Anterograde Conduction Research Articles

His Bundle Refractoriness.

Multiple points of instruction discussed practically in the context of a challenging case make for a memorable learning experience. In this installment of Teaching Rounds in Cardiac Electrophysiology, Nayyar et al1 elucidate the unique findings and analysis in such a manner and take us through to diagnosis and a treatment plan that eliminated arrhythmia without having to ablate all of the abnormal structures identified in their patient. Their case in which 2 unusual arrhythmogenic substrates coexist and interact to result in what appears to be a random and inexplicable series of electrophysiological findings is broken down in logical steps defining each aspect of the arrhythmia.1 These steps include defining the antegrade and retrograde limbs of the putative tachycardia circuit, defining the mechanism of tachycardia, and coming to a conclusion keeping in mind certain difficult differential diagnostic situations and the importance of interpreting His bundle refractory extrastimuli maneuvers. See Article by Nayyar et al When anterograde conduction over the AV node and an accessory pathway is present, the primary maneuver to determine the mechanism of AV conduction is incremental atrial pacing or delivery of coupled atrial extrastimuli. With usual accessory pathway activation, the ventricular beats represent fusion between AV node and accessory pathway conduction, and premature atrial beats progressively delay AV nodal conduction with no significant effect on the pathway. As a result, the stimulus to earliest ventricular activation remains fixed, but the H–V interval becomes progressively negative and the QRS progressively more preexcited. Nayyar et al1 noted that while subtle but significant increase in preexcitation and a more negative H–V interval did occur with atrial extrastimuli, there was a clearly discernible increment in overall conduction time to the ventricle. This finding may be seen with atriofascicular or AV pathways with AV node-like characteristics (incorrectly referred to as …

Evolution of Clinical and Electrophysiological Data in Children with a Preexcitation Syndrome.

With ablation, the follow-up of preexcitation syndrome now is difficult to assess. The purpose was to collect data of children with a preexcitation syndrome studied on two separate occasions within a minimal interval of 1 year. This is a retrospective chart review of 47 children initially aged 12 ± 4 years, who underwent two or more invasive electrophysiological studies (EPS) within 1-25 years of one another (6.3 ± 4.8) for occurrence of symptoms or new evaluation. Among initially symptomatic children (n = 25), four (19%) became asymptomatic and one presented life-threatening arrhythmia. Among asymptomatic children (n = 22), five became symptomatic (22.7%). Anterograde conduction disappeared in seven of 23 children with initially long accessory pathway-effective refractory period, but four of six had still induced atrioventricular reentrant tachycardia (AVRT). AVRT was induced at second EPS in three of 13 asymptomatic preexcitation syndrome with negative initial EPS. There were no spontaneous adverse events in the five children with criteria of malignancy at initial EPS; signs of malignancy disappeared in two. At multivariate analysis, AVRT at initial EPS was the only independent factor of symptomatic AVRT during follow-up. Absence of induced AVRT at initial EPS was the only factor of absence of symptoms and a negative study at the second EPS. There were no significant changes of data in children after 6.3 ± 4.8 years of follow-up. Most children with spontaneous/inducible AVRTs at initial EPS had still inducible AVRT at second EPS. Induced AF conducted with high rate has a relatively low prognostic value for the prediction of adverse events.

“2 for 1 Phenomenon” on Implantable Cardioverter Defibrillator Intracardiac Tracing

"2 for 1 phenomenon" is simultaneous anterograde conduction over the fast and slow pathways of the atrioventricular (AV) nodal pathway, leading to a double ventricular response from each atrial beat. This phenomenon can initiate AV nodal reentrant tachycardia (AVNRT). The unique induction of AVNRT was observed in a patient with an implantable cardioverter defibrillator in our case. Minimal to no retrograde invasion of the slow pathway from the anterogradely conducted fast pathway depolarization is the most accepted explanation.

