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Notes: Introduction: Atrial arrhythmias have emerged as a topic of great interest for clinical electrophysiologists. Noninvasive imaging of electrical function in humans may be useful for computer-aided diagnosis and treatment of cardiac arrhythmias, which can be accomplished by the fusion of data from ECG mapping and magnetic resonance imaging (MRI). Methods and Results: In this study, a bidomain-theory–based surface heart model activation time (AT) imaging approach was applied to paced rhythm data from four patients. Pacing sites were the right superior pulmonary vein, left inferior pulmonary vein, left superior pulmonary vein, coronary sinus, posterior wall of right atrium, and high right atrium. For coronary sinus pacing, the AT pattern of the right atrium was compared with a CARTO map. The root mean square error between CARTO geometry (85 nodal points) and the surface model of the right atrium was 8.6 mm. The correlation coefficient of the noninvasively obtained AT map of the right atrium and the CARTO map was 0.76. All pulmonary vein pacing sites were identified. The reconstructed pacing site of right posterior atrial pacing correlates with the invasively determined pacing catheter position with a localization distance of 4 mm. Conclusion: The individual anatomic model of the atria of each patient enables accurate noninvasive AT imaging within the atria, resulting in a localization error for the pacing sites within 10 mm. Our findings may have implications for imaging of atrial activity in patients with focal arrhythmias or focal triggers. (J Cardiovasc Electrophysiol, Vol. 14, pp. 712-719, July 2003)

Notes: Mapping of Atrial Fibrillation. Introduction: Long linear lesions have been shown to eliminate atrial fibrillation in animal models, but little is known about the electrophysiologic response in one atrium to lesions in the contralateral atrium. Methods and Results: Twelve dogs with chronic atrial fibrillation were randomized to either right atrial ablation (n = 4), left atrial ablation first (n = 4), or a sham procedure (n = 4). Simultaneous biatrial endocardial mapping was performed before and after three linear lesions were applied at specific points in either atrium, using an expandable ablation catheter. Atrial fibrillation was reinducible after single atrial ablation in each dog and no longer inducible after biatrial ablation in five dogs. At baseline, the mean atrial fibrillation cycle length was longer on the trabeculated (117 ± 15 msec) compared with the smooth right (101 ± 16 msec) or left atrium (88 ± 10 msec; P 〈 0.01). Single right and left atrial ablation caused a significant cycle length increase in the ablated atrium. Left atrial ablation increased the cycle length on both the trabeculated (121 ± 18 msec vs 137 ± 11 msec; P 〈 0.05) and smooth right atrium (108 ± 12 msec vs 124 ± 9 msec; P 〈 0.05). Right atrial ablation, however, had no significant effect on left atrial fibrillation cycle length (82 ± 8 msec vs 86 ± 7 msec). Conclusion: Left atrial linear lesions affect right atrial endocardial activation, whereas right atrial lesions do not affect left atrial activation in a canine model of atrial fibrillation. These findings suggest that the left atrium is the driver during chronic atrial fibrillation in this animal model and may explain the limited success of right atrial ablation alone in human atrial fibrillation.

