed from electrodes within the coronary sinus showing activation later than adjacent electrodes (downstream overdrive pacing) during 66 ATs in 62 patients: 20 cavotricuspid isthmus-dependent ATs, 20 perimitral ATs, 13 focal ATs with sequential coronary sinus activation, and 13 other macroreentrant left atrial ATs. The paced cycle length was 10 to 30 milliseconds below the tachycardia cycle length (TCL), and activation at the neighboring upstream electrodes was assessed. Downstream overdrive pacing at 48 sites close to a macroreentrant circuit (PPI-TCL <40 milliseconds, where PPI is postpacing interval) produced constant fusion demonstrated by a long stimulus to upstream atrial electrogram interval (S-Au) >75% TCL and was consistent with orthodromic activation of the upstream site despite its close proximity to the pacing site. In contrast, downstream overdrive pacing at 18 sites during focal AT or remote from the macroreentrant AT circuit (PPI-TCL >40 milliseconds) always demonstrated a comparatively short S-Au <25% of TCL (12±4% versus 89±4% of TCL; P<0.001), consistent with direct activation. CONCLUSIONS: Selection of a downstream activation site for overdrive pacing can facilitate rapid recognition of macroreentry and proximity to the reentry circuit using a single multielectrode catheter by recognizing a PPI-TCL <40 milliseconds and S-Au >75% of TCL. Recognition of intracardiac constant fusion with this method is a novel criterion for transient entrainment.

A case of atrial tachycardia treated with ivabradine as bridge to ablation.

Ivabradine is indicated in cardiac failure and ischemia to reduce sinus rate by inhibition of the pacemaker I(f) current in sinoatrial node. We report a case of an 18-year-old woman with left atrial tachyarrhythmia resistant to several antiarrhythmic drugs and to electric cardioversion who responded only to ivabradine, which significantly reduced heart rate without abolishing the arrhythmia itself. An ectopic focus in the ostium of left pulmonary veins was found and the patient was successfully ablated. We suggest that ivabradine might be therefore useful in the treatment of supraventricular tachyarrhythmias due to an enhanced automaticity.

Ablation of focal atrial tachycardia from the non-coronary aortic cusp: case series and review of the literature.

AIMS: Focal atrial tachycardia successfully ablated from the non-coronary cusp (NCC) is rare. Our aim was to describe the characteristics of mapping and ablation therapy of NCC focal atrial tachycardias and to provide a comprehensive review of the literature. METHODS AND RESULTS: Seven patients (age 40 ± 9 years) with symptomatic, drug-refractory atrial tachycardia were referred for electrophysiological study. Extensive right and left atrial mapping revealed atrial tachycardia near His in all patients but either failed to identify a successful ablation site or radiofrequency applications only resulted in temporary termination of the tachycardia. Mapping and ablation of the NCC were performed retrogradely via the right femoral artery. Mapping of the NCC demonstrated earliest atrial activation during atrial tachycardia 38 ± 14 ms (ranging 17-56 ms) before the onset of the P-wave. Earliest atrial activation in the NCC was earlier than earliest activation in the right atrium and left atrium in all patients. The P-wave morphology was predominantly negative in the inferior leads and biphasic in leads V1 and V2. The tachycardia was successfully terminated by radiofrequency application in 10 ± 6 s (2-16 s), without complications. All patients were free of symptoms during a follow-up of 19 ± 9 months. Literature search revealed 18 reports (91 patients) describing NCC focal atrial tachycardia, with 99% long-term ablation success with a 1% complication rate. CONCLUSION: Symptomatic focal atrial tachycardia near His may originate from the NCC and can be treated safely and effectively with radiofrequency ablation.

Failed anti-tachycardia pacing can be used to differentiate atrial arrhythmias from ventricular tachycardia in implantable cardioverter-defibrillators.

BACKGROUND: Atrial fibrillation/tachycardia (AF/AT) may result in inappropriate therapies in implantable cardioverter-defibrillators (ICDs). The post-pacing interval (PPI) and tachycardia cycle length difference (PPI - TCL) has been previously demonstrated to indicate the proximity of the pacing site to a tachycardia origin. AIMS: We postulated that the PPI and PPI - TCL would be greater in AT/AF vs. ventricular tachycardia (VT) after episodes of failed anti-tachycardia pacing (ATP). METHODS AND RESULTS: This was a single-centre, retrospective study evaluating consecutive patients implanted with dual (DR)/biventricular (BIV) ICDs. Stored electrograms were used to determine whether the ATP captured the arrhythmia and the arrhythmia did not present with primary or secondary termination. Measurements were done using manual calipers. A total of 155 patients were included. There were 79 BIV and 76 DR devices. In total, 39 episodes were identified in 20 patients over a 23-month follow-up period. A total of 76 sequences of ATP (burst/ramp) were delivered, 28 (37%) of them inappropriate. Fifty-one events (18 AT/AF and 33 VT) were compared. The mean PPI was 693 ± 96 vs. 512 ± 88 ms (P < 0.01) and the mean PPI - TCL was 330 ± 97 vs. 179 ± 103 ms (P < 0.01) for AT/AF and VT, respectively. Cut-offs of 615 ms for the PPI [area under curve (AUC) 0.93; 95% confidence interval (CI): 0.84-1.00; P < 0.01] and 260 ms for PPI - TCL (AUC 0.86; 95% CI: 0.74-0.98; P < 0.01) were identified. CONCLUSION: The PPI and PPI - TCL after failed ATP differs significantly between AF/AT and VT and are therefore useful indices to discriminate between supraventricular tachycardia and VT in ICDs.

Clinical significance of early atrial arrhythmia type and timing after single ring isolation of the pulmonary veins.