98-05: Prophylactic Catheter Ablation of the Arrhythmogenic Substrate for Total Cavo-pulmonary Connection Candidates with Isomerism

Background: The substrates of supraventricular tachycardia (SVT) are often associated with right atrial isomerism (RAI) and left atrial isomerism (LAI) that are candidates for total cavo-pulmonary connection (TCPC) procedure. Since SVT can be a serious complication and is mostly difficult to be cured by catheter ablation (CA) because of access limitation to the heart after TCPC. Therefore, pre-operative electrophysiological evaluation seems important to prospect the risk of SVT. The purpose of this study is to delineate the incidence of arrhythmogenic substrates in TCPC candidates with isomerism and evaluate the result of prophylactic CA before TCPC. Patients: From January 2010 to December 2015, we performed electrophysiological study (EPS) upon 20 consecutive patients (RAI in 15 and LAI in 5) before TCPC. Median age was 3 years and median weight was 13 kg. Spontaneous narrow QRS tachycardia had been demonstrated at the palliative operation and/or diagnostic catheterization in all patients. All patients were associated with complete atrioventricular (AV) septal defect. Results: We confirmed that distinct His bundle electrograms recorded at the anterior aspect (1 patients) the posterior aspect (2 patients) or both sides of the common AV valve (17 patients). The type of SVT was AV reentrant tachycardia (AVRT) involving twin AV nodes in 12 patients, uncommon AV nodal reentrant tachycardia (AVNRT) in 1, common atrial flutter (AFL) around common AV valve in 2 and incisional atrial reentrant tachycardia in 5. We achieved successful CA in 19 patients (95%). We could not complete the isthmus block line for AFL in only one failed case after replacement of artificial common AV valve. In 12 patients with AVRT involving twin AV nodes, we performed CA of unilateral AVN which showed recessive anterograde conduction. Iatrogenic ventricular dyssynchrony after CA was never observed in all 12 cases of our series. We could eliminate uncommon AVNRT by modification of one posterior AV node. One clinically significant complication of a stuck artificial common AV valve occurred after successful CA for AFL. The mean follow-up period was 3 years. In all patients after CA no recurrence of SVT was observed. Nineteen patients underwent TCPC procedure successfully and safely. Conclusion: Prophylactic CA of arrhythmogenic substrates in TCPC candidates with isomerism heart may be an effective therapeutic option.

Left-Sided Accessory Pathways with Atrioventricular Node-Like Properties in the Wolff-Parkinson-White Syndrome

Submit Manuscript | http://medcraveonline.com J Cardiol Curr Res 2015, 4(3): 00145 in right-sided pathways, we have previously demonstrated in the study of 55 patients with left-sided AP [12], that 7% of anterograde conduction and 15% of retrograde conduction had decremental conduction over the AP with a maximal decrement of ≥30 ms [12]. Nevertheless, we have found that an additional 27% of the left-sided AP in the anterograde direction, and 29% in the retrograde direction had minimal decremental conduction of less than 30 ms [12]. Therefore, our electrophysiological studies revealed that it is not uncommon to observe minimal decremental conduction over left-sided AP, and stress that care should be taken in the evaluation of conduction over these connections.

Coexistent Types of Atrioventricular Nodal Re-Entrant Tachycardia: Implications for the Tachycardia Circuit.

Background—There is evidence that atypical fast–slow and typical atrioventricular nodal re-entrant tachycardia (AVNRT) do not use the same limb for fast conduction, but no data exist on patients who have presented with both typical and atypical forms of this tachycardia. We compared conduction intervals during typical and atypical AVNRT that occurred in the same patient.Methods and Results—In 20 of 1299 patients with AVNRT, both typical and atypical AVNRT were induced at electrophysiology study by pacing maneuvers and autonomic stimulation or occurred spontaneously. The mean age of the patients was 47.6±10.9 years (range, 32–75 years), and 11 patients (55%) were women. Tachycardia cycle lengths were 368.0±43.1 and 365.8±41.1 ms, and earliest retrograde activation was recorded at the coronary sinus ostium in 60% and 65% of patients with typical and atypical AVNRT, respectively. Thirteen patients (65%) displayed atypical AVNRT with fast–slow characteristics. By comparing conduction intervals during slow–fast and fast–slow AVNRT in the same patient, fast pathway conduction times during the 2 types of AVNRT were calculated. The mean difference between retrograde fast pathway conduction during slow–fast AVNRT and anterograde fast pathway conduction during fast–slow AVNRT was 41.8±39.7 ms and was significantly different when compared with the estimated between-measurement error (P=0.0055).Conclusions—Our data provide further evidence that typical slow–fast and atypical fast–slow AVNRT use different anatomic pathways for fast conduction.

