Atrial Cycle Length Research Articles

Hypertension Editors’ Picks

<i>Hypertension</i> Editors’ Picks

Internal cardioversion of persistent atrial fibrillation in implantable cardioverter defibrillator patients: the juice is not worth the squeeze

Internal cardioversion of persistent atrial fibrillation in implantable cardioverter defibrillator patients: the juice is not worth the squeeze

Relationship Between Complex Fractionated Atrial Electrograms During Atrial Fibrillation and the Critical Site of Atrial Tachycardia That Develops After Catheter Ablation for Atrial Fibrillation

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. 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. 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.

Low efficacy of cardioversion of persistent atrial fibrillation with the implantable cardioverter-defibrillator

AimsAtrial fibrillation (AF) and heart failure are conditions that often coexist. Consequently, many patients with an implantable cardioverter-defibrillator (ICD) present with AF. We evaluated the effectiveness of internal cardioversion of AF in patients with an ICD.MethodsRetrospectively, we included 27 consecutive ICD patients with persistent AF who underwent internal cardioversion using the ICD. When ICD cardioversion failed, external cardioversion was performed.ResultsPatients were predominantly male (89 %) with a mean (SD) age of 65 ± 9 years and left ventricular ejection fraction of 36 ± 17 %. Only nine (33 %) patients had successful internal cardioversion after one, two or three shocks. The remaining 18 patients underwent external cardioversion after they failed internal cardioversion, which resulted in sinus rhythm in all. A smaller left atrial volume (99 ± 36 ml vs. 146 ± 44 ml; p = 0.019), a longer right atrial cycle length (227 (186–255) vs. 169 (152–183) ms, p = 0.030), a shorter total AF history (2 (0–17) months vs. 40 (5–75) months, p = 0.025) and dual-coil ICD shock (75 % vs. 26 %, p = 0.093) were associated with successful ICD cardioversion.ConclusionInternal cardioversion of AF in ICD patients has a low success rate but may be attempted in those with small atria, a long right atrial fibrillatory cycle length and a short total AF history, especially when a dual-coil ICD is present. Otherwise, it seems reasonable to prefer external over internal cardioversion when it comes to termination of persistent AF.

Impact of ganglionated plexi ablation on high-frequency stimulation-induced changes in atrial fibrillation cycle length in the pulmonary vein

BackgroundWe assessed high-frequency stimulation (HFS)-induced changes in the atrial fibrillation (AF) cycle length (AFCL) in the pulmonary vein (PV) after ganglionated plexi (GP) ablation. MethodsTwenty-two patients undergoing catheter ablation for AF were retrospectively enrolled. Sites showing a vagal response (VR) to HFS were defined as GP-positive sites. AFCL was determined in the adjacent PV, distant PV, coronary sinus, and right atrium. Twenty cycles were counted before and after each HFS. After radiofrequency application to the GP site, HFS was repeated. ResultsAt GP-positive sites (n=57), significant shortening of the AFCL was detected in the adjacent PV (17% shortening, 165±38 to 137±27ms, p<0.001) and distant PV (4.8% shortening, p<0.001), but not in the coronary sinus (0.8% shortening, p=0.27) or right atrium (1.8% shortening, p=0.06). However, no significant shortening was observed at GP-negative sites (n=25). At 41 of the 57 sites where VR disappeared after a single radiofrequency application, no significant shortening was observed in the adjacent PV (2.1% shortening, p=0.25). At 16 of the 57 sites where VR was still present, significant shortening was observed in the adjacent PV (16% shortening, p<0.001). ConclusionsHFS of the GP has a strong influence on AFCL in the PV.

