Characteristics of slow pathway conduction after successful AVNRT ablation

Background: AV node slow pathway conduction can persist following successful ablation for AV node reentrant tachycardia (AVNRT). We hypothesized that careful examination of AV nodal conduction curves before and after effective AVNRT ablation in patients with persistent slow pathway conduction could shed light on this apparent paradox.
Methods and Results: Thirty patients (age 40.9 ± 14.3; 8 male) were included. AV node function curves were created based on pre- and postablation atrial extrastimulus testing. Analysis of slow pathway function curves demonstrated significant decrease in AH for any given coupling interval after ablation (mean difference –68.1 [–94.5, –41.7] P < 0.001), graphically indicated by downward displacement of the curve. In addition, mean slow pathway effective refractory period (ERP) increased from 247.9 ± 36.1 msec to 288.6 ± 56.0 msec (P < 0.001); mean maximum AH interval decreased from 361.3 ± 114.2 msec to 306.9 ± 65.2 msec (P = 0.013 ) ; mean difference in minimum and maximum AH interval during slow pathway conduction decreased (from 94.5 ± 75.8 msec to 59.6 ± 46.2 msec (P = 0.016 ). Finally, mean difference between the fast and slow pathway effective refractory periods, the span of coupling intervals over which slow pathway conduction occurred, decreased (from 113.9 ± 61.4 msec to 63.2 ± 41.5 msec, P = 0.001).
Conclusions: Ablation, which successfully eliminates inducible and spontaneous AVNRT in the presence of persistent slow pathway conduction, is associated with significantly altered slow pathway conduction characteristics, indicating the presence of a damaged or different slow pathway after ablation, incapable of sustaining tachycardia.     

Left ventricular conduction delays induced by right ventricular apical pacing: effect of left ventricular dysfunction and bundle branch block

Background: RV apical pacing (RVP) may be deleterious, possibly by simulating LBBB, i.e., prolonging QRS duration (QRSd) and LV activation (LVAT). However, determinants of electrical delays are unknown.
Hypothesis: LV dysfunction (LVEF ≤ 40%, HF) and pre-existing conduction system abnormalities may modulate RVP's effects, compared to LBBB.
Methods: RVP-induced QRSd and LVAT were compared in normal LV to HF, with normal QRS (<120 ms), RBBB, or LBBB. LVAT was estimated by interval from QRS onset to basal inferolateral LV depolarization.
Results: During LBBB and RVP, LVAT/QRSd was ≥85%, i.e., LVAT indicated terminal LV depolarization. In normal LV, LVAT during intrinsic conduction (55 ± 18 ms) was delayed by RVP (129 ± 20 ms, n = 58, P < 0.001). RVP's effects were similar to LBBB (P = NS) and unaffected by baseline conduction disease. In HF overall, RVP-induced delays (QRSd 209 ± 27, LVAT 186 ± 26 ms, n = 102) were greater than RVP in normal LV (P < 0.001). When baseline conduction system disease was present, RVP's effects were exaggerated (RVP wide QRS [>120 ms]: QRSd 216 ± 27, LVAT 191 ± 20 ms, [n = 72] vs RVP normal QRS: QRSd 193 ± 24, LVAT 169 ± 24 ms, n = 31, P < 0.001). In patients with LBBB (n = 41), delays during intrinsic conduction (QRSd 163 ± 29, LVAT 137 ± 33 ms, n = 41) were enhanced by RVP (QRSd 218 ± 28, LVAT 191 ± 22 ms, P < 0.001). RVP's effects were similar in patients with LBBB and RBBB (P = NS).
Conclusion: RVP simulated LBBB in normal LV. In HF, RVP induced greater conduction delays than LBBB, enhanced by accompanying conduction disease. These variations may contribute to RVP's mixed clinical effects.     