Endocardial Electrophysiological Study in an Asymptomatic Competitive Athlete With Ventricular Preexitation due to Conduction via Fasciculoventricular Accessory Pathway

We present a clinical case of a rare form of the WPW phenomenon due to anterograde conduction over fasciculoventricular accessory pathway in 20-year-old competitive athlete. The patient had no history of palpitations or syncope. ECG revealed shortening of PQ interval (112 ms) and wide QRS complex due to conduction via accessory pathway. To address the question of participation in competitive activity and the need for ablation the patient underwent endocardial electrophysiological study in the course of which we verified conduction via fasciculoventricular accessory pathway. The result of the study was used in determination of strategy of further management.

Risk factors responsible for atrial fibrillation development between symptomatic patients with concealed or manifest atrioventricular accessory pathways

BackgroundPatients with manifest atrioventricular accessory pathways (mAPs) have a greater tendency to develop atrial fibrillation (AF) compared with patients with concealed atrioventricular accessory pathways (cAPs). However, the risk factors of developing AF in patients with various atrioventricular accessory pathways (APs) are not clear. MethodsThis retrospective study included 460 symptomatic patients with either cAPs (n=246) or mAPs (n=214) who underwent electrophysiological study and successful radiofrequency catheter ablation of APs. Clinical and electrophysiological characteristics were compared between cAPs and mAPs and between AF and non-AF groups with cAPs or mAPs. Independent risk factors of AF were analyzed using multivariate logistic regression. ResultsAF was more frequent in mAPs group than in cAPs group (23.4% vs 9.8%, p<0.01). Clinical features were similar between cAPs and mAPs. Anterograde conduction properties served as the major electrophysiological feature of mAPs. Multivariate analysis indicated that mAPs, hypertension, post-ablation P wave dispersion (Pd), N-terminal proB-type natriuretic peptide (NT-proBNP) and creatinine were independent risk factors of AF in the complete cohort. Hypertension, post-ablation Pd and high-sensitivity C-reactive protein (hsCRP) were independent risk factors of AF in cAPs group. Post-ablation Pd, NT-proBNP, creatinine and shorter effective refractory period of anterograde accessory pathways (AAP ERP) were independent risk factors of AF in mAPs group. ConclusionsResults from this study demonstrate that the risk factors of AF are not homogenous between concealed and manifest APs, which might suggest heterogeneous pathogenesis of AF in these two types of APs.

Atypical atrioventricular nodal reentrant tachycardia: prevalence, electrophysiologic characteristics, and tachycardia circuit.

This study aimed at assessing the prevalence, electrophysiologic characteristics, and mechanism of atypical atrioventricular nodal reentrant tachycardia (AVNRT). We studied 925 consecutive patients with AVNRT. Atrial-His (AH) and His-atrial (HA) intervals were measured during atypical AVNRT (HA > 70 ms), and compared with measurements in 34 patients with typical (slow-fast) AVNRT. Assuming that conduction velocity over the fast pathway is similar in the anterograde and retrograde directions, the AH interval during the fast-slow form should be smaller than the HA during slow-fast. Atypical AVNRT was diagnosed in 59 patients (6.4%), median age 50 years (range 19-79 years), and 37 (59.7%) of them female. Fast-slow AVNRT was diagnosed in 44 patients (74.5%), and slow-slow AVNRT in 9 patients (15.2%). The remaining six patients (10.2%) could not be reliably classified due to inconsistent AH, and HA/AH patterns or variable intervals. Tachycardia induction with anterograde conduction jumps was seen in two patients with the fast-slow, and in three patients with slow-slow or intermediate forms. Atrial-His in the fast-slow group was significantly longer than HA in the slow-fast group, 99.7 ± 40.5 ms vs. 45.8 ± 7.7 ms, P < 0.001. Tachycardia cycle length was longer in fast-slow compared with slow-fast, 379.1 ± 68.5 ms vs. 317.1 ± 42.8 ms, P < 0.001. Of AVNRT cases, 6.4% are atypical and may display patterns that do not necessarily correspond to the fast-slow or slow-slow conventional types. Atypical fast-slow and typical AVNRT do not appear to utilize the same limb for fast conduction.

