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Notes: AV Nodal Behavior After Ablation. Introduction; The objective of this report is to delineate the atrioventricular (AV) nodal electrophysiologic behavior in patients undergoing fast or slow pathway ablation for control of their AV nodal reentrant tachycardia (AVNRT). Methods and Results: One hundred sixteen consecutive patients with symptomatic AVNRT were included. Twenty-two patients underwent fast pathway ablation with complete abolition of AVNRT in all and development of complete AV block in five patients. Of 17 patients with intact AV conduction postablation, 12 had demonstrated antegrade dual pathway physiology during baseline study, which was maintained in three and lost in nine patients postablation. Two patients with successful fast pathway ablation developed uncommon AVNRT necessitating a slow pathway ablation. Twenty-one patients demonstrated both common and uncommon forms of AV nodal reentry during baseline study. The earliest site of atrial activation was close to the His-bundle recording site (anterior interatrial septum) during common variety and the coronary sinus ostium (posterior interatrial septum) during the uncommon AV nodal reentry in all 21 patients. Ninety-six patients underwent successful slow pathway ablation. Among these, the antegrade dual pathway physiology demonstrable during baseline study (60 patients) was maintained in 25 and lost in 35 patients postablation. Conclusion: These data suggest that: (1) dual pathway physiology may persist after successful ablation, which might be a reflection of multiple reentrant pathways in patients with AVNRT: and (2) the retrograde pathways during common and uncommon AVNRT have anatomically separate atrial breakthroughs. These findings have important electrophysiologic implications regarding the prevailing concept of the AV nodal physiology in patients with AVNRT.

Notes: Linear Lesions Prevent Atrial Fibrillation. Introduction: In the animal model, segmentation of the atria with radiofrequency-generated linear lesions (LL) using the loop catheter has been shown to be highly effective in terminating chronic atrial fibrillation (AF). This study addresses the question whether the same lesion set also would prevent reinduction and sustainability of AF. Methods and Results: We studied two groups of dogs. The AF group included eight dogs in which the atria were paced until chronic AF was present. After 6 months of sustained AF, the dogs were converted to normal sinus rhythm (NSR) by the creation of LL in both atria. Rapid atrial pacing was restarted 6 months later and continued for 4 weeks. In the NSR group, there were nine dogs in NSR without inducible AF at baseline. LL were created, and after 6 months rapid atrial pacing was applied for 4 weeks. Rhythm status was monitored weekly. Transthoracic echocardiography was performed at baseline, before linear lesion placement, and before pacing/repacing. At the conclusion of the study, the hearts were excised and examined. The lesions were stained, and their quality was assessed. AF was induced in a much shorter interval in the dogs in which AF had previously been present than in NSR dogs (8 ± 5 days vs 25 ± 13 days; P 〈 0.05). LL prevented sustainability of AF induced via rapid pacing once the pacing stimulus was stopped. Incomplete lesions were associated with increased inducibility of atrial tachycardia and AF. Conclusion: In this animal model of AF, LL are not only capable of terminating chronic AF, but also lead to self-termination of AF once the rapid pacing is stopped. Self-termination of AF after induction with rapid pacing was not observed in this AF model in the absence of LL. In the dogs with 6 months of AF, the presence of AF led to increased atrial susceptibility to AF induction by rapid pacing, even with LL and after 6 months of recovery. Incomplete LL allows induction of atrial tachycardia and AF.

Notes: Body Surface Laplacian Map. Introduction: The body surface Laplacian electrocardiogram (ECG) mapping provides a noninvasive means for spatiotemporal mapping of cardiac electrical events. The aim of the present study was to explore the relationship between the Laplacian ECG and the underlying cardiac activities during ventricular depolarization in healthy human subjects. Methods and Results: A 95-channel body surface potential ECG was recorded over the anterolateral chest from 11 healthy male subjects. The surface Laplacian (SL) ECG was estimated from the recorded potentials during QRS complex by means of a novel spline SL estimator, as well as by the conventional 5-point SL estimator for comparison purpose. A simulation study was also conducted using a realistic geometry heart-torso model in an attempt to qualitatively interpret the experimental results. For all subjects, more spatial details were observed in the SL ECG maps compared with the potential ECG maps, with spline SL more robust against noise than the 5-point SL. In total, three positive activities (denoted as P1, P2, P3) and four negative activities (denoted as N1, N2, N3, N4) in the spline SL ECG maps were observed during ventricular depolarization. Initial localized P1 and N1 activities were observed in 11 and 8 subjects, respectively. Then, the initial P1 was divided into three positive activities (P1, P2, P3) in 9 subjects. After the appearance of multiple positive activities, three negative activities (N2, N3, N4) appeared in 11, 8, and 9 subjects, respectively. Similar findings were obtained in the computer simulation study. Conclusion: The present study demonstrates that the SL ECG provides more spatial details than the potential ECG, and multiple simultaneously active ventricular activities could be revealed in the SL ECG maps. The results suggest that the SL ECG may provide an alternative for noninvasive mapping of cardiac electrical activity.