Noninvasive determination of atrial fibrillation cycle length by atrial colour tissue Doppler imaging in horses

Atrial fibrillation cycle length (AFCL) is an indicator of atrial electrical remodelling during atrial fibrillation (AF). To compare AFCL measured invasively from an intra-atrial electrogram (AFCLEGM ) with AFCL measured noninvasively by atrial colour tissue Doppler imaging (AFCLTDI ). Prospective descriptive clinical study. Measurements were performed in 31 episodes of AF or flutter in 29 horses (588 ± 61 kg bwt, 9 ± 3 years old) admitted for transvenous electrical cardioversion. The AFCLEGM was measured from an intracardiac electrogram using a bipolar sensing/pacing electrode inserted into the right atrium. The AFCLTDI was measured from atrial colour tissue velocity curves in the following 5 regions: 1) left atrial free wall from a right parasternal 4-chamber view, 2) left atrial free wall from a short-axis view, 3) left atrial free wall from a left parasternal long-axis view, 4) interatrial septum, and 5) right atrial dorsal wall near the tuberculum intervenosum. The AFCLEGM and AFCLTDI from the 5 regions were compared using a one-way repeated-measures ANOVA with Bonferroni correction for multiple comparisons and calculation of the Bland-Altman mean bias and limits of agreement of AFCLEGM and AFCLTDI . The AFCLEGM was 161 ± 18 ms in 29 AF episodes. Two horses showed atrial flutter and had an AFCLEGM of 244 and 324 ms. The mean bias between AFCLTDI and AFCLEGM ranged from -18 to +9 ms depending on the atrial wall region. The AFCLTDI was significantly shorter in the left atrial free wall from the right parasternal 4-chamber view and short-axis view than in the other regions (P<0.001). Tissue Doppler imaging allows noninvasive measurement of AFCL in horses with AF and is able to identify spatial differences within the equine atria. Atrial fibrillation cycle length is an indicator of atrial electrical remodelling and is an important parameter to study AF pathophysiology or the effect of antiarrhythmic drugs.

Prevalence and electrophysiological characteristics of typical atrial flutter in patients with atrial fibrillation and chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is one of the important underlying diseases of atrial fibrillation (AF). However, the prevalence and electrophysiological characteristics of typical atrial flutter (AFL) in patients with AF and COPD remain unknown. The purpose of the present study was to investigate those characteristics. We investigated 181 consecutive patients who underwent catheter ablation of AF. Twenty-eight patients were diagnosed with COPD according to the Global Initiatives for Chronic Obstructive Lung Disease (GOLD) criteria. Forty patients with no lung disease served as a control group. We analysed the electrophysiological characteristics in these groups. Typical AFL was more common in the COPD group (19/28, 68%) than in the non-COPD group (13/40, 33%; P = 0.006). The prevalence of AFL increased with the severity of COPD: 4 (50%) of 8 patients with GOLD1, 13 (72%) of 18 patients with GOLD2, and 2 (100%) of 2 patients with GOLD3. Atrial flutter cycle length and conduction time from the coronary sinus (CS) ostium to the low lateral right atrium (RA) during CS ostium pacing before and after the cavotricuspid isthmus ablation were significantly longer in the COPD group than in the non-COPD group (285 vs. 236, 71 vs. 53, 164 vs. 134 ms; P = 0.009, 0.03, 0.002, respectively). In COPD patients with AF, conduction time of RA was prolonged and typical AFL was commonly observed.

Characteristics of atrial fibrillation cycle length predict restoration of sinus rhythm by catheter ablation

Successful termination of atrial fibrillation (AF) during catheter ablation (CA) is associated with arrhythmia-free follow-up. Preablation factors such as mean atrial fibrillation cycle length (AFCL) predict the likelihood of AF termination during ablation but recurring patterns and AFCL stability have not been evaluated. To investigate novel predictors of acute and postoperative ablation outcomes from intracardiac electrograms: (1) recurring AFCL patterns and (2) localization index (LI) of the instantaneous fibrillatory rate distribution. Sixty-two patients with AF (32 paroxysmal AF; 45 men; age 57 ± 10 years) referred for CA were enrolled. One-minute electrogram was recorded from coronary sinus (CS; 5 bipoles) and right atrial appendage (HRA; 2 bipoles). Atrial activations were detected automatically to derive the AFCL and instantaneous fibrillatory rate (inverse of AFCL) time series. Recurring AFCL patterns were quantified by using recurrence plot indices (RPIs): percentage determinism, entropy of determinism, and maximum diagonal length. AFCL stability was determined by using the LI. The CA outcome predictivity of individual indices was assessed. Patients with terminated atrial fibrillation (T-AF) had higher RPI (P < .05 in CS7-8) and LI than did those with nonterminated atrial fibrillation (P < .005 in CS3-4; P < .05 in CS5-6, CS7-8, and HRA). Patients free of arrhythmia after 3-month follow-up had higher RPI and LI (all P < .05 in CS7-8). All indices except percentage determinism predicted T-AF in CS7-8 (area under the curve [AUC] ≥ 0.71; odds ratio [OR] ≥ 4.50; P < .05). The median AFCL and LI predicted T-AF in HRAD (AUC ≥ 0.75; OR ≥ 7.76; P < .05). The RPI and LI predicted 3-month follow-up in CS7-8 (AUC ≥ 0.68; OR ≥ 4.17; P < .05). AFCL recurrence and stability indices could be used in selecting patients more likely to benefit from CA.