Relation of the Atrial Input Sites to the Dual Atrioventricular Nodal Pathways:

Dual AV Nodal Pathways. Introduction : The usually accepted definition of the dual pathway electrophysiology requires the presence of conduction curves with a discontinuity ("Jump"). However, AV nodal reentrant tachycardia has been ohserved in patients with "smooth" conduction curves, whereas discontinuity of the conduction curve does not guarantee induction of stable reentry. We hypothesize that the duality of AV nodal conduction can be revealed by careful choice of stimulation sites during the generation of AV nodal conduction curves.
Methods and Results : In 21 rabbit heart atrial-AV nodal preparations, programmed electrical stimulation with S1-S2-S3 pacing protocol was applied eitber posteriorly at the crista terminalis input site (CrT) or anteriorly at the lower interatrial septum input site (IAS), or (in 8 preparations with surgically divided input sites) at both. We found tbat in intact preparations with "smooth" conduction curves, pacing at long coupling intervals produced shorter AV nodal conductiim times from the IAS (56 ± 9.8 msec vs 69 ± I 0.1 msec; P < 0.01). At short coupling intervals, in contrast, shorter conduction times were obtained from the CrT (173 ± 21.8 msec vs 188 ± 22.8 msec; P < 0.01). This resulted in a characteristic crossing of the superimposed IAS and CrT conduction curves. After division of the inputs, the IAS site had rapid conduction to the His bundle but a longer refractory period, whereas the CrT site bad long conduction times and sborter refractory periods. Wavefronts entering the AV node from these two inputs can summate, resulting in improved conduction.
Conclusion : Pacing protocols designed to accentuate tbe asymmetry between tbe AV nodal inputs can belp to reveal tbe functional difference between tbe dual pathways and thus to better assess the properties of AV nodal conduction.     

Time and temperature profile of catheter cryoablation of right septal and free wall accessory pathways in children

Introduction: The overall acute success with cryoablation for accessory pathways (APs) has been reported to be lower than with radiofrequency ablation. Generally, prior cryomapping (limited to −30°C) has been used to test for loss of AP conduction and absence of atrioventricular (AV) node impairment. However, the temperature at which loss of AP conduction occurs may be variable. The purpose of this study was to evaluate the time and temperature profile at which loss of AP conduction occurs.
Methods and Results: A retrospective study evaluated 25 patients (mean age 13.3 ± 3.6 years) who underwent cryoablation for right-sided APs (22 manifest/3 concealed). Direct cryoablation (–80°C) without cryomapping was performed using a "time to success" strategy. If AP conduction was successfully interrupted within 25 seconds of the onset of cryoablation, the lesion was continued for 240 seconds; otherwise it was terminated and further mapping was performed. Cryoablation was successful in 24/25 (96%) patients. Temperature at loss of AP conduction was −66.2 ±−16.7°C (range +32 to −84°C) with conduction block at temperatures lower than −30°C for all but 3 APs. Critical time to success (interval from cryoadherence to loss of AP conduction) was significantly shorter for permanently successful cryolesions, compared with transiently successful lesions (6.3 ± 4.1 vs. 11.2 ± 2.2 sec; P < 0.001). There were no major complications.
Conclusions: Cryothermal energy required for successful ablation may be variable and restricting test applications to −30°may limit its efficacy. A "time to success" strategy may improve outcome of cryoablation for right-sided APs in children without compromising safety.     

A rate-independent method of assessing QT-RR slope following conversion of atrial fibrillation

Introduction: Following conversion of atrial fibrillation (AF), QT interval transiently and variably prolongs and can trigger Torsades de Pointes (TdP). However, quantitative analysis of risk in this setting is difficult because cycle length variability during AF makes rate-corrected QT impossible to calculate. In this study, a newly developed method to study heart rate dependence of the QT interval during AF was applied to assess the QT–RR relationships prior to and following cardioversion in patients with AF.
Methods and Results: Cardiac rhythm was digitized for ≥30 minutes prior to and following elective cardioversion to sinus rhythm (SR) in 12 patients. Each QT interval was placed in a "bin" (50 ms), according to the preceding RR interval. All QT intervals within a bin were averaged and RR bin-specific QT values were derived. The slope of the QT–RR relationship was much flatter in AF (0.058 ± 0.02) compared with that predicted by conventionally used QT rate corrections (0.130 [Bazett], 0.096 [Fridericia]) and much steeper after cardioversion (0.238 ± 0.14, P < 0.01 compared with AF). The method also allowed us to establish that QT at any given RR interval prolonged when SR was restored (e.g., at RR interval 800 ms: QT = 0.38 ± 0.03 second [AF] vs 0.46 ± 0.05 second [SR], P < 0.01). The longest QT values were in patients receiving sotalol or quinidine.
Conclusions: The results of this study demonstrate that QT interval can be reliably measured in AF using a method that is independent of heart rate. We also showed that cardioversion of AF acutely increases the QT interval and the steepness of the QT–RR slope.     

