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SATISH, O.S.,et al.: Radiofrequency Catheter Ablation Therapy of Swallowing-Induced Atrioventricular Nodal Reentrant Tachycardia: Report of Two Cases. We describe two patients who presented with a history of recurrent palpitations on swallowing of solid food. The event-recorder and Holter monitoring documented episodic supraventricular tachycardia (SVT) initiated by atrial premature contractions (APCs). During electrophysiological study (EPS), swallowing of solid food consistently induced APCs and their activation sequence, morphology of P wave were suggestive of their right atrial origin in them. Drug challenge did not affect the APC onset during the swallowing. During EPS, slow-fast variety of atrioventricular nodal reentrant tachycardia (AVNRT) was induced and successful radiofrequency (RF) catheter ablation of slow pathway resulted in total relief of their symptoms.(PACE 2005; 28:594–597) [ABSTRACT FROM AUTHOR]

Narrow QRS tachycardia with atrial activation occurring before ventricular activation was induced in a 34-year-old woman with dilated cardiomyopathy. During tachycardia late ventricular extrastimulus delivered when His bundle was refractory failed to reset the tachycardia while early ventricular extrastimulus caused paradoxical delay of the subsequent atrial response and terminated the tachycardia with a QRS not being followed by an atrial response. This is a rare but specific sign for excluding atrial reentry as the mechanism of tachycardia when P wave or atrial activation is registered before QRS response. (PACE 2012; 35:245-248) [ABSTRACT FROM AUTHOR]

Background: The therapeutic effect of low-voltage area (LVA)-guided left atrial (LA) linear ablation for non-paroxysmal atrial fibrillation (non-PAF) is uncertain. We aimed to investigate the efficacy of LA linear ablation based on the preexisting LVA and its effects on LA reverse remodeling in non-PAF patients. Methods: We retrospectively evaluated 145 consecutive patients who underwent radiofrequency catheter ablation for drug-refractory non-PAF. CARTO-guided bipolar voltage mapping was performed in atrial fibrillation (AF). LVA was defined as sites with voltage ≤ 0.5 mV. If circumferential pulmonary vein isolation couldn't convert AF into sinus rhythm, additional LA linear ablation was performed preferentially at sites within LVA. Results: After a mean follow-up duration of 48 ± 33 months, 29 of 145 patients had drugs-refractory AF/LA tachycardia recurrence. Low LA emptying fraction, large LA size and high extent of LVA were associated with AF recurrence. There were 136 patients undergoing LA linear ablation. The rate of linear block at the mitral isthmus was significantly higher via LVA-guided than non-LVA-guided linear ablation. Patients undergoing LVA-guided linear ablation had larger LA size and higher extent of LVA, but the long-term AF/LA tachycardia-free survival rate was higher than the non-LVA-guided group. The LA reverse remodeling effects by resuming sinus rhythm were noted even in patients with a diseased left atrium undergoing extensive LA linear ablation. Conclusions: LVA-guided linear ablation through targeting the arrhythmogenic LVA and reducing LA mass provides a better clinical outcome than non-LVA guided linear ablation, and outweighs the harmful effects of iatrogenic scaring in non-PAF patients. [ABSTRACT FROM AUTHOR]

Identifies the determinants of tachycardia recurrences after radiofrequency ablation of idiopathic ventricular tachycardia. Analysis of clinical and electrophysiologic parameters; Earliest endocardial activation time at the successful ablation site.

