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Unipolar Electrograms (unipolar + electrogram)
Selected AbstractsDetermining the Local Time of Activation from the Unipolar Electrogram: New Methods, New ChallengesJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 10 2000BONNIE B. PUNSKE PH.D. [source] Mechanism of Propensity to Atrial Fibrillation in Patients Undergoing Isthmus Ablation for Typical Atrial FlutterJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2 2005HEMANTH RAMANNA M.D. Background: Patients undergoing isthmus ablation for atrial flutter (AFL) may reveal postablation atrial fibrillation (AF). The electrophysiological mechanism is unclear. In patients with idiopathic AF, enhanced spatial dispersion of right atrial refractoriness was the substrate for the initiation of AF. We hypothesize that dispersion of right atrial refractoriness in patients undergoing AFL ablation is the major cause of postablation AF. Methods: Consecutive patients (n = 42) undergoing isthmus ablation for typical AFL were included. Twelve right atrial unipolar electrograms were recorded. Inducibility of AF was assessed by a pacing protocol, starting with one extrastimulus, followed by more aggressive pacing until AF was induced. Mean fibrillatory intervals were used to assess local refractoriness of each recording site. Spatial dispersion of right atrial refractoriness was calculated as the coefficient of dispersion (CD-value: standard deviation of the mean of all local mean fibrillatory intervals as a percentage of the overall mean fibrillatory interval). A CD-value of 3.0 or less was defined as normal, whereas CD-value greater than 3.0 was considered enhanced dispersion. PES and refractoriness analysis were followed by isthmus ablation. Results: Of the 42 patients, 29 had CD-value of 3.0 or less. In these 29 patients, AF was induced with 1 extrastimulus in only 1 patient, with 2 extrastimuli in 4 patients and burst pacing was required to induce AF in 24 of these 29 patients. Prior to the procedure, 5 of 29 patients had AF episodes, after ablation 6 of 29 patients. Of the 42 patients, 13 had CD-value greater than 3.0, AF was induced with a single extrastimulus in 11 patients, with 2 extrastimuli in the remaining 2 patients. Of the 13 patients, 11 had AF episodes both before and after ablation (P < 0.001). Conclusion: Enhanced spatial dispersion of right atrial refractoriness may be the substrate for propensity to AF in patients with AFL. The substrate was associated with enhanced inducibility of atrial fibrillation. [source] On the Atrial Response to Focal Discharges in ManJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2004HEMANTH RAMANNA M.D. Introduction: Triggers and vulnerability are key factors for the occurrence of atrial fibrillation (AF). The aim of this study was to assess spatial dispersion of atrial refractoriness and vulnerability in response to both focal discharges as well as programmed electrical stimulation in patients undergoing ablation of atrial arrhythmogenic foci. Methods and Results: Twenty-nine patients were studied, and 12 right atrial unipolar electrograms were recorded. Inducibility of AF was assessed by a pacing protocol that started with one extrastimulus, followed by more aggressive pacing until AF was obtained. Mean fibrillatory intervals were used to assess the local refractoriness of each recording site. Spatial dispersion of refractoriness was calculated as the coefficient of dispersion (CD value: standard deviation of the mean of all local mean fibrillatory intervals as a percentage of the overall mean fibrillatory interval). Based on our previous study, a CD value , 3.0 was defined as normal, whereas a CD value >3.0 was considered enhanced spatial dispersion of refractoriness. Fifteen of 29 patients had normal dispersion of refractoriness (mean CD value 1.65 ± 0.43), and AF was inducible with burst pacing only. These patients had focal discharges causing rapid atrial tachycardia with a focal activation pattern. Activation mapping of focal activity was possible in 14 of 15 patients. Focal triggering of AF occurred in only 1 of 15 patients. Fourteen of 29 patients had enhanced dispersion (mean CD value 4.2 ± 0.72). AF was inducible with a single extrastimulus in 11 of 14 patients (P < 0.001). Focal triggering of AF occurred in all 14 patients. Conclusion: Spatial dispersion of atrial refractoriness determines whether focal atrial discharges trigger AF with disorganized activity or, alternatively, only rapid atrial tachycardia. (J Cardiovasc Electrophysiol, Vol. 15, pp. 1-8, June 2004) [source] Endocardial Mapping of Right Ventricular Outflow Tract Tachycardia Using Noncontact Activation MappingJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2003Michael Ribbing M.D. Introduction: Activation mapping and pace mapping identify successful ablation sites for catheter ablation of right ventricular outflow tract (RVOT) tachycardia. These methods are limited in patients with nonsustained tachycardia or isolated ventricular ectopic beats. We investigated the feasibility of using noncontact mapping to guide the ablation of RVOT arrhythmias. Methods and Results: Nine patients with RVOT tachycardia