Biventricular pacing and QT interval prolongation

Introduction: The purpose of this study was to examine BiV pacing-dependent changes in QT interval and the related potential for proarrhythmia. Biventricular (BiV) pacing has emerged as a promising therapy for patients with advanced congestive heart failure (CHF) and bundle branch block (BBB).
Methods and Results: One hundred and seventy-six consecutive patients (123 men and 53 women; mean age 67 ± 16 years) with ischemic (n = 128) or nonischemic (n = 48) cardiomyopathy in New York Heart Association Class II (8%) or III (92%) CHF (ejection fraction 24 ± 9%) underwent atrial synchronous BiV pacing. The QRS, QT, and JT intervals were measured at 30 minutes after initiation of BiV pacing, at 24 hours, and at 1 month postimplant. QT interval was defined as the time interval between the initial deflection of the QRS complex and the point at which the T wave crossed the isoelectric line. At baseline, the average QRS duration was 178 ± 10 ms, attributable to left BBB (n = 158) or intraventricular conduction delay (n = 18). BiV pacing resulted in a small but statistically significant reduction in QRS duration (148 ± 9 ms during BiV pacing vs 178 ± 10 ms at baseline [P < 0.0001]), yet the QT increased to 470 ± 34 ms with BiV pacing versus 445 ± 32 ms at baseline [P < 0.0001]). The JTc interval during BiV pacing was significantly shorter than during LV pacing (290 ± 9 ms vs 320 ± 20 ms, P < 0.0001). During a mean follow-up of 24 ± 6 months, one patient developed recurrent torsade de pointes. That was eliminated once left ventricular pacing was discontinued.
Conclusion: Biventricular pacing prolongs QT interval. However, the occurrence of torsade de pointes is uncommon.     

Adenosine-Sensitive Atrial Reentrant Tachycardia Originating from the Atrioventricular Nodal Transitional Area

Adenosine-Sensitive AT from AVN Area. Introduction : Atrial tachycardia shows wide variations in its electrophysiologic properties and sites of origin. We report an atrial tachycardia with ECG manifestations and electrophysiologic characteristics similar to an atypical form of AV nodal reentrant tachycardia (AVNRT).
Methods and Results : This supraventricular tachycardia was observed in 11 patients. It was initiated by atrial extrastimulation with an inverse relationship between the coupling interval of an extrastimulus and the postextrastimulus interval. Its induction was not related to a jump in the AH interval, and its perpetuation was independent of conduction block in the AV node. Ventricular pacing during tachycardia demonstrated AV dissociation without affecting the atrial cycle length. A very small dose of adenosine triphosphate (mean 3.9 ± 1.2 mg) could terminate the tachycardia. The earliest atrial activation during tachycardia was recorded at the low anteroseptal right atrium with a different intra-atrial activation sequence from that recorded during ventricular pacing, where the tachycardia was successfully ablated in 9 of 10 attempted patients. Bidirectional AV nodal conduction remained unatttched after successful ablation.
Conclusion : There may he an entity of adenosine-sensitive atrial tachycardia probably due to focal reentry within the AV node or its transitional tissues without involvement of the AV nodal pathways. This tachycardia can he ablated without disturbing AV nodal conduction from the right atrial septum.     

The Relationship of Bipolar Left Ventricular Pacing Stimulus Intensity to Cardiac Depolarization and Repolarization in Humans with Cardiac Resynchronization Devices

Background: Myocardial depolarization can be altered by varying pacing stimulus output. This may have implications on response rates for cardiac resynchronization therapy (CRT). The purpose of our study was to determine the relationship of left ventricular (LV) pacing stimulus intensity to measures of depolarization and repolarization in humans with CRT devices.
Methods: In 37 patients with a CRT device and bipolar LV leads, bipolar LV-only pacing from maximum output to threshold was performed. The presence of changes in depolarization was defined by predetermined changes in ECG morphology that accompanied a change in bipolar stimulus amplitude. ECG parameters and the EGMs were analyzed at various LV pacing stimulus intensities.
Results: Changes in ECG morphology were apparent in 70% of patients. These occurred at a mean LV stimulus amplitude of greater than 2.7 ± 0.8 V at 1 ms. Of the patients with changes in surface ECG, the transventricular conduction time decreased from 155 ± 41 ms at low output to 141 ± 39 ms at high output (P < 0.01). Despite a significant reduction in QRS duration with high output, mean QTc and JTc interval increased with increasing LV stimulus strength (539 ± 45 vs 559 ± 46 ms (P < 0.01) and 353 ± 31 ms vs 377 ± 32 (P < 0.01)).
Conclusion: Increased LV stimulus intensity, independent of RV anodal capture, is associated with faster transventricular conduction time, changes in myocardial depolarization, and longer QT intervals. These findings have important implications on the relationship of programmed LV pacing output to pacing-induced proarrhythmia and clinical CRT response rates.     

