Myocardial ischemia-reperfusion damage impacts occurrence of ventricular fibrillation in dogs

To define the relationship between ischemia-reperfusion-induced myocardial damage (IRD) and the occurrence of ventricular tachycardia (VT) and fibrillation (VF), we studied 23 dogs with a three-dimensional activation mapping system. Left anterior descending (LAD) coronary artery occlusion and reperfusion were performed while recording electrograms during VF and atrial pacing. Prior nonischemic sites showing IRD, defined as at least 10% loss of electrogram voltage after reperfusion, had the longest ventricular effective refractory periods (ERPs). IRD sites also occurred more frequently in dogs with reperfusion VF (44 +/- 2 sites, P < 0.01) compared with dogs with VT (18 +/- 5 sites) and no VT (16 +/- 3 sites). In dogs (n = 3) with 3 h of reperfusion, 95% of IRD sites still had lower voltage than those recorded during occlusion. Activation mapping of the first eight complexes of VF had Purkinje or endocardial focal origin in 57%, and complexes originated from IRD sites in 28%. In contrast, dogs with only reperfusion VT also had Purkinje or endocardial focal origin in 79%, but only 5% (P < 0.01 vs. VF dogs) of the sites of origin had IRD. Therefore, dogs with reperfusion VF had more IRD sites where the ERP was longest, and more focal ventricular complexes originated from IRD sites, indicating that IRD may be one important factor in the occurrence of VF during reperfusion.     

Endocardial activation during ventricular fibrillation in normal and failing canine hearts

Because congestive heart failure (CHF) promotes ventricular fibrillation (VF), we compared VF in seven dogs with CHF induced by combined myocardial infarction and rapid ventricular pacing to VF in six normal dogs. A noncontact, multielectrode array balloon catheter provided full-surface real-time left ventricular (LV) endocardial electrograms and a dynamic color-coded display of endocardial activation projected onto a three-dimensional model of the LV. Fast Fourier transform (FFT) analysis of virtual electrograms showed no difference in peak or centroid frequency in CHF dogs compared with normals. The average number of simultaneous noncontiguous wavefronts present during VF was higher in normals (2.4 +/- 1.0 at 10 s of VF) than in CHF dogs (1.3 +/- 1.0, P < 0.005) and decreased in both over time. The wavefront "turnover" rate, estimated using FFT of the noncontiguous wavefront data, did not differ between normals and CHF and did not change over 5 min of VF. Thus the fundamental frequency characteristics of VF are unaltered by CHF, but dilated abnormal ventricles sustain fewer active wavefronts than do normal ventricles.     

Ventricular fibrillation in myopathic human hearts: mechanistic insights from in vivo global endocardial and epicardial mapping

Ventricular fibrillation (VF) is an important cause of sudden cardiac death and cardiovascular mortality in patients with cardiomyopathy. Although it was generally believed that chaotic reentrant wavefronts underlie VF in humans, there is emerging evidence of spatiotemporal organization during early VF. The mechanism of this organization of electrical activity in early VF is unknown in myopathic hearts. We studied early VF in vivo, intraoperatively in five cardiomyopathic patients. Simultaneous electrograms were obtained from the epicardium and endocardium in left ventricular cardiomyopathy and from the endocardium in right ventricular myopathy. The Hilbert transform was used to derive the phase of the electrograms. Rotors were identified by isolating phase singularity points. Rotors were present in all of the myopathic hearts studied during VF and cumulatively lasted a mean of 3.2 +/- 2.0 s of the 7.0 +/- 4.0 s of the VF segments analyzed. For each surface mapped, 3.6 +/- 2.9 rotors were identified for the duration mapped. The average number of cycles completed by these rotors was 4.9 +/- 4.9. The longest rotor lasted 10.2 +/- 6.2 rotations and lasted 2.0 +/- 1.2 s. The rotors on the endocardium had a cycle length of 192 +/- 33 ms compared with 220 +/- 15 ms on the epicardium (P=0.08). There is centrifugal activation of electrical activity from these rotors, and they give rise to domains that activate at faster rates with evidence of conduction block at the border with slower domains. These rotors frequently localized to border regions of myocardium with bipolar electrogram amplitude of <0.5 mV. The organization of electrical activity during early VF in myopathic human hearts is characterized by wavefronts emanating from a few rotors.     