Alternating atrial pacing cycle length during ventricular tachycardia: What is the mechanism?

Case summary A 62-year-old man with a background of ischemic cardiomyopathy and sick sinus syndrome underwent implantation of a cardiac resynchronization therapy defibrillator (CRTD) device (Medtronic Concerto, Minneapolis, MN). Table 1 lists the basic pacing programming of the device. At routine follow-up, a ventricular event was detected that was terminated successfully following 3 antitachycardia pacing therapies. The dot-plot relating to the ventricular event initially demonstrated some variation in the cycle length of the ventricular tachycardia (VT), resulting in V-V intervals drifting above and below the ventricular tachycardia detection interval (VTDI) set at 400 ms (Figure 1). Simultaneous critically short coupled ventricular tracked events during this period of VT were seen in association with those V-V intervals that were just above the VTDI. Careful analysis of the corresponding electrograms also revealed an interesting pattern of atrial pacing with alternating cycle lengths of 680 and 490 ms occurring concurrently in the presence of VT (Figure 2). Further inspection of the episode revealed that once acceleration of the VT occurred with V-V intervals falling consistently below the VTDI, cessation of atrial pacing was seen, followed by the successful detection and subsequent termination of the VT episode with antitachycardia pacing. The questions that arise are as follows. (1) Which algorithm was responsible for the simultaneous critically short coupled ventricular tracked events observed following initiation of VT? (2) Why, despite ongoing VT,

Palpitations in a 19-year-old man, take a second look

Answer to rhythm puzzle It is clear that there is atrial flutter with a variable AV block (2:1–3:1) leading to a ventricular rate of 90–120 beats per min. The atrial flutter cycle length (CL) is 260 msec (Fig. 1). The QRS complex has a rightward axis and is 120 ms wide. The ST-T segments seem normal. Fig. 1 ECG at presentation with in the inlay an enlargement of lead II The combination of findings is obviously unusual in a 19-year-old man. First of all, a typical atrial flutter cycle length is 200 msec (instead of 260 msec) leading to an atrial rate of 300 beats/min. Moreover, in the case of an atrial flutter there usually is a 2:1 block leading to a ventricular rate of 150 beats/min. Hence, in this case the atrial flutter rate is lower than expected and so is the ventricular rate due to hampered AV conduction. Finally, also the conduction in the ventricles is slower than normal as can be judged from the rightward axis and the broad QRS complex (120 msec). Taken together, conduction of the cardiac impulse is slower than expected in all cardiac compartments (atrium, AV node and ventricle). The family history, with a pacemaker implant at age 42 in his mother’s brother, is compatible with an inherited cause of cardiac conduction disease. Indeed, molecular genetic testing revealed the presence of a mutation in the SCN5a gene, the gene encoding for the cardiac sodium channel. Cardiac sodium channel function is crucial for proper conduction of the cardiac impulse at all cardiac levels and loss-of-function mutations give rise to a variety of familial syndromes, including familial conduction disease [1].