Notes: LA Mechanical Function After Linear Lesions. Introduction: The extent of left atrial (LA) mechanical function recovery after creation of linear lesions using the loop catheter has not been determined. Methods and Results: LA mechanical function was assessed before and after linear lesions using transthoracic two-dimensional and Doppler echocardiography in two groups: (I) normal, which consisted of eight healthy dogs in normal sinus rhythm (NSR); and (2) atrial fibrillation (AF), which consisted of nine dogs in spontaneous AF for 6 months following rapid pacing-induced AF. NSR was restored with linear lesions in all AF dogs. All animals were in NSR 5 months after linear lesions. In the normal dogs, the maximal velocity of the transmitral flow “A” wave was reduced by 42% during the first week postablation and by 24% at 5 months versus preablation. At 5 months, no differences in LA function were noted between the normal and the AF group for all measured Doppler parameters. At 5 months, the LA systolic area in AF dogs was reduced by 40% (preablation 12.9 ± 2.9 cm2, postablation 7.6 ± 1.2 cm2; P 〈 0.01) and in the normal dogs by 21% (preablation 10.0 ± 0.9 cm2, postablation 7.8 ± 1.2 cm2; P 〈 0.02), being the same in both groups within 3 months of recovery. Conclusion: The creation of linear lesions with the loop catheter does not result in LA expansion. In normal dogs, LA mechanical activity is reduced for 3 weeks postablation. The time course of LA mechanical function recovery is the same for the AF and the NSR dogs, and it is complete at 3 months postablation. At 5 months, LA systolic function parameters in both groups are reduced by 24% versus the preablation values of the normal dogs. Linear lesions result in a significant reduction in LA size.

Notes: Profibrillatory Effects of Extrastimuli. Multiple extrastimuli are known to cause ventricular Hhrillation in normal hearts. The mechanisms by which multiple extrastimuli facilitate induction of ventricular fibrillation were studied in 10 normal, anesthetized, open chest dogs. Strength-interval curves and latency-interval curves were measured following basic drive (S1S1) and following captured single and double extrastimuli (S2and S3). The zone of relative refractoriness was widened by closely coupled extrastimuli: 44 ± 8 msec after basic drive. 81 ± 19 msec after S2 and 92 ± 15 msec after S2S3 (P 〈0.001 compared to basic drive). The maximum latency between a test stimulus and its propagated response was prolonged by extrastimuli: 95 ± 6 msec after basic drive, 144 ± 11 msec after S2, and 162 ± 12 msec after S3 (P 〈0.001). Extrastimuli that were not closely coupled (i.e., that were delivered 30 or 50 msec following the effective refractory period of the previous beat) had little effect on the zone of relative refractoriness or maximum latency of subsequent stimuli. Catbodal, anodal, and bipolar extrastimuli had similar effects on effective refractory period, zone of relative refractoriness, and latency. Extrastimuli did not cause decreases in threshold for capture and did not exaggerate early diastolic dips in strength-interval curves. Forty episodes of ventricular fibrillation were induced in eight of ten dogs. Latency-interval curves that induced VF had longer maximum latency (P 〈0.001) and wider zones of relative refractoriness (P 〈0.001) than did latency interval curves that did not result in ventricular fibrillation. Prolongation of the relative refractory period resulted in corresponding prolongation of latency with correlation coefficient of 0.97, however, both of these parameters correlated poorly with the coupling interval of The premature stimuli (R = 044 and 043). In conclusion, premature extrastimuli may facilitate induction of ventricular fibrillation by widening the relative refractory period and prolonging latency. However, premature stimuli initiated at coupling intervals of over 30 msec above the ERP of the previous propagated beat eliminate much of the relative refractory period and latency increase, and were not associated with ventricular flbrillation. (J Cardiovasc Electrophysiol, Vol. I, No. 3, pp 197–208, June 1990)

Notes: Introduction: Creation of radiofrequency lesions to isolate the pulmonary veins (PV) and ablate atrial fibrillation (AF) has been complicated by stenosis of the PVs. We tested a cryoballoon technology that can create electrical isolation of the PVs, with the hypothesis that cryoenergy will not result in PV stenosis. Methods and Results: Lesions were created in 9 dogs (weight 31–37 kg). Cryoenergy was applied to the PV-left atrial (LA) interface. Data collected before and after ablation included PV orifice size, arrhythmia inducibility, electrogram activity, and pacing threshold in the PVs. Tissue examination was performed immediately after ablation in 3 dogs and after 3 months (4.8 ± 1.0) in 6 dogs. After ablation there was no localized P wave activity in the ablation zone and no LA-PV conduction. Before ablation, the pacing threshold was 1.9 ± 1.1 mA in each PV. After ablation, the pacing threshold increased significantly to 7.2 ± 1.8 mA , or capture was not possible. Burst pacing did not induce any sustained arrhythmias. Most dogs had hemoptysis during the first 24 to 48 hours. Acute tissue examination revealed hemorrhagic injury of the atrial-PV junction that extended into the lung parenchyma. After recovery, the lesions were circumferential and soft with no PV stenosis. Histologic examination revealed fibrous tissue with no PV-LA interface thickening. Conclusion: This new cryoballoon technology effectively isolates the PVs from LA tissue. No PV stenosis was noted. Acute tissue hemorrhage and hemoptysis are short-term complications of this procedure. After 3 months of recovery, cryoablated tissue exhibits no collagen or cartilage formation. (J Cardiovasc Electrophysiol, Vol. 14, pp. 281-286, March 2003)