Incremental Pacing for the Diagnosis of Complete Cavotricuspid Isthmus Block During Radiofrequency Ablation of Atrial Flutter

Incremental Pacing for the Diagnosis of Cavotricuspid Isthmus Block.   Background: Complete conduction block of the cavotricuspid isthmus (CTI) reduces atrial flutter recurrences after ablation. Incremental rapid pacing may distinguish slow conduction from complete CTI conduction block.
Methods and Results: Fifty-two patients (67 ± 9 years) undergoing 55 CTI ablation procedures were included. With ablation, double potentials (DPs) separated by an isoelectric line of ≥30 ms were obtained. Incremental atrial pacing (600–250 ms) was performed from coronary sinus (CS) and low lateral right atrium (LLRA). A <20 ms increase in the DPs distance during incremental pacing was indexed as complete CTI block. In 8 patients, an initial <20 ms DPs distance increase was noted; direct complete isthmus block was suggested and no additional ablation performed. In the remaining, the CTI line was remapped for conduction gaps and additional radiofrequency energy pulses applied. Complete block, as indexed by incremental pacing, occurred in 46 of 55 procedures, with one flutter recurrence (follow-up 8 ± 2 months): DPs interval variation of 116 ± 20 to 123 ± 20 ms (CS), P = 0.21; and 122 ± 25 to 135 ± 35 ms (LLRA), P = 0.17. The remaining 9 patients (persistent rate-dependent DPs increase) presented 3 flutter recurrences, P = 0.01: DP distance from 127 ± 15 to 161 ± 18 ms (CS), P < 0.001; and 114 ± 24 to 142 ± 10 ms (LLRA), P = 0.007.
Conclusion: Incremental pacing distinguishes complete CTI block from persistent conduction. Such identification, accompanied by additional ablation to achieve block, should minimize flutter recurrences after ablative therapy. (J Cardiovasc Electrophysiol, Vol. 21, pp. 33–39, January 2010)     

Nonuniform Anisotropy is Responsible for Age-Related Slowing of Atrioventricular Nodal Reentrant Tachycardia

Age-Related Slowing of AVNRT. Introduction : AV nodal reentrant tachycardia cycle length has been shown to he longer in the elderly population. Microfibrosis associated with aging producing nonuniform anisotropic conduction or changes in membrane ionic properties could explain this finding.
Methods and Results : Forty-five patients (33 women and 12 men) with typical AV nodal reentrant tachycardia were studied to analyze the effects of age on electrophysiologic characteristics of the tachycardia using high-density catheter mapping of the triangle of Koch. We classified patients into group A (age ≤ 45 years, mean [± SD] 32.7 ± 8.8, n = 27) and group B (age > 45 years, mean [± SD] 61.1 ± 10.2, n =18). Retrograde atrial activation was recorded during tachycardia by means of a 2-mm decapolar catheter at the His bundle, a quadripolar catheter at the high right atrium, a multipolar catheter (6 to 10 poles) in the coronary sinus, and a deflectable quadripolar catheter at the posterior triangle of Koch. The AH interval at the AV junction as well as HA intervals at several atrial sites were measured during tachycardia. HA intervals at all atrial recording sites except in the posterior triangle of Koch were significantly longer in group B, as well as the tachycardia cycle length (362 vs 329 msec, P = 0.01). The mean AH interval was prolonged by 24 msec in group B, but this difference did not reach statistical significance. A sequential pattern of retrograde atrial activation during tachycardia was more frequently recorded in group B.
Conclusions : Since the delayed activation to the atrium was heterogeneous, transverse nonuniform anisotropic conduction is a likely explanation of these age-related modifications of AV nodal reentrant tachycardia characteristics.     