Background: Compared with left atrial (LA) dimension, LA emptying fraction (LAEF) has received less emphasis as a predictor of atrial fibrillation (AF) recurrence after radiofrequency catheter ablation (RFCA). In addition, patients experiencing post-RFCA AF recurrence may respond to previously ineffective antiarrhythmic drugs (AADs). Classifying these patients into a third RFCA outcome category is recommended. Objective: To identify predictors of RFCA outcome classified into three categories, and to build proportional odds logistic regression models for clinical applicability to predict AF recurrence. Methods: Data were retrospectively collected from 483 consecutive patients with drug-refractory AF undergoing RFCA (328 men; age 58.4 ± 11.5 years; 383 paroxysmal). Patients were classified into 3 groups based on the last RFCA outcome: group 1, free from AF without AADs; group 2, free from AF with AADs; and group 3, recurrence of AADs-refractory atrial tachyarrhythmia. Results: After a mean follow-up duration of 64.5 ± 43.2 months and mean ablation procedure number of 1.37 ± 0.68, the RFCA outcome showed 76.0%, 9.5% and 14.5% of patients in groups 1, 2, and 3, respectively. In multivariate analysis, LAEF was the most stable and important predictor of AF recurrence, followed by body mass index, stroke, AF duration, mitral regurgitation, and LA linear ablation. For patients undergoing repeat RFCA, LAEF was the only independent predictor (cutoffs: 43% and 35% for groups 1 and 3, respectively). Conclusion: LAEF provides optimal prognostic information regarding the risk stratification of AF patients undergoing RFCA. [ABSTRACT FROM AUTHOR]

Background Radiofrequency catheter ablation (RFCA) of ventricular arrhythmias (VAs) originating from the left ventricular (LV) papillary muscles (PMs) is challenging. Methods We enrolled 16 consecutive patients who received RFCA for VAs from LV PMs. Three-dimensional electroanatomical mapping was used to construct activation and/or pace maps. RFCA was performed first at the earliest activation site or at the best matched site in the pace maps. When an acceleration or reduction in the incidence of VAs was observed during the first few seconds of the application, the ablation energy was delivered continuously for 60–120 s. Additional ablation was then circumferentially delivered at the base of the PMs. Results RFCA was successfully performed in all 16 patients with no cases of recurrence of VAs after a mean follow-up of 20 ± 12 months. VAs originated from the anterior (n = 8) and posterior (n = 8) PMs. Purkinje potentials were identified at the target sites in seven patients. All VAs were temporarily suppressed by one to two long-duration shots of RFCA at the initial targeted site, but recurrence was subsequently noted. In six patients, the QRS morphologies of the VAs changed after the initial RFCA. A subsequent circumferential approach with multiple ablations applied to the base of the PMs completely eliminated all VAs. In all but one patient, successful RFCA was achieved using an open-irrigated ablation catheter. Conclusions Circumferential RFCA at the base of the PMs overcame anatomical limitations, leading to a high success rate of RFCA for VAs from LV PMs. [ABSTRACT FROM AUTHOR]

Background: L-type calcium current reactivation plays an important role in development of early afterdepolarizations (EADs) and torsades de pointes (TdP). Secondary intracellular calcium (Cai) rise is associated with initiation of EADs. Objective: To test whether inhibition of sarcoplasmic reticulum (SR) Ca2+ cycling suppresses secondary Cai rise and genesis of EADs. Methods: Langendorff perfusion and dual voltage and Cai optical mapping were conducted in 10 rabbit hearts. Atrioventricular block (AVB) was created by radiofrequency ablation. After baseline studies, E4031, SR Ca2+ cycling inhibitors (ryanodine plus thapsigargin) and nifedipine were then administrated subsequently, and the protocols were repeated. Results: At baseline, there was no spontaneous or pacing-induced TdP. After E4031 administration, action potential duration (APD) was significantly prolonged and the amplitude of secondary Cai rise was enhanced, and 7 (70%) rabbits developed spontaneous or pacing-induced TdP. In the presence of ryanodine plus thapsigargin, TdP inducibility was significantly reduced (2 hearts, 20%, p = 0.03). Although APD was significantly prolonged (from 298 ± 30 ms to 457 ± 75 ms at pacing cycle length of 1000 m, p = 0.007) by ryanodine plus thapsigargin, the secondary Cai rise was suppressed (from 8.8 ± 2.6% to 1.2 ± 0.9%, p = 0.02). Nifedipine inhibited TdP inducibility in all rabbit hearts. Conclusion: In this AVB and long QT rabbit model, inhibition of SR Ca2+ cycyling reduces the inducibility of TdP. The mechanism might be suppression of secondary Cai rise and genesis of EADs. [ABSTRACT FROM AUTHOR]