Anterograde conduction to the His bundle during right ventricular overdrive pacing distinguishes septal pathway atrioventricular reentry from atypical atrioventricular nodal reentrant tachycardia.

Distinguishing orthodromic atrioventricular reciprocating tachycardia (ORT) using a retrograde septal accessory pathway (AP) from atypical atrioventricular nodal reentrant tachycardia (AVNRT) may be challenging. Specifically, excluding the presence and participation of an AP may require multiple diagnostic maneuvers. The purpose of this study was to assess the relative value of commonly used right ventricular (RV) pacing maneuvers, including identification of anterograde His-bundle activation with entrainment, to differentiate ORT using a retrograde septal AP from atypical AVNRT. From March 2009 to June 2014, 56 patients (28 female; age 43.9 ± 17.4 years) who underwent electrophysiologic study and ablation for supraventricular tachycardia (26 ORT using septal AP and 30 atypical AVNRT) that exhibited a concentric atrial activation pattern and a septal ventriculoatrial interval >70 ms were analyzed. Overdrive pacing maneuvers or ventricular extrastimuli failed on at least 1 occasion to correctly identify a septal AP. Overall, 16 ORT patients and 26 AVNRT patients had successful RV entrainment, and 12 (75%) ORT patients showed anterograde His capture (11 patients) and/or anterograde septal ventricular capture (3 patients). None of the patients with atypical AVNRT showed anterograde conduction to the His bundle with entrainment. RV pacing maneuvers are useful to exclude an AP in patients with AVNRT having concentric atrial activation sequence and a septal ventriculoatrial interval >70 ms; however, none are consistently diagnostic. When observed in this patient population, anterograde His-bundle or septal ventricular capture during RV entrainment was diagnostic for ORT using a septal AP.

0048: A long accessory pathway refractory period measured by oesophageal atrial stimulation is always associated with a benign form of preexcitation syndrome

Measurement of accessory pathway (AP) refractory period (RP) is required for the evaluation of preexcitation syndrome (PS). The purpose of study was to evaluate the measurement of AP-RP by transesophageal electrophysiological study (EPS) and intracardiac EPS. EPS was performed in 51 patients aged from 13 to 50 years (mean 30±16) for a PS. Atrial stimulation was performed in control state (CS) at a cycle length of 400ms and coupling was decereased until AP6RP or atrial RP. Measurement was repeated after isoproterenol when AP-RP≥250ms in CS. Measurement was performed by transesophageal route and then by intracardiac route, with a delay not >3 months. AP-RP’s were 267±50ms in CS, 233±49ms after isoproterenol at transesophageal EPS, 309±72ms in CS, 280±64ms after isoproterenol at intracardiac EPS (p<0.002). Among 31 patients with initially AP-RP ≥250ms at transesophageal EPS, AP-RP was ≤220ms after isoproterenol in 12 patients. All, but one had an AP-RP≥250ms in CS at intracardiac EPS; one patient with AP-RP of 270ms at esophageal EPS had a value of 240ms at intracardiac EPS in CS but value was 250ms after isoproterenol. Three patients with transesophageal AP-RP in CS and after isoproterenol ≥280ms had lost their anterograde conduction. At transesophageal EPS, AP-RP was <250ms in 20 patients of which only 8 had a short AP-RP at intracardiac EPS and 3 had a short AP-RP after isoproterenol. There was no significant difference for the induction of orthodromic tachycardia at transesophageal and intracardiac EPS (72%) and there was a similar induction of atrial fibrillation at transesophageal EPS (32%) and intracardiac EPS (28%). A long AP refractory period measured at transesophageal EPS excluded the presence of an AP with a short refractory period at intracardiac study even after isoproterenol. There was an adrenergic factor during transesophageal EPS and isoproterenol produced a significant shortening of AP refractory periods in only 39% of patients with AP-RP ≥250ms. When AP-RP is ≥280ms at transesophageal EPS, the loss of anterograde conduction in AP can be expected in the following weeks (15%).