Differential Effect of Adenosine on Anterograde and Retrograde Fast Pathway Conduction in Patients with Atrioventricular Nodal Reentrant Tachycardia

Adenosine and Retrograde Fast Pathway Conduction . Introduction : Several studies have shown that the fast pathway is more responsive to adenosine than the slow pathway in patients with AV nodal reentrant tachycardia. Little information is available regarding the effect of adenosine on anterograde and retrograde fast pathway conduction.
Methods and Results : The effects of adenosine on anterograde and retrograde fast pathway conduction were evaluated in 116 patients (mean age 47 ± 16 years) with typical AV nodal reentrant tachycardia. Each patient received 12 mg of adenosine during ventricular pacing at a cycle length 20 msec longer than the fast pathway VA block cycle length and during sinus rhythm or atrial pacing at 20 msec longer than the fast pathway AV block cycle length. Anterograde block occurred in 98% of patients compared with retrograde fast pathway block in 62% of patients ( P < 0.001). Unresponsiveness of the retrograde fast pathway to adenosine was associated with a shorter AV block cycle length (374 ± 78 vs 333 ± 74 msec, P < 0.01), a shorter VA block cycle length (383 ± 121 vs 307 ± 49 msec, P < 0.001), and a shorter VA interval during tachycardia (53 ± 23 vs 41 ± 17 msec, P < 0.01).
Conclusion : Although anterograde fast pathway conduction is almost always blocked by 12 mg of adenosine, retrograde fast pathway conduction is not blocked by adenosine in 38% of patients with typical AV nodal reentrant tachycardia. This indicates that the anterograde and retrograde fast pathways may be anatomically and/or functionally distinct. Unresponsiveness of VA conduction to adenosine is not a reliable indicator of an accessory pathway.     

Clinical Experience with Dofetilide in the Treatment of Patients with Atrial Fibrillation

Introduction: Dofetilide is the newest drug approved by the United States Food and Drug Administration for the treatment of patients with atrial fibrillation (AF). Few data on the efficacy and safety of dofetilide in a diverse group of patients are available. The aim of this study was to evaluate the results of dofetilide in a consecutive series of 69 patients with AF.
Methods and Results: Sixty-nine patients with persistent (n = 53) or paroxysmal (n = 16) AF were administered dofetilide in-hospital. Prior to starting dofetilide, all patients had been adequately anticoagulated, and concomitant agents contraindicated in the presence of dofetilide were discontinued. Heart rhythms were monitored continuously by telemetry in all patients. The initial dose, which was determined using the Cockroft-Gault calculated creatinine clearance, was 500 μg bid, 250 μg bid, and 125 μg bid in 51, 13, and 5 patients, respectively. Reductions in subsequent dosage occurred in 12 patients, 4 for QT prolongation. Dofetilide was discontinued in-hospital in 7 patients, 2 for adverse arrhythmic events and 3 for unacceptable QT prolongation. Twenty-seven (63%) of 43 patients in AF converted spontaneously to sinus rhythm. Fifty-eight patients were discharged receiving dofetilide treatment and were followed as outpatients for 21 ± 7 months. One third of patients continued to take dofetilide at 1 year. One patient had a cardiac arrest 1 day after hospital discharge.
Conclusion: Dofetilide is a well-tolerated antiarrhythmic drug with a high conversion rate of AF to sinus rhythm. One third of patients maintained sinus rhythm at 1 year. Proarrhythmia can occur and initiation of therapy must be performed in-hospital. (J Cardiovasc Electrophysiol, Vol. 14, pp. S287-S290, December 2003, Suppl.)     

Prevention of Action Potentials During Extracellular Electrical Stimulation of Long Duration

Prevention of Action Potentials by Electrical Stimulation. Introduction : This study investigated if action potentials can be prevented by electrical field stimuli of long duration.
Methods and Results : The transmembrane potential was recorded by a double-barrel micro-electrode during field stimulation given across a papillary muscle from 10 guinea pigs. After 10 stimuli (S) with a 200-msec S-S interval, a 400-msec square wave shock was given Just before or after the end of the effective refractory period following the 10th stimulus through electrodes 1 cm on either side of the papillary muscles. Another two stimuli (S' and S") having the same 200-msec S-S interval were given during the shock pulse to test if the action potentials induced by these two stimuli could be prevented by the shock. The shock strength was increased until the shock field prevented the action potentials induced by the S' and S" stimuli. The resting membrane potential was −85.5 ± 2.9 mV. For shocks causing depolarization at the recording site, the field strength required to prevent S'- and S"-induced action potentials was 1.5 ± 0.4 V/cm, which depolarized the transmembrane potential to −55.3 ± 8.9 mV and −58.1 ± 7.2 mV from the resting membrane potential at the time of the S' and S" stimuli, respectively. The strength of shocks causing hyperpolarization required to prevent S'- and S"-induced action potentials was 5.0 ± 0.8 V/cm, which hyperpolarized the transmembrane potential to −105 ± 6.5 mV and −115.6 ± 6.9 mV from the resting membrane potential at the time of the S' and S" stimuli, respectively.
Conclusion : Both depolarization and hyperpolarization caused by an electrical field can prevent action potentials.     

