Epicardial wavefronts arise from widely distributed transient sources during ventricular fibrillation in the isolated swine heart.

It has been proposed that VF waves emanate from stable localized sources, often called "mother rotors." However, evidence for the existence of these rotors is conflicting. Using a new panoramic optical mapping system that can image nearly the entire ventricular epicardium, we recently excluded epicardial mother rotors as the drivers of Wiggers' stage II VF in the isolated swine heart. Furthermore, we were unable to find evidence that VF requires sustained intramural sources. The present study was designed to test the following hypotheses: 1. VF is driven by a specific region, and 2. Rotors that are long-lived, though not necessarily permanent, are the primary generators of VF wavefronts. Using panoramic optical mapping, we mapped VF wavefronts from 6 isolated swine hearts. Wavefronts were tracked to characterize their activation pathways and to locate their originating sources. We found that the wavefronts that participate in epicardial reentry were not confined to a compact region; rather they activated the entire epicardial surface. New wavefronts feeding into the epicardial activation pattern were generated over the majority of the epicardium and almost all of them were associated with rotors or repetitive breakthrough patterns that lasted for less than 2 s. These findings indicate that epicardial wavefronts in this model are generated by many transitory epicardial sources distributed over the entire surface of the heart.

[Transvenous parasympathetic nerve stimulation in the chronic myocardial infarction phase]. / Transvenöse Stimulation parasympathischer Nerven in der chronischen Infarktphase.

The study describes the electrophysiological effects of transvenous cardiac nerve stimulation in an animal model of myocardial infarction. In ten sheep with recent myocardial infarction, transvenous stimulation of parasympathetic cardiac nerves was achieved from a catheter in the right pulmonary artery. The effects of transvenous cardiac nerve stimulation on sinus rhythm cycle length, ventricular refractory periods and inducibility of monomorphic ventricular tachycardia were evaluated. Sinus rhythm cycle length increased from 620 +/- 24 ms to 723 +/- 30 ms during nerve stimulation with 20 Hz and to 779 +/- 28 ms during stimulation with 40 Hz (p < 0.05). Effective ventricular refractory periods from stimulation sites in non-infarcted right and left ventricular myocardium showed a tendency towards prolongation during cardiac nerve stimulation with shortening after cessation of stimulation. These differences, however, were not significant. In contrast, refractory periods from stimulation sites within the infarcted area remained unchanged during cardiac nerve stimulation. The inducibility of monomorphic ventricular tachycardia by programmed electrical stimulation was reduced during transvenous cardiac nerve stimulation. Pathological examination showed cholinergic nerves in close proximity to the tip of the stimulation catheter in the right pulmonary artery. Transvenous cardiac nerve stimulation in sheep with remote myocardial infarction exhibits electrophysiological effects on the ventricles. Although a parasympathetic effect on the ventricles could not be proven, the observed effects may result from direct stimulation of efferent parasympathetic nerves.

Comparison of the temperature profile and pathological effect at unipolar, bipolar and phased radiofrequency current configurations.

With a multi-electrode catheter, phased radiofrequency (RF) delivers current between each electrode and a backplate as well as between adjacent electrodes. This study compared the tissue heating and lesion dimensions created by phased and standard RF. Ablation was performed on the in vivo thigh muscles in 5 pigs. Six lesions were created on each thigh muscle using phase angle 0 degrees RF, 127 degrees RF, 180 degrees RF with and without a backplate, and standard RF in bipolar and sequential unipolar configurations. Two plunge needles, each with 6 thermocouples 1 mm apart, were inserted into the tissue with one needle beside an electrode and the other midway between electrodes for tissue temperature measurement. The 0 degrees RF created lower tissue temperatures and smaller lesions between electrodes than those beside electrode. With 127 degrees and 180 degrees RF, tissue temperature and lesion dimensions between electrodes were similar to beside electrode, while the 127 degrees RF created higher tissue temperature and deeper lesions than 180 degrees RF (both with and without a backplate) at both sites. Standard RF bipolar ablation created similar tissue temperatures and lesion depths at both sites, but required greater power than the 127 degrees RF. Standard RF sequential unipolar ablation created only a slight temperature increase and no lesions between electrodes 3 and 4. As judged by tissue temperature, lesion depth and uniformity, and RF power requirement, 127 degrees RF may be a better energy configuration for linear ablation than the other RF modalities tested.

Mechanism of ventricular defibrillation for near-defibrillation threshold shocks: a whole-heart optical mapping study in swine.