0035: Unpredictable long-term follow-up of untreated preexcitation syndrome

Accessory pathway (AP) ablation is currently performed in patients with a preexcitation syndrome (PS); natural follow-up is based on old studies. The purpose of the study was to report data of untreated patients with PS, studied 2 times at least one year of interval. 2 baseline electrophysiological study (EPS) were performed within 1 to 25 years of one another (mean 9.5±7) in 104 patients, 58 males, 46 females, aged initially from 4 to 67 y (30±16), with overt PS. First EPS was indicated for syncope (n=10), atrioventricular reentrant tachycardias (AVRT)(n=51), atrial fibrillation (AF)(n=6), spontaneous malignant form (AF conducted at very high rates over AP)(n=4) or for asymptomatic PS (n= 33). The protocol was similar, performed in control state (CS) and after isoproterenol. At 2 nd EPS, among patients studied for syncope at EPS1, 2 have still syncope, 3 have AVRT, 1 has AF, 3 are asymptomatic. Among patients with AVRT at EPS1, 38 (74.5%) have AVRT, 8 are asymptomatic, 3 had syncope, 3 has AF. Among patients with AF, 2 present with a malignant form, 2 had AVRT, 1 is asymptomatic. Among asymptomatic patients, 3 present with a malignant form, 17 (53%) remain asymptomatic, 7 have AVRT, 4 have syncope, 1 has AF.All AVRT or AF but 1 occurred in patients with inducible AVRT or AF at EPS1.The higher rate conducted by AP was lower in CS and after isoproterenol at EPS2 (166±80bpm, 191±90) than at EPS1 (191±67, 243±67)(p<0.01). AP refractory periods increased from 268±73ms to 283±62 in CS (p<0.03) and from 202±46 to 244±54ms after isoproterenol (p<0.03). AP has lost anterograde conduction properties in 28 patients. AVRT was induced in 5 of 27 asymptomatic PS with initially negative EPS. Two patients with initially poor anterograde conduction over AP have a very rapid conduction over AP several years later. We generally report an improvement of electrophysiological data with the time; however AVRT induction remains present in 74.5% of cases; unexpected changes may occur in 2% of patients considered initially at low risk who developed a dramatic shortening of AP refractory period several years after initial measurement.

0037: Is the risk of atrial fibrillation dependent on the mechanism of tachycardia in patients with history of paroxysmal supraventricular tachycardia?

to evaluate the role of the mechanism of paroxysmal supraventricular tachycardia (SVT) on the incidence of spontaneous atrial fibrillation (AF). The relation between SVT and AF is well-known but its frequency could depend on the mechanism of SVT. 1559 patients, mean age 49±19 years, with SVT and without anterograde conduction over an accessory pathway (AP) were referred for electrophysiological study (EPS), performed in control state and after isoproterenol. SVT was related to atrioventricular nodal re-entrant tachycardia (AVNRT) in 1262 patients (group I), either typical (n=1180)(group IA) or atypical (n=183)(group IB). In 297 patients SVT was related to atrioventric-ular re-entrant tachycardia (AVRT) due to a concealed AP (group II). At the initial evaluation 47 group I patients (4%)(44 of group IA, 4%, 3 of group IB, 2%), 6 of group II (2%) had presented at least one episode of sustained AF (NS). During follow-up (mean 3±2 years), 97 patients developed AF, 86 of group I (7%)(71 of group IA, 6%, 15 of group IB, 8%),11 of group II (4%). AF risk was higher in group I than in group II (p<0.045); differences remain significant for group IA/IB. When patients with AF at first study were excluded AF risk was similar in all groups: 5% of group I)(4% of group IA; 6.5% of group IB)(0.06) and 3% of group II. Ablation of slow pathway/AP was performed in 1099 patients, 67% of group I (69% of group IA, 51% of group IB), 64% of group II (NS). AF risk was paradoxically higher in patients in whom ablation was performed in group I (6.7% in group I, 7% in group IA, 13% in group IB), compared to patients without ablation (4% in group I, 4% in group IA, 3% in group IB)(p<0.022) and was unchanged in group II (4% after ablation and 3% in patients without ablation). AF-related SVT was rare (3%), independent on the mechanism of SVT. The risk of subsequent AF after a follow-up of 3 years increased to 6% and was near 5% in patients without AF at initial evaluation; it was only higher in patients with atypical AVNRT than in patients with AVRT. The risk was not affected by the ablation of the slow pathway or the AP.