Radiofrequency Ablation of Atrial Insertion of Left-Sided Accessory Pathways Guided by the "W Sign"

AP Ablation and the "W Sign." introduction: The aim of this study was to evaluate the efficacy of radiofrequency (RF) ablation of the atrial insertion of left-sided aceessory pathways with guidance by a specific morphologic characteristic of the local electrogram, which we call the "W sign." This represents the shortest local atrioventricular (AV) interval during sinus rhythm in patients with manifest preexcitation or the shortest local VA interval during AV reciprocating tachycardia and/or ventricular pacing in patients with concealed accessory pathways.
Methods and Results: The transseptal technique was used in 31 patients (18 men, 13 women; aged 32 ± 13 years), and RF ablation of 33 accessory pathways (26 manifest and 7 concealed) was attempted. Patients presented with palpitations (n = 16), presyncope (n = 10), or syncope (n = 5). The clinical arrhythmia was AV reciprocating tachycardia (n = 24) or atrial fibrillation (n = 7). In 21 patients (68%) electrophysiologic study and RF ablation were performed at a single session. Accessory pathways were left posteroseptal (n = 5) or left free wall (n = 28). The "W sign," formed from merging of the local atrial and ventricular electrograms, was identified at all successful sites prior to ablation. Ablation was successful in all patients. A median of 7 RF lesions were delivered per patient. The fluoroscopy time was 76 ± 48 minutes; total procedure time was 5.4 ± 1.9 hours. No significant complications occurred. Early recurrence (≤ 24 hours) occurred in I patient; during 6 ± 4 months, accessory pathway conduction recurred in another patient.
Conclusion: We conclude that RF ablation of the atrial insertion of left accessory pathways can be very successful when guided by the "W sign."     

Effects of Lidocaine on Shock-Induced Vulnerability

Introduction: Lidocaine is known to increase the defibrillation threshold (DFT) of monophasic shocks (MS) and have no effect on DFT of biphasic shocks (BS). The aim of this study was to enhance our understanding of the mechanisms of vulnerability and defibrillation through the investigation of this difference.
Methods and Results: We studied the effect of 15 μM lidocaine on shock-induced vulnerability using fluorescent imaging of Langendorff-perfused rabbit hearts. Vulnerability was assessed as vulnerable window with shock strengths of 15 to 150 V and vulnerable period (VP) with shock delivery phase of 0% to 100% of action potential duration (% APD). With MS, lidocaine caused a significant increase in both the upper limit of vulnerability (ULV, 71 ± 17 V vs 120 ± 1.5 V, P < 0.01) and upper limit of VP (91 ± 8.0% APD vs 110 ± 4.2% APD, P < 0.01). With BS, lidocaine had no effect on ULV (40 ± 3.4 V vs 45 ± 4.5 V) and did not increase the upper limit of VP (78 ± 8.9% APD vs 96 ± 12% APD, P < 0.01). Lidocaine caused reduction of the conduction velocity during pacing (0.58 ± 0.08 m/s vs 0.44 ± 0.05 m/s, P < 0.01), shock-induced break excitation (0.82 ± 0.17 m/s vs 0.30 ± 0.07 m/s, P < 0.01), and postshock reentry (0.34 ± 0.07 m/s vs 0.19 ± 0.08 m/s, P < 0.01). Lidocaine had no effect on shock-induced virtual electrode polarization.
Conclusion: Lidocaine increased MS ULV due to slowing of shock-induced break-excitation wavefronts, which resulted in enhanced probability of survival of virtual electrode induced phase singularity. Lidocaine had no effect on BS ULV because no break excitation was induced by BS. Reduction of conduction velocity by lidocaine resulted in increased dispersion of repolarization and led to upper limit of VP increase for both MS and BS. (J Cardiovasc Electrophysiol, Vol. 14, pp. S237-S248, October 2003, Suppl.)     