Dantrolene was reported to suppress ventricular fibrillation (VF) in failing hearts with acute myocardial infarction, but its antiarrhythmic efficacy in regional ischemia-reperfusion (IR) hearts remains debatable. Heart failure (HF) was induced by right ventricular pacing. The IR rabbit model was created by coronary artery ligation for 30 min, followed by reperfusion for 15 min in vivo in both HF and non-HF groups (n = 9 in each group). Simultaneous voltage and intracellular Ca2+ (Cai) optical mapping was then performed in isolated Langendorff-perfused hearts. Electrophysiological studies were conducted and VF inducibility was evaluated by dynamic pacing. Dantrolene (10 μM) was administered after baseline studies. The HF group had a higher VF inducibility than the control group. Dantrolene had both antiarrhythmic (prolonged action potential duration (APD) and effective refractory period) and proarrhythmic effects (slowed conduction velocity, steepened APD restitution slope, and enhanced arrhythmogenic alternans induction) but had no significant effects on ventricular premature beat (VPB) suppression and VF inducibility in both groups. A higher VF conversion rate in the non-HF group was likely due to greater APD prolonging effects in smaller hearts compared to the HF group. The lack of significant effects on VPB suppression by dantrolene suggests that triggered activity might not be the dominant mechanism responsible for VPB induction in the IR model. [ABSTRACT FROM AUTHOR]

Background Macroreentrant atrial tachycardia (MRAT) is frequently unresponsive to antiarrhythmic drugs. The application of three-dimensional (3D) mapping and entrainment pacing contributes to a high success rate for radiofrequency ablation, but programmed electrical pacing may either terminate or transform clinical tachyarrhythmias. On the basis of clinical experiences of the use of ventricular tachycardia ablation, channels with continuous activation are suitable for reentrant circuits, and ablation at these channels can lead to noninducibility of ventricular tachycardias. We reviewed patients referred for symptomatic MRAT with identified channels with continuous activation and evaluated the efficacy of MRAT ablation by targeting these channels. Methods Fifteen consecutive patients (10 men, 49 ± 14 years) with MRAT illustrated by endocardial activation maps using a 3D electroanatomical mapping system (CARTO™, Biosense Webster, Diamond Bar, CA, USA) were included in this study. Continuous activation was defined as double or continuous potentials without an isoelectric interval, and sites with continuous activation were tagged for measurements of channel properties. Radiofrequency ablation was performed at those targeted sites located within the reentrant circuit. Results Radiofrequency ablation successfully eliminated MRAT in all patients. The mean cycle length was 283 ± 60 ms, and the longest activation duration was 112 ± 38 ms. The minimal and maximal bipolar voltage amplitudes were 0.13 ± 0.1 mV and 0.7 ± 0.6 mV, respectively. The targeted ablation length and width were 28.9 ± 15.3 mm and 9.4 ± 3.3 mm, respectively. Conclusion Radiofrequency ablation of MRAT targeting channels with continuous activation using a 3D electroanatomical mapping system yields a high success rate. [ABSTRACT FROM AUTHOR]

Dantrolene in Failing Hearts with AMI Introduction Dantrolene prevents arrhythmogenic Ca2+ release during heart failure (HF). However, direct evidence to support its antiarrhythmic effects in failing hearts with acute myocardial infarction (AMI) is lacking. Methods and Results HF was induced by right ventricular pacing (312 beats/min, 4 weeks) in 19 rabbits. AMI was induced by coronary artery ligation in rabbits surviving chronic pacing (n = 17). The hearts were quickly excised and Langendorff-perfused for simultaneous membrane potential and intracellular Ca2+ (Cai) optical mapping when ventricular fibrillation (VF) occurred or 4 hours after AMI. The VF inducibility was defined as the ability to provoke sustained VF (>2 minutes) by pacing. Dantrolene (10 μM) was administered after baseline studies. Spontaneous VF occurred in 5 rabbits (SVF group). The ventricular premature beat (VPB) burden was significantly higher in the SVF group than the non-SVF group (P < 0.05). Dantrolene suppressed VPB burden (P = 0.03) and prolonged action potential duration (APD; P < 0.05) to reduce VF inducibility (P < 0.05). However, dantrolene shortened immediate postshock APD50 even if VF storm was suppressed. Conclusion In failing hearts with AMI, VPB burden plays a pivotal role in SVF occurrence. Dantrolene suppresses VPBs and/or prolongs repolarization to inhibit spontaneous VF and reduce VF inducibility. [ABSTRACT FROM AUTHOR]