Notes: Atrial Fibrillation Organization. Introduction: Atrial fibrillation is not entirely random, but little is known about the spatiotemporal endocardial organization and its surface ECG manifestations.Methods and Results: In 16 patients with atrial fibrillation (chronic, n = 14), endocardial mapping of the trabeculated, the posteroseptal smooth right atrium, and the coronary sinus was performed using multipolar catheters. The surface ECG was analyzed by determining “fibrillation wave” (F wave) amplitude, rate, and polarity. During 50 minutes of atrial fibrillation, an organized activation was present 72%± 32% of the analyzed time on the trabeculated, 19%± 15% on the smooth right atrium (P 〈 0.01), and 51%± 33% along the coronary sinus (P 〈 0.05). The direction of organized activation was craniocaudal in 72%± 16%. caudocranial in 10%± 9% (P 〈 0.01), and indeterminable in 18%± 11%. The mean surface F wave amplitude in lead V1 was 0.128 ± 0.06 mV during 28 seconds of atrial fibrillation with a craniocaudal direction of activation and 0.065 ± 0.02 mV during a disorganized activation (P 〈 0.01). A stable relation between surface F waves and organized trabeculated right atrial activation was observed, and the mean F wave cycle length (190 ± 27 msec) was highly comparable to the simultaneously measured endocardial cycle length (191 ± 27 msec, correlation coefficient 0.97). F wave polarity in V1 was positive in 12 of 14 patients during craniocaudal and negative in 11 of 14 patients during caudocranial rigbt atrial free-wall activation.Conclusion: An organized activation during atrial fibrillation with a predominant craniocaudal direction on the trabeculated right atrium is frequently present and influences the appearance of “coarse” or “fine” atrial fibrillation as well as F wave polarity on the surface ECG.

Notes: Global P Wave Duration on the 65-Lead ECG. Introduction: Pacing is believed to prevent atrial fibrillation by reducing atrial activation time. Exact correlation between P wave duration (PWD) on surface ECG and endocardial atrial activation time is still unexplored. Methods and Results: In 15 patients without structural heart disease (9 women, age 45 ± 14 years), single site [high right atrium (HRA), coronary sinus ostium (CSos), distal CS (CSd), high RA septum (Bachmann's bundle, BB)] and dual-site pacing (various combinations) was performed after ablation of supraventricular tachycardia. A 65-lead surface ECG was recorded simultaneously. Endocardial atrial activation time was measured off-line (stimulus – last bipolar recording), and the respective PWD was assessed using the root mean square and 65-channel summary plots. PWD during pacing from BB was significantly shorter (96 ± 12 msec) than during HRA (121 ± 15 msec), CSos (108 ± 9 msec), and CSd pacing (126 ± 14 msec; P 〈 0,01, respectively). PWD during dual-site pacing (HRA + BB, 91 ± 14 msec; HRA + CSos, 96 ± 7 msec; HRA + CSd, 90 ± 7 msec; BB + CSd, 96 ± 12 msec) was not significantly shorter than during pacing from BB. Correlation between endocardial atrial activation time and PWD was 0.83. Conclusion: PWD during single-site and dual-site atrial pacing represents endocardial atrial activation time and can be measured precisely using the 65-lead surface ECG. The fact that high septal pacing results in the shortest PWD may have implications for preventive pacing in patients with atrial fibrillation.

Notes: Introduction: Biventricular pacing has been shown to improve the clinical status of patients with congestive heart failure, but little is known about its influence on ventricular repolarization. The aim of our study was to evaluate the effect of biventricular pacing on ECG markers of ventricular repolarization in patients with congestive heart failure. Methods and Results: Twenty-five patients with congestive heart failure, sinus rhythm (SR), and complete LBBB (6 females; age 61 ± 8 years; NYHA class II–III; echocardiographic ejection fraction 21 ± 5%; QRS ≥ 130 ms) underwent permanent biventricular DDDR pacemaker implantation. A high-resolution 65-lead body-surface ECG recording was performed at baseline and during right-, left-, and biventricular pacing, and the total 65-lead root mean square curve of the QRST complex and the interlead QT dispersion were assessed. The QRS duration was increased during right (RV)- and left ventricular (LV) pacing (127 ± 26% and 117 ± 40%; P 〈 0.05), as compared to SR (100%) and biventricular pacing (93 ± 16%; ns). The QTc interval was increased during RV and LV pacing (112 ± 12% and 114 ± 14%; P 〈 0.05) as compared to SR (100%) or biventricular pacing (99 ± 12%). There was no effect on JT interval during all pacing modes. The Tpeak-end interval was increased during right (120 ± 34%; P 〈 0.01) and LV pacing (113 ± 29%; P 〈 0.05) but decreased during biventricular pacing (81 ± 19%; P 〈 0.01). A similar effect was found for the Tpeak-end integral and the Tpeak amplitude. QT dispersion was increased during right ventricular (129 ± 16 ms; P 〈 0.05) and decreased during biventricular pacing (90 ± 12 ms; P 〈 0.01), as compared to SR (114 ± 22 ms). Conclusions: Using a high-resolution surface ECG, biventricular pacing resulted in a significant reduction of ECG markers of ventricular dispersion of repolarization.