Diagnostic Clues From the Surfaee ECG to Identify Idiopathic (Fascicular) Ventricular Tachycardia: Correlation with Electrophysiologic Findings

ECG in Idiopathic Fascicular VT. Introduction : An RS interval > 100 msec in precordial leads has been recently described for the diagnosis of ventricular tachycardia (VT). The aim of this study was to assess the value of this criterion when applied to patients with right bundle branch block pattern, left-axis deviation (fascicular) VT sensitive to verapamil.
Methods and Results : Eleven patients (mean age 31 ± 11 years; range 16 to 51) had a mean heart rate of 164 ± 37 beats/min (range 107 to 230) during VT, The QRS complex axis was -92°± -15° (range -80 to -115). The mean QRS duration was 121 ± 9 msec (range 105 to 140). The mean RS interval was 67 ± 9 msec (range 60 to 80). Fusion beats were present in 2 patients (18%), and AV dissociation confirmed by electrophysiologic study was found on ECG in 8 (73%) of 11. During tachycardia, the QRS-H'interval was 19 ± 10 msec (range 10 to 30) in 6 of 11 patients. In seven patients, a fast, unique (or double) presystolic potential lasting 32 msec (range 12 to 40) occurring before the onset of the QRS complex was found at the site of origin of VT, localized in the inferior apical left ventricular septum. In all cases, VT was successfully treated by catheter ablation.
Conclusion : A wide QRS complex tachycardia with right bundle branch block and left-axis deviation sensitive to verapamil observed in a young patient without structural heart disease should not be confused with supraventricular tachycardia with aberrancy but rather suggests the presence of fascicular VT. As opposed to VT associated with structural heart disease, the RS interval is < 80 msec in all precordial leads in all cases. Independent of this parameter, AV dissociation detectable on surface ECG has a sensitivity of 73%, which increases to 82% in the presence of fusion beats.     

The VA relationship after differential atrial overdrive pacing: a novel tool for the diagnosis of atrial tachycardia in the electrophysiologic laboratory

Introduction: Despite recent advances in clinical electrophysiology, diagnosis of atrial tachycardia (AT) originating near Koch's triangle remains challenging. We sought a novel technique for rapid and accurate diagnosis of AT in the electrophysiologic laboratory.
Methods: Sixty-two supraventricular tachycardias including 18 ATs (10 ATs arising from near Koch's triangle), 32 atrioventricular nodal reentrant tachycardias (AVNRTs), and 12 orthodromic reciprocating tachycardias (ORTs) were studied. Overdrive pacing during the tachycardia from different atrial sites was performed, and the maximal difference in the postpacing VA intervals (last captured ventricular electrogram to the earliest atrial electrogram of the initial beat after pacing) among the different pacing sites was calculated (delta-VA interval).
Results: The delta-VA intervals were >14 ms in all AT patients and <14 ms in all AVNRT/ORT patients, and thus, the delta-VA interval was diagnostic for AT with the sensitivity, specificity, and positive and negative predictive values all being 100%. When the diagnostic value of the delta-VA interval and conventional maneuvers were compared for differentiating AT from atypical AVNRT, both a delta-VA interval >14 ms and "atrial-atrial-ventricular" response after overdrive ventricular pacing during the tachycardia were diagnostic. However, the "atrial-atrial-ventricular" response criterion was available in only 52% of the patients because of poor ventriculoatrial conduction.
Conclusions: The delta-VA interval was useful for diagnosing AT irrespective of patient conditions such as ventriculoatrial conduction.     