A Study of the Atrial Fibrillatory Cycle Length Derived From the 12-Lead ECG: Longer Cycle Length Activity is Associated With More Advanced Electroanatomic Remodelling

A Study of the Atrial Fibrillatory Cycle Length Derived From the 12-Lead ECG: Longer Cycle Length Activity is Associated With More Advanced Electroanatomic Remodelling

Effects of dronedarone and amiodarone on atrial fibrillatory rate in patients with persistent atrial fibrillation

Current guidelines for the management of atrial fibrillation (AF) recommend dronedarone for the prevention of recurring AF [1]. Especially in patients with structural heart disease, e.g. hypertension with left ventricular hypertrophy, dronedarone is a welcome alternative to amiodarone due to its favorable safety profile. However, the antiarrhythmic efficacy of dronedarone is lower than that of amiodarone as exemplified in the DIONYSOS trial [2]. This observation is supported by experimental studies showing much weaker atrial electrophysiologic effects and anti-AF efficacy of dronedarone compared with amiodarone in a canine AF model [3]. However, there is a lack of studies investigating specific antiarrhythmic effects of amiodarone and dronedarone in human AF that are, moreover, restricted to in-vitro experiments of human atrial myocytes [4]. Consequently, we applied time–frequency analysis to the surface ECG for determination of atrial fibrillatory rate (AFR) as a measure of atrial refractoriness for in-vivo monitoring of amiodarone and dronedarone effects in patients with persistent AF. In patients with persistent AFN7 days but b1 year, 2-minute 12 lead ECG recordings were made at baseline and after 3 days of antiarrhythmic drug treatment with all subjects relaxed in a supine position after a 5-minute equilibration period. Dronedarone (2×400 mg/day) or amiodarone (1,200 mg/day loading dose) was initiated prior to external electrical cardioversion on an inpatient basis under continuous electrocardiographic monitoring. All patients were adequately anticoagulated using either oral anticoagulation therapy with an international normalized ratio between 2 and 3 or weight-adapted low molecular weight heparin following exclusion of left atrial thrombus formation by transesophageal echocardiography. Twenty-one consecutive patients treated with dronedarone were prospectively included in our AF registry and matched for age and genderwith 20patientswhowere treatedwith amiodarone. The clinical characteristics of the study population are summarized in Table 1 and showed no difference between the two groups. All patients provided informed consent for study participation, i.e. acquisition and analysis of baseline and on-treatment ECG for evaluation of drug effects. Time–frequency analysis was performed a posteriori on ECG lead V1 as described previously (Fig. 1) [5]. Briefly, after analog-to-digital conversion (1,000 Hz, 12 bit, 0.05–300 Hz) and high-pass filtering to remove baseline wander, QRST complexes were subtracted using spatiotemporal QRST cancelation (Fig. 1, top). One frequency estimate of the atrial signal was obtained every second from overlapping 2.5-second windows by short-term Fourier transform (segment-wise Fast Fourier transform). Thus, this instantaneous signal was represented in a spectral profile. Subsequently, the frequency of the atrial signal was trended as a function of time and mean atrial frequency determined. Frequencies were converted to AFR with its unit fibrillations per minute (fpm; AFR=frequency∗60). All continuous variables are presented as mean±one standard deviation. ECG parameters before and after drug administration were compared using Student's t-test for paired data. Differences in ECG parameter changes between dronedarone and amiodarone were evaluated using t-test for unpaired data. A p valueb .05 was considered statistically significant. The authors of this manuscript certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology. At baseline, mean AFR measured 396±44 fpm in the dronedarone group, comparable to 410±32 fpm in the amiodarone group. AFR was reduced by 25±23 fpm with dronedarone (pb .001 for on-treatment vs. baseline) and by 70±29 fpm with amiodarone (pb .001 for on-treatment vs. baseline). The amiodarone-induced AFR reduction was significantly higher than the AFR reduction with dronedarone (pb .001 for amiodarone vs. dronedarone; Fig. 2, left). Ventricular rate at baseline showed no difference between the dronedarone and the amiodarone group. Both drugs slowed ventricular rate significantly; dronedarone by 18±19 beats per minute (bpm, pb .001 for on-treatment vs. baseline) and amiodarone by 9±12 bpm, (p=.002 for on-treatment vs. baseline). There was a trend for greater magnitude of ventricular rate slowingwith dronedarone comparedwith amiodarone (p=.086; Fig. 2, right). Class I and III antiarrhythmic drugs have been shown to increase atrial cycle length (decrease AFR) which coincides with increased refractoriness and decreased conduction velocity [6]. Previous studies [5,7–9] have subsequently demonstrated a substantial AFR