Notes: Prediction of Left Atrial Linear Lesions. Introduction: Continuity of radiofrequency (RF) lesions for a catheter-based cure of atrial fibrillation is essential in order to avoid reentrant tachycardias. In the present study, we assessed the value of intracardiac echocardiography and preablation electrode-tissue interface parameters for creation of left atrial linear lesions. Methods and Results: In six healthy dogs, two left atrial linear lesions (lesion 1, along the inferior posterior left atrium; lesion 2, from the appendage to the left atrial roof) were attempted via a transseptal approach using a deflectable catheter with six 7-mm coil electrodes. In a randomized fashion, one lesion was performed under echocardiographic guidance and one with blinded echocardiographic monitoring. The following preablation parameters were assessed for every coil electrode: (1) mean atrial electrogram amplitude of six consecutive sinus beats; (2) diastolic pacing threshold; and (3) temperature response to application of 5 W for 10 seconds. After ablation (target temperature 70°C, maximum power 50 W, duration 60 sec), the excised left atrium was examined macroscopically and histologically for lesion length, continuity, and presence or absence of lesions associated with each coil.Out of 12 attempted RF lesions, 7 were continuous (length, 47 ± 5 mm, lesion 2, n = 6) and 5 were discontinuous (lesion 1, n = 5). Fifty-two of 70 coil electrodes (74%) had pathologic evidence of lesion creation. Intracardiac echocardiography was superior to fluoroscopy with respect to the actual number of coil electrodes creating lesions, and lesion continuity was correctly predicted in 9 of 12 lesions. Intracardiac echocardiography was 85% sensitive and 54% specific in predicting lesions created by individual coils. The correlation between the mean 60-second ablation temperature and the preablation parameters was 0.45 for the electrogram amplitude, -0.67 for the pacing threshold, and 0.81 for the temperature response to low-power application. Sensitivity and specificity for prediction of lesions created by individual coils, respectively, were 84% and 48% for the electrogram amplitude. 90% and 68% for the pacing threshold, and 96% and 76% for the low-power RF application. Conclusion: Long linear lesions can be safely and effectively performed in the canine left atrium, using a tip-deflectable multielectrode catheter. Intracardiac echocardiography may be helpful for positioning the ablation catheter in some parts of the left atrium, and preablation parameters, especially a nontraumatic low-power RF application, are able to predict ultimate lesion creation with high accuracy.