Abstract: Background: Piceatannol, a hydroxystilbene natural product, has been reported to exert antiarrhythmic action via I Na inhibition and slow I Na inactivation in ischemia-reperfused (IR) rat hearts. The present study aimed to clarify the proarrhythmic property of piceatannol during regional IR injury in failing rabbit hearts. Methods: Heart failure (HF) was induced by rapid right ventricular pacing for 4weeks. The IR model was created by coronary artery ligation for 30min, followed by reperfusion for 15min in vivo. Simultaneous voltage and intracellular Ca2+ (Cai) optical mapping was then performed in isolated Langendorff-perfused hearts (n =11 in each HF and control group). Action potential duration (APD) restitution, arrhythmogenic alternans and VF inducibility were evaluated by a dynamic pacing protocol. Conduction velocity was measured along lines across the IR and non-IR zones during pacing. Piceatannol (10μM) was administered after baseline studies. Results: In the HF group, piceatannol decreased conduction velocity, induced rate-dependent regional inhomogeneity of conduction delay and wavelength shortening, slowed Cai decay, and facilitated arrhythmogenic alternans instead of APD prolongation to increase VF inducibility. In the control group, the proarrhythmic effects of piceatannol on APD restitution, arrhythmogenic alternans and conduction delay were offset by its antiarrhythmic effects (APD and wavelength prolongation), resulting in a neutral effect on VF inducibility. Conclusions: Piceatannol (10μM) is proarrhythmic in failing rabbit hearts with regional IR injury. The increased VF inducibility by piceatannol in HF suggests that its undesirable effects are more pronounced than its benefits in failing hearts. [Copyright &y& Elsevier]

Background The effects of SEA0400, a Na+/ Ca2+ exchanger (NCX) blocker, on dynamic factors and arrhythmogenic alternans in 1-month myocardial infarction (MI) hearts remain unknown. Methods Simultaneous voltage and intracellular Ca2+ (Cai) optical mapping was performed in 12 rabbit hearts with MI for 1 month and six normal rabbit hearts as control. Western-blot studies were performed in both groups in an additional six hearts for each. Action potential duration (APD) restitution was constructed and arrhythmogenic alternans was induced by dynamic pacing. SEA0400 (0.03, 3 μM) was administered after baseline studies. Results SEA0400 suppressed pacing-induced ventricular premature beats in a concentration-dependent manner. SEA0400 at 0.03 μM steepened APD restitution slopes and enhanced spatially discordant alternans (SDA), which became insignificant at 3 μM. The VF inducibility was seven of nine at baseline, nine of nine at 0.03 μM SEA0400, and five of nine at 3 μM SEA0400 (P = NS). Significant upregulation of NCX in the remote but not periinfarct zone and less degree downregulation of DHP1α in the remote versus periinfarct zone may play a role in enhancing SDA induction by SEA0400 in 1-month MI hearts. Conclusions In 1-month MI hearts, SEA0400 suppresses pacing-induced ventricular premature beats, but also is proarrhythmic by steepening APD restitution and enhancing SDA via NCX inhibition. Heterogeneous upregulation of NCX and downregulation of DHP1α may contribute to SDA augmentation by SEA0400 in this model. The insignificant effect of SEA0400 on VF inducibility suggests that suppression of both reentry and triggered activity is required to suppress VF induction in this model. [ABSTRACT FROM AUTHOR]