A Reappraisal on Lidocaine-Sensitive Repetitive, Uniform Atrial Tachycardia

Lidocaine sensitive, repetitive atrial tachycardia is an unusual arrhythmia whose electrophysiologic substrate remains undefined. We aimed to analyze the electropharmacologic characteristics of this arrhythmia with emphasis on its cellular substrate and response to drug challenges. We retrospectively analyzed a series of 18 patients from an electrocardiographic and electrophysiologic perspective and the response to pharmacological challenge. There was no evidence of structural heart disease in 12 patients, 4 patients presented with systemic hypertension; one patient had a prior myocardial infarction and one a mitral valve prolapse. The arrhythmia depicted a consistent pattern in nine patients. The first initiating ectopic beat showed a long coupling interval, the cycle length of the second atrial ectopic beat presented the shortest cycle length and a further prolongation was apparent towards the end of the atrial salvos. Conversely, in the other nine cases, the atrial tachycardia cycle length was erratic. The arrhythmia was suppressed by asynchronous atrial pacing at cycle lengths longer than those of the atrial tachycardia. Intravenous lidocaine eliminated the arrhythmia in all patients, but intravenous verapamil suppressed the atrial tachycardia in only two patients while adenosine caused a transient disappearance in 2/8 patients. Only one patient responded to all the three agents. Radiofrequency ablation was successfully performed in 10 patients. Repetitive uniform atrial tachycardia can be sensitive to lidocaine. In few cases, this rare focal arrhythmia may be also suppressed by adenosine and/or verapamil, which suggests a diversity of electrophysiologic substrates that deserve to be accurately identified.

Abstract 8927: Double-hump Syndrome: The Presence Of Extreme Interatrial Conduction Delay is Associated With Regularization and Progressive Slowing of Atrial Arrhythmias in a Subgroup of Patients With Hypertrophic Cardiomyopathy

Background: In patients with hypertrophic cardiomyopathy (HCM) extreme interatrial activation delay (IAD), indicated by complete separation of the right and left atrial activation on the surface ECG (double hump P wave), was associated with regularization and increase of the cycle length (CL) of recurrent atrial tachycardias (ATs).We aimed to determine the prevalence and the predisposing clinical factors for this clinical entity. Methods: We used data from our HCM registry (n=174 pts, mean age: 53±14 yrs). Data of patients with separated P wave, regularization and slowing of ATs (group I, 5 pts, 2.9%) were compared with 122 control patients with HCM without ATs (group II.). The following parameters were analyzed: P wave morphology and change in P wave duration (ΔP and Pmax), changes in AT CL (ΔATCL), echocardiography parameters including interatrial septal thickness (IAS-T), E/A ratio, E/E prime ratio and fractional shortening (FS) and results of genetic testing. Results: Overall, 9 pts (5.1%) had double hump P waves. This was associated with AT CL prolongation in 5 pts, who were older (66±11 yr vs. 50±14 yr, p=0.016) and had longer follow-up (13,8±1,8 years vs. 7,8± 4,7 years, p=0.005). The ΔATCL was 121±134 ms (range [40-360]) in group I. Echocardiography confirmed double mitral and tricuspid inflow A waves in all group I. pts. Pmax and ΔP were significantly larger in group I (166±33 ms vs. 105±22 ms, p&lt;0.001; 52±26 ms vs. 9±13 ms, p&lt;0.001, respectively). Group I. had an increased LA size as compared to group II. (58±12 mm vs. 45±8 mm, p=0.001) and higher E/A and E/E prime ratios (1,99±1,2 vs. 1,23±0,5, p=0.005 and 20,9±13 vs. 13,1±6,0, p=0.011, respectively). There were no differences in IAS-T and in FS (superior IAS: 4,4±0,1 mm vs. 5,2±1,7 mm, p=NS; inferior IAS: 5,8±0.1 mm vs. 5,7±2,2 mm, p=NS; 38,4±5 % vs. 40,4±9 %, p=NS, respectively). All identified mutations were typical Dutch founder mutations of the MYBPC3 gene. Conclusions: A subgroup of HCM patients have an unique combination of symptoms of separated P wave, regularization and slowing of ATs. Interatrial conduction delay is not related to IAS-T, however, it is associated with larger atria and higher LA pressures. The presence of double hump syndrome is associated with MYBPC3 myosin binding protein mutations.