AIMS: Early atrial arrhythmia following atrial fibrillation (AF) ablation is associated with higher recurrence rates. Few studies explore the impact of early AF (EAF) and atrial tachycardia (EAT) on long-term outcomes. Furthermore, EAF/EAT have not been characterized after wide pulmonary vein isolation. We aimed to characterize EAF and EAT and its impact on late AF (LAF) and AT (LAT) after single ring isolation (SRI). METHODS AND RESULTS: We recruited 119 (females 21, age 58 ± 10 years) consecutive patients with AF (paroxysmal 76, persistent 43) undergoing SRI. Early atrial fibrillation/ early atrial tachycardia was defined as AF/AT within 3 months post-procedure (blanking period). Patients were followed for median 2.8[2.2-4] years. Early atrial fibrillation occurred in 28% (n = 33) and EAT in 25% (n = 30). At follow-up, 25% (n = 30) had LAF and 28% (n = 33) had LAT. Patients with EAF and EAT had higher rates of LAF (48 vs. 16%, P<0.0001) and LAT (60 vs. 16%, P < 0.0001), respectively. Independent predictors of LAF were EAF (3.53(1.72-7.29) P = 0.001); and of LAT were EAT (5.62(2.88-10.95) P < 0.0001) and procedure time (1.38/ h(1.07-1.78) P = 0.04). Importantly, EAF did not predict LAT and EAT did not predict LAF. Early atrial fibrillation late in the blanking period was associated with higher rates of LAF (73% for month 3 vs. 25% for Months 1-2, P = 0.004). However, EAT timing did not predict LAT. CONCLUSION: Early atrial fibrillation and EAT are predictive of LAF and LAT, respectively. Early atrial fibrillation late in the blanking period has greater predictive significance for LAF. This timing is not relevant for LAT. Early arrhythmia type and timing have important prognostic significance following SRI. CLINICAL TRIAL REGISTRATION: http://www.anzctr.org.au;ACTRN12606000467538.

Relationship between complex fractionated atrial electrograms during atrial fibrillation and the critical site of atrial tachycardia that develops after catheter ablation for atrial fibrillation.

INTRODUCTION: Complex fractionated atrial electrograms (CFAEs) are a substrate modification target in patients with atrial fibrillation (AF). However, whether CFAEs can be also arrhythmogenic grounds of atrial tachycardia (AT) presenting after AF ablation remains to be determined. We investigated the relationship between CFAEs and the critical site of AT after CFAE-guided AF ablation. METHODS AND RESULTS: Seventy-two patients showing AT after pulmonary vein isolation and further CFAE-guided ablation were included. The termination sites of the 95 distinct ATs were annotated on color-coded CFAE cycle maps. Of the 95 ATs, 61 (64.2%) had a termination site at the border zone of CFAE or in a highly dense CFAE area. The cycle length (CL) of the ATs terminated in the CFAE area was significantly shorter than the CL of those terminated in the non-CFAE area. The cut-off CL for ATs terminated at the CFAE area was 270 milliseconds, with sensitivity/specificity of 70%/75%. In 67.2% of the ATs terminating at the CFAE-related area, the major termination sites were the anterior wall near the LA appendage, septum and roof, whereas the peri-mitral isthmus was the most common termination site of ATs in the non-CFAE area. CONCLUSIONS: The areas showing CFAE and their border zones were frequently associated with termination of ATs presenting after AF ablation. The mean CL of ATs originating near CFAEs was significantly shorter than that of those terminated in non-CFAE areas. The targeted CFAE areas also provided the arrhythmogenic milieu for AT developing after AF ablation.

The presence of extensive atrial scars hinders the differential diagnosis of focal or macroreentrant atrial tachycardias in patients with complex congenital heart disease.

AIMS: Atrial tachycardias (ATs) frequently develop in patients with congenital heart defects (CHDs). This study aimed to evaluate the effects of extensive atrial scar formation on the total atrial activation time (TAAT) and its relation to the tachycardia cycle length (CL) to classify AT. METHODS AND RESULTS: Seventy-one patients were included and divided into two groups: patients without CHD (Group I, 35 patients) and with CHD (Group II, 36 patients). All patients underwent CARTO electroanatomical activation mapping. Two subgroups were created: centrifugal (CAT) or macroreentrant AT (MRAT). Total atrial activation time, CL, and mean bipolar signal amplitude (BiSA) were analysed. In Group I, 18 patients (51.4%) had CAT and 17 (48.6%) MRAT. The mean BiSA for Group I was 1.30 ± 0.32 mV. Total atrial activation time/CL ratios were different between CAT and MRAT (28.4 ± 16.9 vs. 66.6 ± 14.3%, P < 0.001). In Group II, 18 patients (50%) had CAT and 18 patients (50%) MRAT. The mean BiSA was 0.94 ± 0.50 mV and was not different for CAT and MRAT subgroups (1.04 ± 0.64 vs. 0.85 ± 0.29, P = 0.243). Total atrial activation time/CL ratios were comparable between CAT and MRAT patients (69.0 ± 40.4 vs. 83.6 ± 8.3%, P = 0.243). A significant lower BiSA was found for CAT with TAAT/CL ratios above 40% (0.62 ± 0.11 vs. 1.90 ± 0.18 mV, P < 0.001). A strong negative correlation was identified between the BiSA and the TAAT/CL ratio in patients with CAT in Group II (-0.742; P < 0.001). CONCLUSION: Low mean BiSA values in CHD patients are associated with altered impulse propagation, making TAAT- and CL-based diagnostic tools inaccurate. Further diagnostic tests are needed to determine the correct mechanism of ATs.