Defining the substrate for ventricular tachycardia ablation: The impact of rhythm at the time of mapping

BackgroundVoltage mapping is critical to define substrate during ablation. In ventricular tachycardia, abnormal potentials may be targets. However, wavefront of activation could impact local signal characteristics. This may be particularly true when comparing sinus rhythm versus paced rhythms. We sought to determine how activation wavefront impacts electrogram characteristics.MethodsPatients with ischemic cardiomyopathy, ventricular tachycardia, and without fascicular or bundle branch block were included. Point by point mapping was done and at each point, one was obtained during an atrial paced rhythm and one during a right ventricular paced rhythm. Signals were adjudicated after ablation to define late potentials, fractionated potentials, and quantify local voltage. Areas of abnormal voltage (defined as <1.5 mV) were also determined.Results9 patients were included (age 61.3 ± 9.2 years, 56% male, mean LVEF 34.9 ± 8.6%). LV endocardium was mapped with an average 375 ± 53 points/rhythm. Late potentials were more frequent during right ventricular pacing (51 ± 21 versus 32 ± 15, p < 0.01) while overall scar area was higher during atrial pacing (22 ± 11% vs 13 ± 7%, p < 0.05). In 1/9 patients, abnormal potentials were seen during a right ventricular paced rhythm that were not apparent in an atrial paced rhythm, ablation of which resulted in non-inducibility.ConclusionRhythm in which mapping is performed has an impact on electrogram characteristics. Whether one rhythm is preferable to map in remains to be determined. However, it is possible defining local signals during normal conduction as well as variable paced rhythms may impart a greater likelihood of elucidating arrhythmogenic substrate.     

Can Right Ventricular Pacing be Useful in the Assessment of Cavo-tricuspid Isthumus Block?

Background

Cavo-tricuspid isthmus (CTI) block is currently assessed by coronary sinus (CS) pacing or low lateral and septal atrial pacing. Occasionally, CS catheterization through the femoral route can be difficult to perform or right atrial pacing can be problematic because of catheter instability or saturation of the atrial electrograms recorded near the catheter.

Objectives

Our aim was to evaluate the feasibility of assessing cavo-tricuspid isthmus block by means of right ventricular (RV) pacing in patients with ventriculo-atrial conduction, comparing it with CS pacing.

Methods

Circumannular activation was analyzed during CS and RV pacing in consecutive patients in sinus rhythm undergoing CTI ablation for typical atrial flutter. Patients without ventriculo-atrial conduction were excluded from the study. The linear lesion was created during RV pacing and split atrial signals on the ablation line were analyzed. CTI block was confirmed by analyzing local electrograms on the line of block and circumannular activation during CS and RV pacing.

Results

Out of 31 patients, 20 displayed ventriculo-atrial conduction (64%) and were included in the study. Before ablation, during RV stimulation, the collision front of circumannular activation shifted counterclockwise in contrast with the pattern observed during CS pacing. After ablation, circumannular activation was similar during CS and RV pacing, showing fully descending lateral right atrium activation, even if double potentials registered on the ablation line were less widely split during RV pacing than CS pacing (111±26 ms vs 128±30 , p=0.0001).

Conclusions

In patients with ventriculo-atrial conduction, tricuspid annulus activation during CS and RV pacing is similar, before and after CTI ablation. The occurrence of split atrial electrograms separated by an isoelectric interval registered on the line of block can be detected during CS or RV pacing. In patients with difficult CS catheterization via the femoral vein, before trying the subclavian or internal jugular route, if retrograde ventriculo-atrial conduction is present, RV pacing can be an easy trick to assess isthmus block.     

Noninvasive electrocardiographic imaging for cardiac electrophysiology and arrhythmia

Over 7 million people worldwide die annually from erratic heart rhythms (cardiac arrhythmias), and many more are disabled. Yet there is no imaging modality to identify patients at risk, provide accurate diagnosis and guide therapy. Standard diagnostic techniques such as the electrocardiogram (ECG) provide only low-resolution projections of cardiac electrical activity on the body surface. Here we demonstrate the successful application in humans of a new imaging modality called electrocardiographic imaging (ECGI), which noninvasively images cardiac electrical activity in the heart. In ECGI, a multielectrode vest records 224 body-surface electrocardiograms; electrical potentials, electrograms and isochrones are then reconstructed on the heart's surface using geometrical information from computed tomography (CT) and a mathematical algorithm. We provide examples of ECGI application during atrial and ventricular activation and ventricular repolarization in (i) normal heart (ii) heart with a conduction disorder (right bundle branch block) (iii) focal activation initiated by right or left ventricular pacing, and (iv) atrial flutter.     