BACKGROUND: To study the mechanism by which shocks succeed (SDF) or fail (FDF) to defibrillate, global cardiac activation and recovery and their relationship to defibrillation outcome were investigated for shock strengths with approximately equal SDF and FDF outcomes (DFT(50)). METHODS AND RESULTS: In 6 isolated pig hearts, dual-camera video imaging was used to record optically from approximately 8000 sites on the anterior and posterior ventricular surfaces before and after 10 DFT(50) biphasic shocks. The interval between the shock and the last ventricular fibrillation activation preceding the shock (coupling interval, CI) and the time from shock onset to 90% repolarization of the immediate postshock action potential (RT(90)) were determined at all sites. Of 60 shocks, 31 were SDF. The CI (59+/-7 versus 52+/-6 ms) and RT(90) (108+/-19 versus 88+/-8 ms) were significantly longer for SDF than FDF episodes. Spatial dispersions of CI (36+/-5 versus 34+/-3 ms) and RT(90) (40+/-16 versus 40+/-8 ms) were not significantly different for SDF versus FDF episodes. The first global activation cycle appeared focally on the left ventricular apical epicardium 78+/-32 ms after the shock. CONCLUSIONS: For near-threshold shocks, defibrillation outcome correlates with the electrical state of the heart at the time of the shock and on RT. Global dispersion of RT was similar in both SDF and FDF episodes, suggesting that it is not crucial in determining defibrillation outcome after DFT(50) shocks.

Atrial defibrillation thresholds of electrode configurations available to an atrioventricular defibrillator.

INTRODUCTION: Little investigation has been conducted to assess the atrial defibrillation thresholds of electrode configurations using electrodes designed for internal ventricular defibrillation (right ventricle [RV], superior vena cava [SVC], and pulse generator housing [Can]) combined with coronary sinus (CS) electrodes. We hypothesized that a CS-->SVC+Can electrode configuration would have a lower atrial defibrillation threshold than a standard configuration for defibrillation, RV-->SVC+Can. We also tested the atrial defibrillation thresholds of five other configurations. METHODS AND RESULTS: In 12 closed chest sheep, we situated a two-coil (RV, SVC) defibrillation catheter, a left-pectoral subcutaneous Can, and a CS lead. Atrial fibrillation was burst induced and maintained with continuous infusion of intrapericardial acetyl-beta-methylcholine chloride. Using fixed-tilt biphasic shocks, we determined the atrial defibrillation thresholds of seven test configurations in random order according to a multiple-reversal protocol. The peak voltage and delivered energy atrial defibrillation thresholds of CS-->SVC+Can (168+/-67 V, 2.68+/-2.40 J) were significantly lower than those of RV-->SVC+Can (215+/-88 V, 4.46+/-3.40 J). The atrial defibrillation thresholds of the other test configurations were RV+CS-->SVC+Can: 146+/-59 V, 1.92+/-1.45 J; RV-->CS+SVC+Can: 191+/-89 V, 3.53+/-3.19 J; CS-->SVC: 188+/-98 V, 3.77+/-4.14 J; SVC-->CS+ Can: 265+/-145 V, 7.37+/-9.12 J; and SVC-->Can: 516+/-209 V, 24.5+/-15.0 J. CONCLUSIONS: The atrial defibrillation threshold of CS-->SVC+Can is significantly lower than that of RV-->SVC+Can. In addition, the low atrial defibrillation threshold of RV+CS-->SVC+Can merits further investigation. Based on corroboration of low atrial defibrillation thresholds of CS-based configurations in humans, physicians might consider using CS leads with atrioventricular defibrillators.

Right atrial septal electrode for reducing the atrial defibrillation threshold.

BACKGROUND: The atrial defibrillation threshold (ADFT) energy of the standard lead configuration, right atrial appendage (RAA) to coronary sinus (CS), was reduced by >50% with the addition of a third electrode traversing the atrial septum in a previous study. This study determined whether the ADFT would be lowered by a more clinically practical third electrode placed in the right atrium along the atrial septum (RSP). METHODS AND RESULTS: Sustained atrial fibrillation was induced in 8 closed-chest sheep with burst pacing and maintained with pericardial infusion of acetyl-beta-methylcholine chloride. A custom-made, dual-defibrillation catheter was placed with electrodes in the lateral RA, CS, and RSP. A separate defibrillation catheter was also placed in the RAA. ADFT characteristics of RAA-->CS and 6 other single- or sequential-shock configurations were determined in random order by using biphasic, truncated-exponential waveforms in a multiple-reversal protocol. The delivered-energy, peak-voltage, and peak-current ADFTs for the sequential-shock configuration CS-->RSP/RA-->RSP (0.53+/-0.31 J, 86+/-22 V, and 1.6+/-0.6 A, respectively) were significantly lower than those of RAA-->CS (1.14+/-0.64 J, 157+/-34 V, and 2.5+/-1.1 A, respectively). The ADFT characteristics of RAA-->CS and RA-->CS were not significantly different, nor were those of CS-->RSP/RA-->RSP and CS-->RSP/RAA--> RSP. CONCLUSIONS: The ADFT of the standard RAA-->CS configuration may be markedly reduced with an additional electrode situated at the RSP.

Purkinje and ventricular contributions to endocardial activation sequence in perfused rabbit right ventricle.