Background Nicorandil (a KATP opener) administration is reported to reduce ventricular arrhythmias 4.8 ± 2.2 hours after myocardial infarction (MI). The electrophysiological changes and the effects on dynamic factors and dynamically induced spatially discordant alternans by nicorandil during phase-2 MI are unclear. Methods Simultaneous voltage and intracellular Ca2+ (Cai) optical mapping was performed in nine Langendorff-perfused hearts 4-5 hours after coronary artery ligation and nine control hearts. Action potential duration (APD) restitution was constructed and arrhythmogenic alternans was induced by dynamic pacing. Western blot studies (Kir6.1 and Kir6.2) were performed in six more hearts for both groups. Nicorandil (100 μM) was administered after baseline studies. Results Phase-2 MI hearts showed longer APD, slower conduction velocity (CV), and higher ventricular fibrillation (VF) inducibility than the control hearts. Nicorandil shortened and restored APD without significant arrhythmogenic effects, and also increased the rate of Cai reuptake and flattened CV restitution to suppress spatially discordant alternans, which might account for a tendency toward higher VF threshold with nicorandil infusion in phase-2 MI hearts. Immunoblotting studies showed significant down-regulation of KATP protein expression, which was functionally correlated to the blunted APD shortening response to nicorandil. Conclusions KATP expression is down-regulated in phase-2 MI hearts. Nicorandil restores APD, increases the rate of Cai reuptake, and flattens CV restitution to suppress spatially discordant alternans induction, which ameliorates its proarrhythmic effects during phase-2 MI. [ABSTRACT FROM AUTHOR]

Background: Clopidogrel is a prodrug that undergoes in vivo bioactivation to show its antiplatelet effects. Recent studies have shown that cytochrome P450 (CYP), ATP-binding cassette transporters (ABCB1), and paraoxonase-1 (PON1) play crucial roles in clopidogrel bioactivation. Here, we aim to determine the effects of genetic polymorphisms of CYP (CYP 2C19*2, CYP 2C19*3, and CYP 2C19*17), ABCB1 (ABCB1 3435C>T, ABCB1 129T>C, and ABCB1 2677G>T/A), and PON1 (PON1 Q192R, PON1 L55M, and PON1 108C.T) on the development of stent thrombosis (ST) in patients receiving clopidogrel after percutaneous coronary intervention (PCI). Methods and Results: We evaluated the incidence of ST (0.64%) in 4964 patients who were recruited in the CAPTAIN registry (Cardiovascular Atherosclerosis and Percutaneous TrAnsluminal INterventions). The presence of genetic polymorphisms was assessed in 20 subjects who developed ST after aspirin and clopidogrel therapy and in 40 age- and sex-matched control subjects who did not develop ST, which was documented after 9 months of angiographic follow-up. ST was acute in 5 subjects, subacute in 7, late in 7, and very late in 1. The presence of CYP 2C19*2 allele was significantly associated with ST (adjusted odds ratio [ORadj]: 4.20, 95% confidence interval [CI], 1.263-9.544; P = 0.031). However, genetic variations in PON1 and ABCB1 showed no significant association with ST. Conclusion: We conclude that in a Taiwanese population, PON1 Q192R genotype is not associated with ST development after PCI. However, the presence of CYP 2C19*2 allele is a risk factor for ST development after PCI. [ABSTRACT FROM AUTHOR]

Objectives: The purpose of this study was to provide direct evidences that rotor ablation suppresses atrial fibrillation (AF) inducibility. Background: Micro–re-entrant wavefronts have been suggested to serve as sources of rapid activations during AF. Whether AF inducibility is suppressed by elimination of rotors remains unknown. Methods: We used optical mapping to study Langendorff-perfused left pulmonary vein (PV)–left atrium (LA) preparations from 13 dogs with pacing-induced heart failure. Atrial arrhythmias were induced by pacing and mapped during acetylcholine infusion (1 μmol/l). Rotors were identified from optical recordings. Epicardial ablation was performed targeting the rotor anchoring sites in preparations with sustained (>10 min) or incessant spontaneous AF. Non-rotor ablation was performed in 4 preparations. Repeated pacing was performed to test the AF inducibility after ablation. Results: Sustained AF (n = 12) and incessant spontaneous AF (n = 1) were induced after acetylcholine infusion. Pulmonary vein focal discharge was found in 9 preparations (9.2 ± 4.2 beats/s), and rotor anchoring was found at the left superior PV-LA junction in 13 preparations (9.1 ± 4.6 beats/s) and at the ligament of Marshall-PV-LA junction in 1 preparation. Epicardial rotor ablation successfully inhibited the inducibility of sustained AF in 12 of 13 preparations (p < 0.01), including 4 with the maximal dominant frequency sites located on the PV-LA junctional rotor zones (direct elimination of mother rotors). The longest AF duration was shortened significantly by rotor ablation (Wilcoxon Z = 3.60, p = 0.002, n = 13), but not by non-rotor ablation (Wilcoxon Z = 1.00, p = 0.317, n = 4). Conclusions: Epicardial ablation of the rotor anchoring sites suppresses AF inducibility. The arrhythmogenicity at the maximal dominant frequency sites is directly/indirectly suppressed by the rotor ablation. [ABSTRACT FROM AUTHOR]