0164: Evolution of preexcitation syndrome in children

Previous studies reported a spontaneous disappearance of preexcitation syndrome (PS) in patients with a long accessory pathway (AP) effective refractory period (ERP) and in children <12 years (y), but stability in children >12 y with inducible SVT and short AP-ERP. The purpose of the study was to collect the data of untreated children with a PS, studied 2 times at least one year of interval. 2 baseline electrophysiological studies (EPS) were performed within 1 to 25 years of one another (mean 6±years) in 39 children and teenagers, 17 boys, 22 girls, aged initially from 1 to 19 years (12.5±4), with overt PS. First EPS (EPS1) was indicated for syncope (n=4), atrioventricular reentrant tachycardias (AVRT)(n=17) or for asymptomatic PS (n=18). The protocol was similar, performed in control state (CS) and after isoproterenol. At EPS2, among patients studied for syncope at EPS1, 1 has still syncope, 2 have AVRT, 1 is asymptomatic. Among patients with AVRT at EPS1, 14 (82%) have still AVRT, 3 are asymptomatic. Among asymptomatic patients, 13 (72%) remain asymptomatic, 2 have AVRT, 3 have syncope. AVRT in children presenting initially with syncope or initially asymptomatic children occurred in 2/4 with inducible AVRT at EPS1. The higher rate conducted by AP was similar in CS and after isoproterenol at EPS2 (178±72bpm, 203±81) and at EPS1 (188±62, 237±83)(p<0.01). AP-ERP’s were similar in CS at EPS2 (283±68ms) and 1 (281±91.5) and tended to increase from 211±72 at ESP1 to 234±58ms at EPS2 (p<0.07) after isoproterenol. AP has lost anterograde conduction in 6 children with initially long APERP but all 5 children with initially inducible AVRT had still inducible AVRT. Two children with initially a long AP-ERP had shorter AP-ERP at EPS2. AVRT was induced at EPS2 in asymptomatic PS with initially negative EPS in 3 children. Contrary to previous studies, we did not find significant changes of clinical and electrophysiological data in children after a mean follow-up of 6±5 years. Most of children with spontaneous or inducible AVRT’s at the first evaluation have still inducible AVRT’s at the second evaluation. AP-ERP did not increase significantly.

Electroanatomic mapping guided cryoablation of Mahaim pathways in children with limited fluoroscopy exposure.

The presence of Mahaim accessory pathways (MAP) with anterograde decremental conduction is a disorder that leads to antidromic atrioventricular reentrant tachycardia. There are rare reports of cryoablation use in MAP. This study aims at sharing our experience with using cryoablation to treat MAP in children. Electrophysiology study and catheter ablation were performed in 14 patients diagnosed with Mahaim tachycardia between January 2010 and December 2013. Cryoablation was used in nine of the cases. A three-dimensional navigation system with surface electrode patches (EnSite System, St. Jude Medical Inc., St. Paul, MN, USA) was used for all procedures. The patients (two girls and seven boys) had a median age of 11.5 years (8-18 years) and a median weight of 67 kg (31-80 kg). Mahaim conduction was localized in the right posterolateral (n = 4), right lateral region (n = 2), right posteroseptal (n = 1), right anterolateral (n = 1), and right anterior (n = 1). A pathway potential was noted in six of nine cases at the tricuspid annulus. Catheter choices and acute success rates were as follows: cryoablation in four (three of four successful), radiofrequency catheter ablation (RFA) and cryoablation in five (successful in four of five). No fluoroscopy was used in six of nine patients. The mean procedure duration was 249 ± 90 minutes. No major complications were observed. The final long-term success rate for cryoablation was seven of nine (78%). Cryoablation can be used as a reliable and effective alternative to RFA in the treatment of Mahaim accessory conduction pathways in children. Prospective comparative studies are necessary in order to further evaluate the long-term efficacy of this method.

Mechanisms and clinical significance of adenosine-induced dormant accessory pathway conduction after catheter ablation.