Noninvasive three-dimensional electrocardiographic imaging of ventricular activation sequence

Imaging the myocardial activation sequence is critical for improved diagnosis and treatment of life-threatening cardiac arrhythmias. It is desirable to reveal the underlying cardiac electrical activity throughout the three-dimensional (3-D) myocardium (rather than just the endocardial or epicardial surface) from noninvasive body surface potential measurements. A new 3-D electrocardiographic imaging technique (3-DEIT) based on the boundary element method (BEM) and multiobjective nonlinear optimization has been applied to reconstruct the cardiac activation sequences from body surface potential maps. Ultrafast computerized tomography scanning was performed for subsequent construction of the torso and heart models. Experimental studies were then conducted, during left and right ventricular pacing, in which noninvasive assessment of ventricular activation sequence by means of 3-DEIT was performed simultaneously with 3-D intracardiac mapping (up to 200 intramural sites) using specially designed plunge-needle electrodes in closed-chest rabbits. Estimated activation sequences from 3-DEIT were in good agreement with those constructed from simultaneously recorded intracardiac electrograms in the same animals. Averaged over 100 paced beats (from a total of 10 pacing sites), total activation times were comparable (53.3 +/- 8.1 vs. 49.8 +/- 5.2 ms), the localization error of site of initiation of activation was 5.73 +/- 1.77 mm, and the relative error between the estimated and measured activation sequences was 0.32 +/- 0.06. The present experimental results demonstrate that the 3-D paced ventricular activation sequence can be reconstructed by using noninvasive multisite body surface electrocardiographic measurements and imaging of heart-torso geometry. This new 3-D electrocardiographic imaging modality has the potential to guide catheter-based ablative interventions for the treatment of life-threatening cardiac arrhythmias.     

Thoracic vein ablation terminates chronic atrial fibrillation in dogs

The thoracic vein hypothesis of chronic atrial fibrillation (AF) posits that rapid, repetitive activations from muscle sleeves within thoracic veins underlie the mechanism of sustained AF. If this is so, thoracic vein ablation should terminate sustained AF and prevent its reinduction. Six female mongrel dogs underwent chronic pulmonary vein (PV) pacing at 20 Hz to induce sustained (>48 h) AF. Bipolar electrodes were used to record from the atria and thoracic veins, including the vein of Marshall, four PVs, and the superior vena cava. Radio frequency (RF) application was applied around the PVs and superior vena cava and along the vein of Marshall until electrical activity was eliminated. Computerized mapping (1,792 electrodes, 1 mm resolution) was also performed. Sustained AF was induced in 30.6 +/- 6.5 days, and ablation was done 17.3 +/- 8.5 days afterward. Before ablation, the PVs had shorter activation cycle lengths than the atria, and rapid, repetitive activations were observed in the PVs. All dogs converted to sinus rhythm during (n = 4 dogs) or within 90 min of completion of RF ablation. Rapid atrial pacing afterward induced only nonsustained (<60 s) AF in all dogs. Average AF cycle lengths after reinduction were significantly (P = 0.01) longer (183 +/- 31.5 ms) than baseline (106 +/- 16.2 ms). There were no activation cycle length gradients after RF application. We conclude that thoracic vein ablation converts canine sustained AF into sinus rhythm and prevents the reinduction of sustained AF. These findings suggest that thoracic veins are important in the maintenance of AF in dogs.     

Comparative effects of single- and linear triple-site rapid bipolar pacing on atrial activation in canine models