Notes: 62-Lead QRST Subtraction Algorithm. Introduction: Atrial activity on the surface ECG during premature beats and supraventricular arrhythmias frequently is obscured by the superimposed QRST complex of the previous cardiac cycle. This study examines the performance of a newly developed automatic QRST subtraction algorithm to isolate ectopic P waves from the preceding T-U wave. Methods and Results: The 62-lead ECG recordings were obtained during (1) sinus rhythm and programmed right atrial stimulation in 12 patients (group A); and (2) sinus rhythm and atrial premature beats, atrial tachycardia, or paroxysmal atrial fibrillation in 5 patients (group B). Pacing in group A patients was conducted at a slow drive cycle length to generate an ectopic P wave not obscured by the previous QRST complex and by delivering single premature extrastimuli at progressively shorter coupling intervals to produce an ectopic P wave obscured by the upsloping (early T-U wave), peak (middle T-U wave), and downsloping component of the T-U wave (late T-U wave). All ectopic P waves in group B patients were concealed by the preceding T-U wave. Automatic QRST subtraction was attained using an adaptive template constructed from averaged QRST complexes (mean 83 ± 25 complexes) obtained during sinus rhythm (groups A and B) or atrial overdrive pacing (group A). P wave integral maps subsequently were computed, visually compared, and mathematically correlated. A high correspondence in spatial map pattern was observed between integral maps of “nonobscured” and previously “obscured” paced P waves obtained in group A patients (mean r = 0.88 ± 0.07) as well as between integral maps of two to three previously obscured P waves with the same atrial arrhythmia morphology obtained in group B patients (mean r = 0.94 ± 0.05). Improved morphologic P wave replication in group A patients was acquired when concealment occurred in the early (mean r = 0.90 ± 0.08) or late part of the T-U wave (mean r = 0.90 ± 0.06) as opposed to the middle T-U wave (mean r = 0.85 ± 0.07) (P = NS and P 〈 0.05 for early vs middle and late vs middle T-U wave, respectively). Conclusion: This novel automatic 62-lead QRST subtraction algorithm enables discrete isolation of T-U wave obscured ectopic atrial activity on the surface ECG while retaining the intricate spatial detail in P wave morphology. Future clinical application of the algorithm may enable improved ECG localization of focal triggers of paroxysmal atrial fibrillation, atrial tachycardia, and the atrial insertion of accessory pathways.

Notes: Animal models and human studies of atrial activation mapping and entrainment have considerably enhanced our understanding of the anatomical substrate for atrial flutter and created the basis for a definite cure with radiofrequency catheter ablation. As atrial flutter has now become a curable arrhythmia, emphasis is shifting to understand the most common arrhythmia: atrial fibrillation. Furthermore, from clinical observation, it is apparent that there is a relationship between atrial fibrillation and atrial flutter in patients with atrial arrhythmias. Techniques that have informed our understanding of the anatomical basis of atrial flutter may also be useful in understanding the relationship between atrial fibrillation and flutter, including animal models, clinical endocardial mapping, and intracardiac anatomical imaging. Thus, atrial anatomy and its relationship to electrophysiological findings, and the role of partial or complete conduction barriers around which reentry can and cannot occur, may be of importance for atrial fibrillation as well. Ultimately, the relationship between atrial fibrillation and atrial flutter may inform our understanding of the mechanisms of atrial fibrillation itself, and help to develop new approaches to device, catheter-based, and pharmacological therapy for atrial fibrillation.

Notes: As pacemaker generator longevity is dependent on current consumption and resistance of the pacing lead, the use of a high impedance pacing lead theoretically results in an extension of battery longevity. Therefore, the effect of high versus standard impedance ventricular leads on generator longevity was studied. In 40 patients (21 women, age 73 ± 13 years) with a standard dual chamber pacemaker indication, a bipolar standard impedance ventricular lead was implanted in 20 patients, the remaining patients received a bipolar high impedance lead in a randomized fashion. All patients received identical pacemaker generators and atrial leads. The estimated longevity of the generator was calculated automatically by a programmed pacemaker algorithm. After a mean follow-up of 39 ± 4.8 months, no significant differences were observed with respect to mean pacing and sensing thresholds of the atrial and ventricular leads in both groups. However, the high impedance leads displayed a significantly higher impedance and a significantly lower current drain as compared to standard impedance leads (1,044 ± 139 vs 585 ± 90 Ω, and 2.2 ± 0.4 vs 4.3 ± 1.1 mA). The extrapolated generator longevity was significantly longer in the high impedance lead group, as compared to the standard impedance lead group (107.3 ± 8.5 vs 97.6 ± 9.0 months; P = 0.02). In conclusion, implantation of a high impedance lead for ventricular pacing results in a clinically relevant extension of generator longevity. (PACE 2003; 26:2116–2120)