Renal Sympathetic Denervation Provides Ventricular Rate Control But Does Not Prevent Atrial Electrical Remodeling During Atrial Fibrillation

Renal denervation (RDN) reduces renal efferent and afferent sympathetic activity thereby lowering blood pressure in resistant hypertension. The effect of modulation of the autonomic nervous system by RDN on atrial electrophysiology and ventricular rate control during atrial fibrillation (AF) is unknown. Here we report a reduction of ventricular heart rate in a patient with permanent AF undergoing RDN. Subsequently, we investigated the effect of RDN on AF-induced shortening of atrial effective refractory period, AF inducibility, and ventricular rate control during AF maintained by rapid atrial pacing in 12 pigs undergoing RDN (n=7) or sham procedure (n=5). During sinus rhythm, RDN reduced heart rate (RR-interval, 708±12 versus 577±19 ms; P=0.0021) and increased atrioventricular node conduction time (PQ-interval, 112±12 versus 88±9 ms; P=0.0001). Atrial tachypacing for 30 minutes increased AF inducibility and decreased AF cycle length. This was not influenced by RDN. RDN reduced ventricular rate during AF episodes by ≈24% (119±9 versus 158±19 bpm; P=0.0001). AF episodes were shorter after RDN compared with sham (12±3 versus 34±4 s; P=0.0091), but atrial effective refractory period was not modified by RDN. RDN reduced heart rate and reduced atrioventricular node conduction time during sinus rhythm and provided rate control during AF. AF-induced atrial electrical remodeling, AF inducibility, and AF cycle length were not modified, but duration of AF episodes was shorter after RDN. Modulation of the autonomic nervous system by RDN might provide rate control and reduce susceptibility to AF. Whether RDN may provide rate control in a larger number of patients with AF deserves further clinical studies.

Nodal recovery, dual pathway physiology, and concealed conduction determine complex AV dynamics in human atrial tachyarrhythmias

The genesis of complex ventricular rhythms during atrial tachyarrhythmias in humans is not fully understood. To clarify the dynamics of atrioventricular (AV) conduction in response to a regular high-rate atrial activation, 29 episodes of spontaneous or pacing-induced atrial flutter (AFL), covering a wide range of atrial rates (cycle lengths from 145 to 270 ms), were analyzed in 10 patients. AV patterns were identified by applying firing sequence and surrogate data analysis to atrial and ventricular activation series, whereas modular simulation with a difference-equation AV node model was used to correlate the patterns with specific nodal properties. AV node response at high atrial rate was characterized by 1) AV patterns of decreasing conduction ratios at the shortening of atrial cycle length (from 236.3 ± 32.4 to 172.6 ± 17.8 ms) according to a Farey sequence ordering (conduction ratio from 0.34 ± 0.12 to 0.23 ± 0.06; P < 0.01); 2) the appearance of high-order alternating Wenckebach rhythms, such as 6:2, 10:2, and 12:2, associated with ventricular interval oscillations of large amplitude (407.7 ± 150.4 ms); and 3) the deterioration of pattern stability at advanced levels of block, with the percentage of stable patterns decreasing from 64.3 ± 35.2% to 28.3 ± 34.5% (P < 0.01). Simulations suggested these patterns to originate from the combined effect of nodal recovery, dual pathway physiology, and concealed conduction. These results indicate that intrinsic nodal properties may account for the wide spectrum of AV block patterns occurring during regular atrial tachyarrhythmias. The characterization of AV nodal function during different AFL forms constitutes an intermediate step toward the understanding of complex ventricular rhythms during atrial fibrillation.