Nonuniform conduction may cause block and/or delay, thereby providing a substrate for the onset and maintenance of reentrant atrial arrhythmias. We tested the hypothesis that linear triple-site, bipolar, rapid pacing (LTSBRP) of the right atrium generates more uniform wave-front propagation compared with single-site, bipolar, rapid pacing (SSBRP), thereby reducing and/or eliminating conduction block and delay that is otherwise present. Five dogs with pericarditis and three normal dogs were studied. Three plunge-wire electrode pairs were placed 5-7 mm apart in both perpendicular and parallel configurations at the superior aspect of the crista terminalis and were used to pace at 200- and 300-ms cycle lengths for < or =6 s. During pacing, 380 electrograms were recorded simultaneously from electrode arrays placed epicardially on the atria, which produced activation sequence maps for each pacing episode. Local conduction-velocity vectors were computed for each site during each episode. Histograms of absolute velocity vector angles from the x-axis (of the crista terminalis) were plotted to assess uniformity of wave-front propagation, and the magnitude of each vector was computed to assess the local speed. LTSBRP showed 1) more uniform linear activation wave fronts compared with SSBRP, 2) velocity vectors with a more uniform magnitude and direction compared with SSBRP, 3) a predominant absolute velocity vector angle vs. a scattered angle distribution with SSBRP, and 4) shorter right atrial activation time and faster mean epicardial speed than SSBRP for each pacing cycle length. LTSBRP created a more uniform wave-front propagation with less or no conduction block and/or delay compared with SSBRP.     

High-density activation map of atrial tachycardia within left atrial appendage

Identification of the critical isthmus of the reentrant tachycardia is essential to maximize the effect of catheter ablation (CA) and to minimize the myocardial injury of CA. An 81-year-old woman presented recurrent palpitations after CA of atrial fibrillation (AF) and atrial tachycardia (AT). She had moderate aortic valve stenosis and coronary artery disease. She had received a pulmonary vein isolation, left atrial (LA) posterior wall isolation, and LA anterior linear ablation for atrial fibrillation 1 year prior. At the start of the procedure, she was in sinus rhythm. Atrial burst pacing induced an AT (230msec). High-density mapping revealed a figure-of-eight activation pattern within the LA appendage (LAA), accounting for 99% of the tachycardia cycle length. The critical isthmus was identified at the mid LAA and the local electrogram of the critical isthmus was not fractionated. A single radiofrequency application at the critical isthmus of the AT, terminated the AT. She was free from any ATs for 28 months.Radiofrequency ablation of the localized reentrant AT was usually performed targeting long fractionated electrograms. In our case, the local electrogram at the critical isthmus was not fragmented compared with the LAA distal part. Long fractionated electrograms were recorded at a more distal part of the LAA than the common isthmus and we could avoid the potential risk of a perforation. A recent developed 3-dimensional electro-anatomical mapping system can identify the critical isthmus and allow us to select a new therapeutic strategy for a critical isthmus ablation of an AT within the LAA.     

Transitions among atrial fibrillation, atrial flutter, and sinus rhythm during procainamide infusion and vagal stimulation in dogs with sterile pericarditis

The mechanism of atrial flutter and fibrillation induced by rapid pacing in 22 dogs with 3-day-old sterile pericarditis was investigated by computerized epicardial mapping of atrial activation before and after administration of agents known to modify atrial electrophysiologic properties: procainamide, isoproterenol, and electrical stimulation of the vagosympathetic trunks. Before the administration of any of these agents, a total of 30 episodes of sustained atrial flutter (greater than 1 min duration, monomorphic; regular cycle length, 127 +/- 12 ms, mean +/- SD) was induced in 15 out of 22 dogs and 9 episodes of unstable atrial flutter (duration, less than 1 min; cycle length, 129 +/- 34 ms; monomorphic, alternating with fibrillation) were induced in the remaining 7 preparations. In the latter, administration of procainamide transformed unstable atrial flutter and atrial fibrillation to sustained atrial flutter (cycle length, 142 +/- 33 ms; n = 9 episodes). During control atrial flutter, atrial maps displayed circus movement of excitation in the right atrial free wall with faster conduction parallel to the orientation of intra-atrial myocardial bundles. Vagal stimulation changed atrial flutter to atrial fibrillation in 32 of 73 trials; this was associated with acceleration of conduction in the lower right atrium, leading to fragmentation of the major wave front. Isoproterenol produced a 6-25% increase of the atrial rate in 6 out of 14 trials of atrial flutter and induced atrial fibrillation in 4. After procainamide, the reentrant pathway was lengthened and conduction was slowed further in the right atrium. Maps obtained during unstable atrial flutter showed incomplete circuits involving the right atrium. Following procainamide infusion, the area of functional dissociation or block was enlarged and a stable circus movement pattern, which was similar to the pattern seen in control atrial flutter, was established in the right atrium. We conclude that (1) the transitions among atrial fibrillation, atrial flutter, and sinus rhythm occur between different functional states of the same circus movement substratum primarily located in the lower right atrial free wall, and (2) the anisotropic conduction properties of the right atrium may contribute to these reentrant arrhythmias and may be potentiated by acute pericarditis.     