Adenosine can unmask dormant pulmonary vein conduction after isolation. The role of adenosine in uncovering dormant accessory pathway (AP) conduction after AP ablation is unknown. We evaluated 109 consecutive patients (age, 41 ± 28 years; 62 [57%] men) who were administered adenosine after successful AP ablation. Dormant AP conduction was defined as adenosine-induced recurrent AP conduction, as demonstrated by recurrent preexcitation or change in retrograde ventriculoatrial activation patterns. Dormant AP conduction was identified in 13 (12%) patients. Adenosine led to transient retrograde AP conduction in 6 patients and transient anterograde AP conduction in 8 patients. In all these cases, adenosine-induced AP conduction occurred during the bradycardia phase of adenosine effect and resulted in dormant AP conduction times shorter than atrioventricular nodal conduction times before adenosine administration. On the basis of analysis of timing of occurrence of dormant AP conduction, the mechanism of adenosine-induced AP conduction was determined to be caused by AP excitability recovery in ≥ 12 (92%) cases. The presence of dormant AP conduction was a significant predictor of chronic recurrent AP conduction requiring repeat ablation (odds ratio, 8.54; 95% confidence interval, 1.09-66.9; P=0.041). Adenosine can unmask dormant AP conduction after catheter ablation. Direct effects of adenosine on the AP, possibly via AP membrane potential hyperpolarization, are the dominant mechanism of adenosine-induced AP conduction after ablation. Dormant AP conduction is associated with higher rates of recurrent AP conduction requiring repeat ablation.

Acute effects of simvastatin to terminate fast reentrant tachycardia through increasing wavelength of atrioventricular nodal reentrant tachycardia circuit.

Simvastatin (SV) leads to reduction of ventricular rhythm during atrial fibrillation on rabbit atrioventricular (AV) nodes. The aim of our study was (i) to determine the frequency-dependent effects of SV in a functional model, and (ii) to assess the effects of SV to suppress experimental AV nodal reentrant tachycardia (AVNRT). Selective stimulation protocols were used with two different pacing protocols, His to atrial, and atrial to atrial (AA). An experimental AVNRT model with various cycle lengths was created in three groups of perfused rabbit AV nodal preparations (n=24) including: SV 3μm, SV 7μm, and verapamil 0.1μm. SV increased nodal conduction time and refractoriness by AA pacing. Different simulated models of slow/fast and fast/slow reentry were induced. SV caused inhibitory effects on the slow anterograde conduction (origin of refractoriness) more than on the fast anterograde conduction time, leading to an increase of tachycardia cycle length, tachycardia wavelength and termination of slow/fast reentrant tachyarrhythmia. Verapamil significantly suppressed the basic and frequency-dependent intrinsic nodal properties. In addition, SV decreased the incidence of gap and echo beats. The present study showed that SV in a concentration and rate-dependent manner increased the AV effective refractory period and reentrant tachycardia wavelength that lead to slowing or termination of experimental fast AVNRT. The direction-dependent inhibitory effect of SV on the anterograde and retrograde dual pathways explains its specific antireentrant actions.

Abstract 18485: Transgenic Expression of a Kir6.1 Gain-of-Function Mutation in the Mouse Heart Results in Av Nodal Conduction Abnormalities