We hypothesize that remodelling of action potential and intracellular calcium (Cai) dynamics in the peri-infarct zone contributes to ventricular arrhythmogenesis in the postmyocardial infarction setting. To test this hypothesis, we performed simultaneous optical mapping of Cai and membrane potential ( Vm) in the left ventricle in 15 rabbit hearts with myocardial infarction for 1 week. Ventricular premature beats frequently originated from the peri-infarct zone, and 37% showed elevation of Cai prior to Vm depolarization, suggesting reverse excitation–contraction coupling as their aetiology. During electrically induced ventricular fibrillation, the highest dominant frequency was in the peri-infarct zone in 61 of 70 episodes. The site of highest dominant frequency had steeper action potential duration restitution and was more susceptible to pacing-induced Cai alternans than sites remote from infarct. Wavebreaks during ventricular fibrillation tended to occur at sites of persistently elevated Cai. Infusion of propranolol flattened action potential duration restitution, reduced wavebreaks and converted ventricular fibrillation to ventricular tachycardia. We conclude that in the subacute phase of myocardial infarction, the peri-infarct zone exhibits regions with steep action potential duration restitution slope and unstable Cai dynamics. These changes may promote ventricular extrasystoles and increase the incidence of wavebreaks during ventricular fibrillation. Whereas increased tissue heterogeneity after subacute myocardial infarction creates a highly arrhythmogenic substrate, dynamic action potential and Cai cycling remodelling also contribute to the initiation and maintenance of ventricular fibrillation in this setting. [ABSTRACT FROM AUTHOR]

YEH, K.-H.,et al.: Long-Term Performance of Transvenous, Steroid-Eluting, High Impedance, Passive-Fixation Ventricular Pacing Leads. The long-term performance of two high impedance, steroid-eluting, passive-fixation ventricular leads, porous platinum iridium electrode CPI Selute Picotip 4035 (131 patients), and platinized platinum electrode Medtronic Capsure Z 5034 (57 patients), was compared with one conventional 8.0-mm2 porous platinum iridium electrode CPI Selute 4285 (38 patients). The mean follow-up period was 28± 14 months. Capture threshold, R wave amplitude, and pacing impedance were measured at the time of implantation, immediately after implantation, 1 week, 1, 3, and 6 months after implantation and then every 6 months thereafter. The two high impedance leads revealed a higher sensing slew rate than the conventional lead, the R wave amplitude was similar among the three groups, but the voltage threshold at 0.5-ms pulse width was significantly higher in porous platinum iridium groups at the time of implantation. During follow-up, the conventional lead revealed a significantly higher R wave amplitude within the first 3 months, however, this pattern disappeared after 3 months. Pacing impedance was significantly higher in the high impedance porous platinum iridium electrode groups. Voltage threshold at 0.5-ms pulse width was similar among the three groups in the first 3 months, however, it increased gradually and was significantly higher in porous platinum iridium electrode groups subsequently. The energy threshold at 0.5 ms was significantly lower in the two high impedance groups than the conventional group, but no difference was found in the two high impedance groups. Lead related complications were similar among the three groups. In conclusion, high impendence electrodes with different design and materials had different properties; platinized platinum electrode showed a lower pacing impedance but had a more stable long-term capture threshold as compared to the porous platinum iridium electrode. Further studies are mandatory for the development of an ideal pacing lead.(PACE 2004; 27:1399–1404) [ABSTRACT FROM AUTHOR]