Diurnal variations of the dominant cycle length of chronic atrial fibrillation

High-resolution digital Holter recording was carried out in 21 patients (15 men, 64 +/- 12 yr) with chronic atrial fibrillation. Dominating atrial cycle length (DACL) was derived by frequency domain analysis of QRST-reduced electrocardiograms. Daytime mean DACL was 150 +/- 17 ms, and nighttime mean was 157 +/- 22 ms (P = 0. 0002). Diurnal fluctuation in DACL differed among patients: it tended to be virtually absent in those with a short mean DACL, but in those with longer DACL the night-day difference was as much as 23 ms (R = 0.72, P < 0.001, correlation of mean DACL to night-day difference). Mean DACL also correlated with ventricular cycle length (R = 0.40, P < 0.001), particularly at night (r = 0.49). The shorter cycle lengths found in this study during the day are consistent with sympathetic and/or other physiological modulation, but since increased vagal tone shortens atrial refractoriness in most models, parasympathetic influences are not likely to play a major role. Alternatively, atrial effective refractory period may not be the sole determinant of atrial cycle length during atrial fibrillation.     

起搏器术后新发房性心律失常的影响因素分析

目的:探讨起搏器术后新发房性心律失常的发生情况及其相关影响因素。方法:选择2006年1月至2007年12月于沈阳军区总医院首次植入永久起搏器的107例患者,男性50例,平均年龄65.0±11.9岁,术前通过追问病史及相关检查均排除房性心律失常(房颤、房扑、房速),术后平均随访3.9年,观察新发房性心律失常情况。按术后是否出现房性心律失常,将患者分为新发房性心律失常组和无房性心律失常组,比较两组患者术前和术后心脏超声结果的变化、心室起搏比例、起搏部位及起搏模式,并通过logistic回归分析起搏器术后发生房性心律失常的影响因素。结果:新发房性心律失常组26例(24.3%),其中房颤17例(15.9%),房扑2例(1.9%),房速7例(6.5%);无房性心律失常组81例。与无房性心律失常组比较,新发房性心律失常组左房内径明显增加(P=0.040)、二尖瓣返流程度较重(P=0.032)及左室射血分数明显下降(P=0.001),心室起搏百分比(VP%)显著升高(P=0.017)。心尖部起搏患者房性心律失常的发生率明显高于间隔部起搏(33.3%vs 16.9%,P<0.05),双腔起搏组患者房性心律失常发生率明显低于单腔起搏器组(18.7%vs 37.5%,P<0.05)。Logistic回归分析显示术后新发房性心律失常的发生与高比例的心室起搏(P=0.006)、VVI(R)起搏模式(P=0.014)及右心室起搏电极导线植于心尖部(P=0.024)显著相关。结论:起搏模式、心室起搏百分比、起搏部位是起搏器术后发生房性心律失常的影响因素。     

A Three-Dimensional Human Atrial Model with Fiber Orientation. Electrograms and Arrhythmic Activation Patterns Relationship

The most common sustained cardiac arrhythmias in humans are atrial tachyarrhythmias, mainly atrial fibrillation. Areas of complex fractionated atrial electrograms and high dominant frequency have been proposed as critical regions for maintaining atrial fibrillation; however, there is a paucity of data on the relationship between the characteristics of electrograms and the propagation pattern underlying them. In this study, a realistic 3D computer model of the human atria has been developed to investigate this relationship. The model includes a realistic geometry with fiber orientation, anisotropic conductivity and electrophysiological heterogeneity. We simulated different tachyarrhythmic episodes applying both transient and continuous ectopic activity. Electrograms and their dominant frequency and organization index values were calculated over the entire atrial surface. Our simulations show electrograms with simple potentials, with little or no cycle length variations, narrow frequency peaks and high organization index values during stable and regular activity as the observed in atrial flutter, atrial tachycardia (except in areas of conduction block) and in areas closer to ectopic activity during focal atrial fibrillation. By contrast, cycle length variations and polymorphic electrograms with single, double and fragmented potentials were observed in areas of irregular and unstable activity during atrial fibrillation episodes. Our results also show: 1) electrograms with potentials without negative deflection related to spiral or curved wavefronts that pass over the recording point and move away, 2) potentials with a much greater proportion of positive deflection than negative in areas of wave collisions, 3) double potentials related with wave fragmentations or blocking lines and 4) fragmented electrograms associated with pivot points. Our model is the first human atrial model with realistic fiber orientation used to investigate the relationship between different atrial arrhythmic propagation patterns and the electrograms observed at more than 43000 points on the atrial surface.     