While consensus exists that Kir6.2 gives rise to the pore forming subunit of KATP channels in mouse heart, there is growing evidence that Kir6.1 is also present in mouse cardiomyocytes. Furthermore, Kir6.1 gain-of-function mutation (GOF) is associated with Early Repolarization (ERS) and Brugada Syndromes. It is unclear, however, whether the consequences of the Kir6.1 GOF result from abnormalities in cardiomyocytes, or other cell types in the heart. To assess the consequence of Kir6.1 GOF in cardiomyocytes, we generated Kir6.1[G343D] (GOF) mice under α-myosin heavy chain promoter. Patch-clamp data shows decreased sensitivity to ATP inhibition in GOF myocytes (EC50 = 43.5 ± 6.1 μM in GOF, 8.3 ± 3.1 μM in WT; p = 0.0007), with no significant change in peak current density (WT: 128 ± 23 pA/pF; GOF: 103 ± 24 pA/pF, p = NS). In vivo electrophysiology testing using programmed electrical stimulation (PES) shows slowed sinus cycle length (SCL, ms) (WT:120 ± 8.7; GOF: 134.0 ± 19.7, p = 0.04), and prolonged atrioventricular interval (AVI, ms) for GOF (WT: 38.0 ± 4.3; GOF: 46.7 ± 4.3, p = 0.02). Kir6.1 GOF mice show prolonged atrioventricular effective refractory period (AVERP, ms) (WT: 49.2 ± 6.6; GOF: 65.7 ± 8.4, p = 0.0001) and diminished anterograde AV node conduction, as seen by right atrial (RA) pacing resulting in 1:1 capture (pacing cycle length, ms) (WT: 73.0 ± 8.4, GOF: 85.0 ± 5.0, p = 0.02), Wenckebach (WT: 68.0 ± 8.4; GOF: 79.3 ± 6.1, p = 0.049) and 2:1 capture (WT: 54 ± 4.2; GOF: 63.6 ± 6.3, p = 0.049). However, the Kir6.1 GOF mice did not show any differences in either atrial refractory period (AERP, ms) (WT: 37.5 ± 2.7, GOF: 37.1 ± 10.75, p = NS) or ventricular refractory period (VERP, ms) (WT: 45 ± 9.4, GOF: 44.2 ± 7.36, p = NS). In summary, Kir6.1 GOF mice display significant AV nodal conduction abnormalities, providing a potential model of Kir6.1-dependent ERS.

Comparison of the “Real-life” Diagnostic Value of Two Recently Published Electrocardiogram Methods for the Differential Diagnosis of Wide QRS Complex Tachycardias

The diagnostic values of the aVR lead or "Vereckei algorithm," and the lead II R-wave peak time (RWPT) criterion, recently devised for the differential diagnosis of wide QRS complex tachycardias (WCTs), were compared. A total of 212 WCTs (142 ventricular tachycardias [VTs], 62 supraventricular tachycardias [SVT], and eight preexcitation SVTs) from 145 patients with proven electrophysiologic diagnoses were retrospectively analyzed by seven examiners blinded to the electrophysiologic diagnoses. The overall test accuracy of the Vereckei algorithm was superior to that of the RWPT criterion (84.3% vs. 79.6%; p = 0.0003). The sensitivity of the Vereckei algorithm for VT diagnosis was greater than that of RWPT criterion (92.4% vs. 79.1%; p < 0.0001). The negative predictive value (NPV) for the Vereckei algorithm was also greater (77.8%; 95% confidence interval [CI] = 73.6% to 82.1%) than that of the RWPT criterion (61.6%; 95% CI = 57.6% to 65.6%). The specificity of the Vereckei algorithm was lower than that of the RWPT criterion (64.7% vs. 80.9%; p < 0.0001). The positive predictive value (PPV) was also lower for the Vereckei algorithm (86.4%; 95% CI = 84.4% to 88.4%) than for the RWPT criterion (90.9%; 95% CI = 89.1% to 92.8%). Incorrect diagnoses made by the Vereckei algorithm were mainly due to misdiagnosis of SVT as VT (65.7% of cases), and those made by the RWPT criterion were due to the more dangerous misdiagnosis of VT as SVT (72.5% of cases). The Vereckei algorithm was superior in overall test accuracy, sensitivity, and NPV for VT diagnosis and inferior in specificity and PPV to the RWPT criterion. All of these parameters were lower in "real life" than those reported by the original authors for each of the particular electrocardiographic methods.

Permanent junctional reciprocating tachycardia in a dog

A 5-year-old male English Bulldog was presented with a 1-year history of paroxysmal supraventricular tachycardia (SVT) partially responsive to amiodarone. At admission the surface ECG showed sustained runs of a narrow QRS complex tachycardia, with a ventricular cycle length (R–R interval) of 260 ms, alternating with periods of sinus rhythm. Endocardial mapping identified the electrogenic mechanism of the SVT as a circus movement tachycardia with retrograde and decremental conduction along a concealed postero-septal atrioventricular pathway (AP) and anterograde conduction along the atrioventricular node. These characteristics were indicative of a permanent junctional reciprocating tachycardia (PJRT). Radiofrequency catheter ablation of the AP successfully terminated the PJRT, with no recurrence of tachycardia on Holter monitoring at 12 months follow-up.