Notes: Implantation of a subcutaneous array to improve the defibrillation threshold of an existing transvenous defibrillation lead system without the need for lead extraction is discussed. (J Cardiovasc Electrophysiol, Vol. 14, pp. 314-315, March 2003)

Notes: AVITALL, B., et al.: The Ablation of Atrial Fibrillation with the Loop Catheter Design: What We Have Learned From the Animal Model. Ablation of chronic atrial fibrillation (AF) with the use of transcutaneous catheter ablation is yet to become a clinical tool. This article summarizes the development of the technology and the technique for the ablation of AF that was tested on the rapidly paced AF dog model. The current ablation technology using the standard ablation technique used in humans is not suitable for the creation of transmural contiguous linear lesions, and such technology is subjecting the patient to the prolonged procedures with considerable risk of complication. The use of the loop catheter design or other designs of ablation technology, which is specifically targeted for the creation of linear lesions, should be developed if the catheter approach for the ablation of AF is to succeed. This article describes the data available for the loop catheter design that is currently undergoing human feasibility studies.

Notes: LIAN, J., et al.: Estimation of Noise Level and Signal to Noise Ratio of Laplacian Electrocardiogram During Ventricular Depolarization and Repolarization. Body surface Laplacian ECG (LECG) has demonstrated its enhanced capability to localize cardiac electrical sources closest to the recording site. The aim of the present study was to evaluate the noise level and signal to noise ratio (SNR) in the LECG as compared to the potential ECG (PECG). Such evaluation is important to determine the applicability of the LECG to localizing and imaging of cardiac electrical activity in an experimental setting. Experimental studies were conducted in six healthy men. A 150-channel PECG was recorded from the anterolateral chest and the LECG was estimated using the finite difference algorithm. The noise level in the PECG and LECG was evaluated using multiple estimation protocols. The signal level during ventricular depolarization and repolarization was also estimated, and the corresponding SNR was calculated. Different filtering techniques were examined to evaluate their effects on the noise level and SNR of the LECG and PECG. The experimental results indicate that with basic signal processing techniques (baseline adjustment, three-point moving average filter, and Wiener spatial filter), the SNR of the LECG is about 30–40% of that of the PECG. Furthermore, the SNR estimated during ventricular depolarization is about three times that obtained during ventricular repolarization for the PECG and LECG. The present study indicates that the LECG derived from the PECG using a local finite difference estimation procedure has satisfactory SNR during the periods of ventricular depolarization and repolarization, and suggests the feasibility of estimating the LECG from the recorded PECG in human subjects in an experimental setting.

Notes: During the generation of radiofrequency (RF) lesions in the ventricular myocardium, the maintenance of adequate electrode-tissue contact is critically important. In this study, lesion dimensions and temperature and impedance changes were evaluated while controlling electrode-tissue contact levels (−5, 0, +1, and +3 mm) and power levels (10, 20, and 30 W). This data was used to assess the ability of impedance and temperature monitoring to provide useful information about the quality of electrode-tissue contact. The results show that as the electrode-tissue contact increases, so does the amount of temperature rise. Witb the electrode floating in blood (-5 contact), the average maximum temperature increase with 20 and 30 W was only 7 ± 1 and 11 ± 2°C, respectively. At 20 and 30 W the temperature plateaued sbortly after the initiation of power application. With good electrode-tissue contact (+1 mm or +3 mm), the temperature increase within the first 10 seconds was significantly greater than the temperature increase from baseline with poor contact (0 mm or −5 mm) and reached a maximum of 60 ± 1°C after 60 seconds of power application. As the electrode-tissue contact increased, so did the rate and level of impedance decrease. However, the rate of impedance decrease was slower compared to the rate of temperature rise. With the electrode floating in blood, the maximum impedance decreases with 20 and 30 W were 6 ± 6 Ω and 9 ± 5 Ω, respectively. The impedances plateaued after a few seconds of power application. With the electrode in good contact, the maximum impedance decreases with 20 and 30 W were 25 ±2Ω and 20 ± 6 Ω, respectively. In these cases the rate of the impedance decrease plateaued after 40 seconds of power application.The increase in lesion diameter and depth correlate well with decreasing impedance and increasing temperature. However, lesion depth appears to correlate better with impedance than temperature. We conclude that, since the electrode-tissue contact is not known prior to the application of power to the endocardium, in the absence of a temperature control system, the power should initially be set at a low level. The power sbould be increased slowly over 20–30 seconds, and then maintained at its final level for at least 90 seconds to allow for maximal lesion depth maturation. The power level should be lowered if the impedance drop exceeds 15 Ω.