Assessment of spatial organization in the atria during paroxysmal atrial fibrillation and adrenergic stimulation.

Non-linear parameters were computed to assess the extent of spatial organization in the atria in terms of coupling/synchronization between electrograms recorded in different atrial sites. Recordings of 9 patients suffering from paroxysmal atrial fibrillation were tested during four clinical experimental conditions: sinus rhythm and atrial fibrillation, both before and after isoproterenol infusion, a drug mimicking adrenergic activation. Two non-linear metrics were investigated: an index of non-linear association (NLA) and a synchronization (S) index based on the cross-conditional entropy. Results evidence the presence of reduced coupling after drug infusion in both sinus rhythm and atrial fibrillation. Moreover, passing from the NLA to the S index, the capability of the parameter to capture the subtle changes due to isoproterenol administration increased.     

Optical mapping of Langendorff-perfused human hearts: establishing a model for the study of ventricular fibrillation in humans

Our objective was to establish a novel model for the study of ventricular fibrillation (VF) in humans. We adopted the established techniques of optical mapping to human ventricles for the first time to determine whether human VF is the result of wave breaks and singularity point formation and is maintained by high-frequency rotors and fibrillatory conduction. We describe the technique of acquiring optical signals in human hearts during VF, their characteristics, and the feasibility of possible analyses that could be performed to elucidate mechanisms of human VF. We used explanted hearts from five cardiomyopathic patients who underwent transplantation. The hearts were Langendorff perfused with Tyrode solution (95% O(2)-5% CO(2)), and the potentiometric dye di-4-ANEPPS was injected as a bolus into the coronary circulation. Fluorescence was excited at 531 +/- 20 nm with a 150-W halogen light source; the emission signal was long-pass filtered at 610 nm and recorded with a mapping camera. Fractional change of fluorescence varied between 2% and 12%. Average signal-to-noise ratio was 40 dB. The mean velocity of VF wave fronts was 0.25 +/- 0.04 m/s. Submillimetric spatial resolution (0.65-0.85 mm), activation mapping, and transformation of the data to phase-based analysis revealed reentrant, colliding, and fractionating wave fronts in human VF. On many occasions the VF wave fronts were as large as the entire vertical length (8 cm) of the mapping field, suggesting that there are a limited number of wave fronts on the human heart during VF. Phase transformation of the optical signals allowed the first demonstration ever of phase singularity point, wave breaks, and rotor formation in human VF. This method provides opportunities for potential analyses toward elucidation of the mechanisms of VF and defibrillation in humans.     

AAI to DDD pacing mode inappropriate switches in a dual chamber pacemaker due to ventricular blanking period

A 90-year-old woman received a dual chamber pacemaker (PM) for a sick sinus syndrome. The PM was programmed with SafeR AAI-DD pacing mode at 60 bpm. During a standard follow up, some memorized electrograms (EGMs) were found in SafeR diagnostics, with atrial pacing (Ap) not followed by any ventricular sensing/pacing event, due to simultaneous junctional activity falling into ventricular blanking period during Ap and, for this reason, unsensed by the PM. Blanking periods can affect PM functioning if not revealed and adjusted.     

Synchronization of ventricular fibrillation with real-time feedback pacing: implication to low-energy defibrillation