Atrial tachycardia caused by a superior vena cava fibrillation with conduction block

AT caused by SVC fibrillationHere, we report a case of a 62-year-old man with a history of incessant atrial tachycardia (AT) for several years. An electrophysiological study revealed rapid and irregular activity in the superior vena cava (SVC), but the surface 12-lead electrocardiogram (ECG) exhibited a relatively regular AT (atrial cycle length=240ms). CARTO mapping of the right atrium (RA) demonstrated that the earliest atrial activation occurred at the posterior septum of the upper RA (the SVC–RA junction). Intravenous administration of 20mg adenosine triphosphate (ATP) led to an acceleration of the SVC–RA conduction up to 1:1 conduction, and the atrial cycle length decreased, consequently converting the AT to transient atrial fibrillation (AF). Application of single radiofrequency energy at the earliest atrial activation site during tachycardia terminated the AT and achieved isolation of the SVC from the RA, despite the continued presence of fibrillation in the SVC. We speculated that SVC fibrillation with spontaneous conduction block at the SVC–RA junction was the cause of this AT.

Catheter ablation of three macroreentrant atrial tachycardias after surgical repair of Double-Outlet Right Ventricle

A 54-year-old man with a surgically repaired double-outlet right ventricle (DORV) presented with palpitations and worsening right heart failure. His 12-lead ECG showed atrial tachycardia (AT) with an atrial cycle length (CL) of 300ms and an inverted saw-tooth F-wave pattern in the inferior leads II, III, and aVF typical of atrial flutter. Electrophysiological study and radiofrequency catheter ablation were performed. A total of 3 sustained ATs (AT1–AT3) were induced. Using the electroanatomical mapping system, CARTO3, and conventional mapping techniques, the ATs were identified as macroreentrant tachycardias circling around an incisional line on the free wall of the right atrium (AT1), the tricuspid annulus (AT2), and low voltage area in the lateral wall including the right septum (AT3). Accuracy of CARTO3 in three-dimensional reconstruction was sufficient to elucidate anatomical features (including catheter sites, incision, and low voltage areas) and macroreentrant circuits. However, conventional mapping techniques were also necessary to identify the mechanism of the tachycardias, and therefore to eliminate all of them successfully. This case demonstrates that the use of combined conventional and electroanatomical mapping techniques, such as CARTO3, can be helpful in identifying the critical isthmus for catheter ablation of macroreentrant AT in patients with surgically corrected congenital heart disease (CHD).

Irregular atrial flutter following pulmonary vein isolation for persistent atrial fibrillation

A 65-year-old man with a history of refractory paroxysmal atrial fibrillation (AF) underwent catheter ablation for persistent AF lasting 2 months. AF was not terminated after complete isolation of the 4 pulmonary veins (PV). Instead, it was transformed to a sustained atrial tachyarrhythmia with beat-to-beat variability in the atrial cycle length. A 12-lead electrocardiogram during tachycardia showed negative flutter-like waves in the inferior leads. Entrainment pacing along the tricuspid annulus confirmed the diagnosis of irregular cavotricuspid isthmus (CTI)-dependent typical atrial flutter (AFL). Linear ablation of the CTI terminated AFL and restored sinus rhythm.

Deglutition-Induced Atrial Tachycardia

A 56-year-old man with gastroesophageal reflux disease had severe but transient palpitations during swallowing with every meal. He continued to have symptoms despite cessation of alcohol and caffeine consumption. Although he was occasionally able to reproduce his symptoms with dry swallowing, they were more prominent after swallowing solid food or carbonated beverages. He reported no palpitations unrelated to deglutition. A 24-hour Holter monitor revealed numerous runs of atrial tachycardia (AT) during meals with varying atrial cycle lengths between 320–500 ms (Figure 1). An echocardiogram was normal. Figure 1. Holter recordings of clinical arrhythmia. Three channel recordings of runs of atrial tachycardia with and without aberrancy are shown during periods of swallowing as patient is having lunch. He was initially placed on β-blockers, which had minimal therapeutic effect and were not tolerated due to fatigue. He was then placed on flecainide, which reduced but did not abolish the arrhythmias. Because of his daily symptoms despite antiarrhythmic medications, he underwent an invasive electrophysiology study. During electrophysiology study, an AT with varying cycle lengths between 300–510 ms was reproducibly induced with swallowing and was found to arise from the left atrium. A circular mapping catheter was placed in the right superior pulmonary …