and three patients with ectopic beats were studied using noncontact mapping. A multielectrode array catheter was introduced into the RVOT and tachycardia was analyzed using a virtual geometry. The earliest endocardial activation estimated by virtual electrograms was displayed on an isopotential color map and measured33 ± 13 msecbefore onset of QRS. Virtual unipolar electrograms at this site demonstrated QS morphology. Guided by a locator signal, ablation was performed with a mean of6.9 ± 2.2radiofrequency deliveries. Acute success was achieved in all patients. During follow-up, one patient had a recurrence of RVOT tachycardia. Compared with patients(n = 21)who underwent catheter ablation using a conventional approach, a higher success rate was achieved by noncontact mapping. Procedure time was significantly longer in the noncontact mapping group. Fluoroscopy time was not significantly different in the two groups. Conclusion: Noncontact mapping can be used as a reliable tool to identify the site of earliest endocardial activation and to guide the ablation procedure in patients with RVOT tachycardia and in patients with ectopic beats originating from the RVOT. (J Cardiovasc Electrophysiol, Vol. 14, pp. 602-608, June 2003) [source] Restitution Properties and Occurrence of Ventricular Arrhythmia in LQT2 Type of Long QT SyndromeJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 9 2002SOU YAMAUCHI M.D. Mechanisms of Ventricular Arrhythmia in LQT2 Heart.Introduction: The aim of this study was to clarify the ventricular tachyarrhythmia mechanism induced by the IKr -blocking agent E4031, simulating the LQT2 form. Electrophysiologic properties were examined in 13 canines before and after administration of E4031. Method and Results: Thirty-six needle electrodes were inserted into the anterior left ventricular wall. From each needle, local unipolar electrograms were obtained from four intramural sites. Activation time (AT) and activation-recovery interval (ARI) were measured. To evaluate the susceptibility to ventricular arrhythmia, intramural ARI dispersions and the restitution relationship between ARI and diastolic interval were calculated. After E4031 administration, ARI prolonged uniformly in each myocardial layer. However, ARI dispersion was not augmented compared with control. The slope of the ARI restitution curve after E4031 was significantly steeper than control. A steep slope may result from augmented ARI alternans. In 11 of the 13 canines, ventricular tachyarrhythmia was induced by programmed stimulation after E4031, whereas no arrhythmia was induced by the same protocol in control. Conclusion: Steepness of electrical restitution may play a major role in arrhythmogenicity in LQT2 hearts. [source] Arrhythmogenesis of T Wave Alternans Associated with Surface QRS Complex Alternans and the Role of Ventricular Prematurity: Observations from a Canine Model of LQT3 SyndromeJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2002MASAOMI CHINUSHI M.D. Intramural TWA and Its Arrhythmogenesis.Introduction: T wave alternans (TWA) is characterized by cycle-to-cycle changes in the QT interval and/or T wave morphology. It is believed to amplify the underlying dispersion of ventricular repolarization. The aim of this study was to examine the mechanisms and arrhythmogenesis of TWA accompanied by QRS complex and/or blood pressure (BP) waveform alternans, using transmural ventricular electrogram recordings in an anthopleurin-A model of long QT syndrome. Methods and Results: The cardiac cycle length was gradually shortened by interruption of vagal stimulation, and TWA was induced in six canine hearts. Transmural unipolar electrograms were recorded with plunge needle electrodes from endocardial (Endo), mid-myocardial (Mid), and epicardial (Epi) sites, along with the surface ECG and BP. The activation-recovery interval (ARI) was measured to estimate local refractoriness. During TWA, ARI alternans was greater at the Mid than the Epi/Endo sites, and it was associated with the development of marked spatial dispersion of ventricular repolarization. As TWA increased, ventricular activation of the cycles associated with shorter QT intervals displayed delayed conduction at the Mid sites as a result of a critically longer ARI of the preceding cycle and longer QT interval, while normal conduction was preserved at the Epi site. Delayed conduction at the Mid sites manifested as surface ECG QRS and BP waveform alternans, and spontaneous ventricular tachyarrhythmias developed in absence of ventricular prematurity. In other instances, in absence of delayed conduction during TWA, ventricular premature complexes infringed on a prominent spatial dispersion of ventricular repolarization of cycles with long QT intervals and initiated ventricular tachyarrhythmia. Conclusion: TWA accompanied by QRS alternans may signal a greater ventricular electrical instability, since it is associated with intramural delayed conduction, which can initiate ventricular tachyarrhythmia without ventricular premature complexes. [source] Prolongation of Activation-Recovery Interval over a Preexcited Region before and after Catheter Ablation in Patients with Wolff-Parkinson-White SyndromeJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2001YASUYA INDEN M.D. Activation-Recovery Interval in WPW Syndrome. Introduction: Preexisting changes in repolarization properties play an important role in T wave abnormalities (cardiac memory) after ablation in patients with Wolff-Parkinson-White (WPW) syndrome. However, no report has provided direct evidence for prolongation of action potential duration (APD) over a preexcited region before and after ablation. Methods and Results: We studied 10 patients with ventricular preexcitation due to a left-sided accessory pathway (AP) (group M) and 12 patients with concealed left-sided AP (group C) to clarify prolongation of APD using activation-recovery intervals (ARIs) from epicardial and endocardial unipolar electrograms in patients with WPW syndrome. ARI was calculated from unipolar electrograms at the His bundle and the coronary sinus adjacent to the AP during atrial pacing (100 beats/min) before and 30 minutes after ablation. Before ablation, ARIs at the AP site were significantly longer in group M than in group C (255 ± 21 msec vs 211 ± 24 msec; P < 0.01), whereas ARIs at the His bundle did not differ between the two groups (255 ± 20 msec vs 245 ± 27 msec; P = NS). After ablation, group M showed no significant changes in ARIs at the AP and His bundle (256 ± 19 msec and 253 ± 15 msec) compared with before ablation. Conclusion: We found by direct analysis of ARIs from the epicardium that APD prolongation over the preexcited region was present before catheter ablation and persisted after catheter ablation. The gradual changes in repolarization properties, including APD prolongation after discontinuation of AP, may be one mechanism of cardiac memory after catheter ablation in patients with WPW syndrome. [source] Laplacian Electrograms and the Interpretation of Complex Ventricular Activation Patterns During Ventricular FibrillationJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 10 2000PH.D., RUBEN CORONEL M.D. Laplacian Electrograms and Ventricular Fihrillation. Introduction. During ventricular fibrillation (VF) interpretation of a local electrogram and determination of the local activation moment are hampered by remote activity or intervening repolarization waves. Successful defibrillation depends on critical timing of the shock relative to local activation. We tested the applicabillity of Laplacian electrograms for detection of the moment of local activation during VF. Methods and Results. From isolated perfased porcine infact heart, 247 local unipolar electrograms were recorded simultaneously (13 × 19 matrix, interelectrode distance 0.3 mm) from the left ventricular wall during sinus rhythm, following pacing or during VF, Activation maps were constructed based on local unipolar electrograms, and Laplacian electrograms were calculated from local electrograms ane its eight neighbors. The Laplacian electrogram displayed a sharp R/S complex with local activation iodicted by the moment of zero crossing without interference from remote activity or repolarization waves. Its amplitude increased with decreasing interelectrode distance, Following epicardial stimulation, Laplacian amplitude was significantly larger than during complexes with different morphology. Collision of wavefronts was associated with entirely positive Laplacian waveforms; "focal" appearancce of acitivity was associated with an entirely negative waveform. Activation block in the activation maps was correlated with the appearance of substanined episodes of negativity or positivity in the Laplacian electrogram (depending on the location of the recording site relative to the line of block). Conclusion. Laplacian electrograms allow detection of the moment of local activation without interference from remote activity or repolarization, especially during complex arrhythmias. The technique applied toe automatic sensing devices, such its the internal defibrillator, may optimize defibrtilation success. (J Cardiovasc Electrophysiol, Vol. 11, pp. 1119-1128, October 2000) [source] Atrial Activation Sequence During Junctional Tachycardia Induced by Thermal Stimulation of Koch's Triangle in Canine Blood-Perfused Atrioventricular Node PreparationPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 5 2002ATSUSHI IWASA IWASA, A., et al.: Atrial Activation Sequence During Junctional Tachycardia Induced by Thermal Stimulation of Koch's Triangle in Canine Blood-Perfused Atrioventricular Node Preparation. Junctional tachycardia is observed during radiofrequency ablation of the slow pathway. The authors investigated the atrial activation sequence during junctional tachycardia induced with thermal stimulation in canine blood-perfused atrioventricular node (AVN) preparation. The canine heart was isolated (n = 7) and cross-circulated with heparinized arterial blood of the support dog. The activation sequence in the region of Koch's triangle (15 × 21 mm) was determined by recording 48 unipolar electrograms. Atrial sites anterior to the coronary sinus ostium (site AN), close to the His-potential recording site (site N) and superior to site N (site F), were subjected to a continuous temperature rise from 38°C to 50°C with a