Wavefront synchronization is an important aspect preceding the termination of ventricular fibrillation (VF). We evaluated the defibrillation efficacy of a novel multisite pacing algorithm using optical recording-guided synchronized pacing (SyncP) in the excitable gaps. We compared the effects of SyncP with traditional overdrive pacing (ODP) at 90% of the VF cycle length (VFCL) and high-frequency pacing (HFP; 43-215 Hz) on spontaneous VF termination in isolated rabbit hearts. For SyncP, the pacing current was triggered by the activation of a reference site and was delivered when the optical potential of the pacing site was in an excitable gap. We measured VFCL and the spatial dispersion of VFCL (SDCL) from five points (3 points in the paced area and 2 points in the nonpaced area) and the distribution of phase singularities during the prepacing, pacing, and postpacing periods. The results showed that 1) the VF termination rate of SyncP (16.0%, n = 106) was higher than that of ODP (2.1%, n = 48, P < 0.01) or HFP (1.6%, n = 129, P < 0.0001); 2) energy consumption for SyncP (7.6 +/- 9.3 mJ) was significantly lower than that of ODP (14.0 +/- 14.8 mJ, P < 0.0001); and 3) SyncP, but not ODP or HFP, decreased SDCL in the paced area during the pacing (P < 0.01) and postpacing (P < 0.05) periods compared with the prepacing period. We conclude that SyncP is effective in inducing wavefront synchronization and is more effective at facilitating spontaneous VF termination than non-SyncP.     

What are the post-ablation insular residual electrograms in the posterior left pulmonary veins electrically connected to?

A 67-year-old man underwent a third ablation procedure for a recurrent atrial tachycardia (AT) after an extensive pulmonary vein (PV) isolation, linear ablation along the left atrial (LA) roof and posterolateral mitral isthmus (MI), and defragmentation of persistent atrial fibrillation and an induced perimitral AT. High-resolution mapping during the clinical AT using the Rhythmia system (Boston Scientific) suggested that the AT was a ridge-related reentrant AT and exhibited a reconnection of the left PVs (LPVs). The residual electrograms in the posterior LPVs were surrounded by endocardial scar, which was like an island consisting of residual LPV electrograms. Retrograde venography of the vein of Marshall (VOM) demonstrated that the VOM reached the posterior left superior PV through the ridge between the LA appendage and left inferior PV and then the LPV carina. An ethanol infusion into the VOM resulted in a simultaneous AT termination and complete electrical isolation of the LPVs, that is, the disappearance of the residual LPV electrograms. The insular residual LPV electrograms in the present case did not appear to be endocardially connected to the LA, because the LPV electrograms were surrounded by endocardial scar and there was a large time gap between the earliest activation in the posterior LPVs and activation in the surrounding area. The VOM course on the venography and elimination of the residual LPV electrograms with an ethanol infusion into the VOM suggested that the insular residual LPV electrograms were electrically connected to the posterolateral LA via the VOM and its branches.     

Chronic atrial fibrillation does not further decrease outward currents. It increases them

Rapid atrial pacing causes electrical remodeling that leads to atrial fibrillation (AF). AF can further remodel atrial electrophysiology to maintain AF. Our previous studies showed that there was a marked difference in the duration of AF in dogs that have been atrial paced at 400 beats/min for 6 wk. We hypothesized that this difference is based on the changes in the degree of electrical remodeling caused by rapid atrial pacing versus that by AF. Right atrial cells were isolated from control dogs (Con, N = 28), from dogs with chronic AF (cAF dogs, N = 13, episodes lasting at least 6 days), or from dogs with nonsustained or brief episodes of AF (nAF dogs, N = 10, episodes lasting minutes to hours). Both transient outward (Ito) and sustained outward K+ current (Isus) densities/functions were determined using whole cell voltage-clamp techniques. In nAF cells, Ito density was reduced by 69% at +40 mV: from 7.1 +/- 0.5 pA/pF (Con, n = 59) to 2.2 +/- 0.2 pA/pF (nAF, n = 24) (P < 0.05). The voltage dependence of inactivation of Ito was shifted positively and decay kinetics were changed; however, recovery from inactivation was not altered in nAF cells. In contrast, Ito density in cAF cells was both significantly different from Con cells and larger than that in nAF cells [at +40 mV, 3.5 +/- 0.3 pA/pF (cAF, n = 29), P < 0.05]. In cAF cells, recovery from inactivation and decay of Ito were both slow; yet, voltage dependence inactivation of Ito approached that of Con cells. Furthermore, "recovered" Ito of cAF cells was more sensitive to tetraethylammonium than currents of Con and nAF cells. Isus densities of nAF and cAF cells did not differ. Both nAF and cAF cells have reduced Ito versus Con cells, but Ito remodeling of nAF cells differed from that of cAF cells. Ito in cAF dogs was likely remodeled by AF per se, whereas that in nAF dogs was likely the consequence of the rapid rate in the absence of sustained AF.