DP+1: another simple endpoint for atrial flutter ablation

Background:  When double potentials (DP) on the line of block are difficult to see, we propose another simple method to verify complete bidirectional block (CBDB) at the end of an atrial flutter ablation. We measured the interval between the electrograms immediately on either side of the line of block on a multipole catheter spanning the isthmus. We called this interval "DP+1" because it is one pair of electrodes away from the DP on the line of block.
Methods:  Fifty consecutive patients (age 62 ± 13 years, LVEF 54 ± 11%, mean cycle length 241 ± 34 ms) underwent an atrial flutter ablation using a duodecapolar catheter with 2–10 mm spacing with the distal tip inserted into the mid-coronary sinus and the rest of the poles spanning the isthmus and the low lateral right atrium. Radiofrequency ablation was performed using a 10-mm tip electrode (EP Technologies). The ablation endpoint was the creation of a craniocaudal activation pattern of the opposite wall to the pacing site (septal and lateral of the line of block).
Results:  The ablation endpoint was achieved in 48 of 50 (96%) patients with 8 ± 2 RF applications. Adequate DP were found in only 22 of 50 patients (44%), but the DP+1 interval was measurable in all patients. When no block was present, the DP+1 interval was 81 ± 10 ms, and 160 ± 18 ms when complete bidirectional block was present (P < 0.001). A DP+1 interval of >140 ms had 100% specificity, 96% sensitivity, 100% positive predictive value for verifying complete bidirectional block. After a follow-up of 528 ± 253 days, there were no recurrences of AFL, but there were four recurrences of AF (8%).
Conclusion:  When DP cannot be seen, another simple method for verifying CBDB in ablation of typical atrial flutter is a DP+1 interval > 140 ms.     

Pulmonary vein conduction is the major finding in patients with atrial tachyarrhythmias after intraoperative maze ablation

Introduction: Electrophysiological (EP) data from patients with recurrent atrial tachyarrhythmias (ATa) after intraoperative maze ablation are limited. Furthermore, the clinical course after accomplishing pulmonary vein (PV) isolation using the double lasso technique (DLT) is unknown.
Methods and Results: EP study and catheter ablation (CA) was guided by a three-dimensional electroanatomic mapping system (3-D EA, CARTO, Biosense-Webster) combined with simultaneous ipsilateral PV mapping using the DLT. Defined endpoints were: (1) identification of conduction gaps within the ipsilateral PVs, (2) elimination of all PV spikes, and (3) ablation of clinical ATas.
CA was performed in eight patients (four females, 62 ± 5 years, LA: 50 ± 6 mm) with drug refractory ATa (9.1 ± 6.3 years) despite non-"cut and sew" maze operation. Electrical PV conduction was demonstrated in the majority of patients (7/8). All endpoints were achieved. Repeat ablations were required in three patients. Second ablation was due to typical atrial flutter (n = 1) and atrial fibrillation (n = 2). One patient required three ablations due to a left atrial macroreentrant tachycardia. During a mean follow-up of 15.5 ± 4.8 months, 7/8 patients were free of ATa recurrences.
Conclusion: Incomplete lesions after non-"cut and sew" maze operation are associated with PV conduction and recurrence of ATas. Electrical isolation of ipsilateral PVs and completion of linear lesions guided by 3-D EA mapping is feasible and successful in maintaining sinus rhythm during mid term follow-up. Completeness of linear lesions using EP endpoints should be confirmed during the initial surgical procedure to minimize ATa recurrences.     

Interatrial conduction measured during biventricular pacemaker implantation accurately predicts optimal paced atrioventricular intervals

Background: Optimizing atrioventricular (AV) delay during biventricular (BiV) pacemaker implantation can require substantial resources. Hence, a simpler method is desirable. We hypothesized that interatrial conduction time (IACT), measured at the time of BiV device implant, could be a surrogate value for the optimal AV delay.
Objective: This study determined the relationship between paced IACT and the optimal paced AV delay (PAV), as determined by echocardiography.
Methods: Consecutive subjects (N = 25; age = 66 ± 10 years; M/F: 17/8) undergoing BiV pacemaker implantation and in sinus rhythm were included. Cannulation of the coronary sinus (CS) was at the operator's discretion. A quadripolar electrophysiology catheter was inserted via the guiding sheath into the inferiolateral CS to measure left atrial depolarization. The IACT was calculated as the interval between right atrial stimulation artifact and earliest deflection on the coronary sinus catheter electrogram. Subsequently, during atrial pacing the PAV was determined using transmitral pulsed wave Doppler echocardiography (iterative method). The relationship between paced IACT and PAV was then determined.
Results: The mean ± SD paced IACT and PAV were 126 ± 25 msec and 157 ± 23 msec, respectively. There was a strong positive correlation between the paced IACT and PAV (r = 0.73, P < 0.001). The equation describing the relationship was PAV = 0.68 * (IACT + 104) msec.
Conclusions: The paced IACT has a strong correlation with the echo derived optimal PAV. This method may be used to program PAV intervals without need for echocardiography in patients undergoing BiV pacemaker implantation.