heating probe. The temperature of the tissue adjacent to the heating site was monitored simultaneously. Junctional tachycardia at a rate of 92 ± 12 beats/min with the His potential preceding the atrial one in the His-bundle electrogram was induced during thermal stimulation at site AN (temperature 42.1°C ± 0.9°C) in all seven preparations, whereas junctional tachycardia was induced during stimulation at site N in one and at site F in none. In each case, the temperature rose only at the site of stimulation. The earliest activation site during junctional tachycardia induced by site AN stimulation was at the His-potential recording site in five preparations and the middle of Koch's triangle in the other two. After creating an obstacle between sites AN and N, atrial tachycardia at a rate of 85 ± 11 beats/min was induced during site AN stimulation. The earliest activation site during this tachycardia was site AN. Thus, junctional tachycardia induced by thermal stimulation was suggested to originate from the AN thermal stimulation site. The impulse from the stimulation site appeared to conduct via the posterior input to the compact AVN and junctional tachycardia was generated. When the posterior input was interrupted, atrial tachycardia was generated. [source] Chronic Amiodarone Effects on Epicardial Conduction and Repolarization in the Isolated Porcine HeartPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 7 2000DOMINIQUE LACROIX Amiodarone is a potent antiarrhythmic agent with complex chronic effects, notably on repolarization and conduction, that are not fully understood. Its low arrhythmogenic potential has been related to a lack of increase in repolarizution dispersion. Since its effects are not documented in pigs we conducted a mapping study of activation and repolarization in isolated perfused porcine hearts. Amio20 female pigs (n = 7) received amiodarone 20 mg/kg per day over 4 weeks while Amio 5O female pigs (n = 7) received 50 mg/kg per day over 4 weeks. Concentrations of the drug encompassed values found in clinical studies. Then, activation patterns and activation-to-recovery intervals (ARI) were mapped epicardially from 128 unipolar electrograms in isolated perfused hearts in corroboration of epicardial action potential recordings. Mean ARI was longer in Amio20 experiments compared to the seven control hearts (325 ±11 ms vs 288 ± 5 m.s at 1,000 ms), whereas ARI dispersion was not different, being comprised between 7 and 11 ms and generating smooth gradients. In Amio5O experiments, mean ARI was further prolonged (390 ±10 ms at 1,500 ms) with an exaggerated reverse rate dependence concomitant with a depressant effect on the plateau of the action potential. Again, ARI dispersion did not differ from controls. Finally, the drug depressed the maximal rate of depolarization (Vmax) and slowed conduction in a rate dependent and concentration dependent fashion. In conclusion, chronic amiodarone induces Class I and Class HI antiarrhythmic effects in ventricular porcine epicardium that are concentration dependent but does not affect dispersion of repolarization. This may partly explain its low arrhythmogenic potential. [source] Effect of Underlying Heart Disease on the Frequency Content of Ventricular Fibrillation in the Dog HeartPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2 2000JASON T. JACOBSON Although prior studies have examined the frequency content of heal electro-gram characteristics during fibrillation, little is know about the effects of underlying heart disease on these parameters. This study was designed to compare the frequency content of local electrograms during VF in canine models of acute ischemia, subacute infarction, and chronic myocardial infarction (MI) to those in control animals to test the hypothesis that underlying heart disease can alter the basic characteristics of VF. VF was induced using burst pacing in three groups of mongrel dogs. Five dogs were evaluated 8 weeks after LAD occlusion MI, five were evaluated 5 days after experimental MI, and 5 had VF induced before (control) and immediately after LAD occlusion (ischemia). During VF, unipolar electrograms were recorded from 112 sites on the anterior LV and electrograms were evaluated 15 and 30 seconds after VF initiation in each group. Electrograms were analyzed by fast Fourier transform. No significant time dependent changes in VF characteristics were noted. The peak frequency was highest in control animals and 8-week MI, intermediate in 5-day MI, and lowest in acute ischemia (P < 0.01 for pairwise comparisons). In contrast, the fractional of energy within a bandwidth of 25% peak amplitude was highest in acute ischemia, (P < 0.001) and similar in the other three groups. Infarction decreased total energy by approximately 50%. In conclusion, the pressure of ischemia or infarction alters the frequency content of VF in a complex fashion. In addition to decreasing the peak frequency, the shape of the power spectral curve is altered in models of structural heart disease. These results suggest that the electrophysiological changes produced by infarction or ischemia alter the structural organization of ventricular fibrillation. [source] | ||||||||||