Interactions between peripheral conduction system and myocardial wave fronts control the ventricular endocardial activation sequence. To assess those interactions during sinus and paced ventricular beats, we recorded unipolar electrograms from 528 electrodes spaced 0.5 mm apart and placed over most of the perfused rabbit right ventricular free wall endocardium. Left ventricular contributions to electrograms were eliminated by cryoablating that tissue. Electrograms were systematically processed to identify fast (P) deflections separated by >2 ms from slow (V) deflections to measure P-V latencies. By using this criterion during sinus mapping (n = 5), we found P deflections in 22% of electrograms. They preceded V deflections at 91% of sites. Peripheral conduction system wave fronts preceded myocardial wave fronts by an overall P-V latency magnitude that measured 6.7 +/- 3.9 ms. During endocardial pacing (n = 8) at 500 ms cycle length, P deflections were identified on 15% of electrodes and preceded V deflections at only 38% of sites, and wave fronts were separated by a P-V latency magnitude of 5.6 +/- 2.3 ms. The findings were independent of apical, basal, or septal drive site. Modest changes in P-V latency accompanied cycle length accommodation to 125-ms pacing (6.8 +/- 2.6 ms), although more pronounced separation between wave fronts followed premature stimulation (11.7 +/- 10.4 ms). These results suggested peripheral conduction system and myocardial wave fronts became functionally more dissociated after premature stimulation. Furthermore, our analysis of the first ectopic beats that followed 12 of 24 premature stimuli revealed comparable separation between wave fronts (10.7 +/- 5.5 ms), suggesting the dissociation observed during the premature cycles persisted during the initiating cycles of the resulting arrhythmias.

Critically timed auxiliary shock to weak field area lowers defibrillation threshold.

INTRODUCTION: This study tested the hypothesis that the defibrillation threshold (DFT) can be lowered by delivering a weak auxiliary shock in conjunction with a stronger primary shock to the cardiac region where the primary shock electric field is weakest. METHODS AND RESULTS: Eight swine were studied in each of two study parts. In both parts, DFTs were determined for dual shocks delivered through two electrode pairs. The biphasic primary shock was delivered through electrodes in the right ventricle and superior vena cava. The auxiliary shock was delivered through a separate electrode in the superior vena cava and a left ventricular electrode placed where the primary shock field was presumed to be weakest. In part I, a monophasic auxiliary shock of 50, 100, or 150 V was delivered either simultaneously with or 1, 20, or 40 msec before primary shock. When auxiliary shock was delivered simultaneously with or 1 msec before primary shock, DFT energy was reduced by approximately 50% compared with primary shock alone. In part II, a 150-V monophasic or biphasic auxiliary shock of either polarity was delivered 1 msec before or after primary shock. Regardless of waveform or polarity, all auxiliary shock delivered before primary shock lowered DFT energy by approximately 30% compared with primary shock alone. Depending on waveform and polarity, auxiliary shock delivered after primary shock either did not significantly change the DFT or elevated the DFT compared with primary shock alone. CONCLUSION: Application of a small auxiliary shock, just before or simultaneously with a primary shock, to the cardiac region where the primary shock field is weakest significantly lowers DFT.

Reentry site during fibrillation induction in relation to defibrillation efficacy for different shock waveforms.

INTRODUCTION: Unsuccessful defibrillation shocks may reinitiate fibrillation by causing postshock reentry. METHODS AND RESULTS: To better understand why some waveforms are more efficacious for defibrillation, reentry was induced in six dogs with 1-, 2-, 4-, 8-, and 16-msec monophasic and 1/1- (both phases 1 msec) 2/2-, 4/4-, and 8/8-msec biphasic shocks. Reentry was initiated by 141+/-15 V shocks delivered from a defibrillator with a 150-microF capacitance during the vulnerable period of paced rhythm (183+/-12 msec after the last pacing stimulus). The shock potential gradient field was orthogonal to the dispersion of refractoriness. Activation was mapped with 121 electrodes covering 4 x 4 cm of the right ventricular epicardium, and potential gradient and degree of recovery of excitability were estimated at the sites of reentry. Defibrillation thresholds (DFTs) were estimated by an up-down protocol for the same nine waveforms in eight dogs internally and in nine other dogs externally. DFT voltages for the different waveforms were positively correlated with the magnitude of shock potential gradient and negatively correlated with the recovery interval at the site at which reentry was induced by the waveform during paced rhythm for both internal (DFT = 1719 + 64.5VV - 11.1RI; R2 = 0.93) and external defibrillation (DFT = 3445 + 150VV - 22RI; R2 = 0.93). CONCLUSION: The defibrillation waveforms with the lowest DFTs were those that induced reentry at sites of low shock potential gradient, indicating efficacious stimulation of myocardium. Additionally, the site of reentry induced by waveforms with the lowest DFTs was in myocardium that was more highly recovered just before the shock, perhaps because this high degree of recovery seldom occurs during defibrillation due to the rapid activation rate during fibrillation.

Reduction in atrial defibrillation threshold by a single linear ablation lesion.

INTRODUCTION: This study investigated a hybrid approach to reduce the atrial defibrillation threshold (ADFT) by determining the effect of a single linear radiofrequency ablation (RFA) lesion on both the ADFT and activation patterns during atrial fibrillation (AF). METHODS AND RESULTS: In 18 open chest sheep (45 to 57 kg), coil defibrillation electrodes were placed in a superior vena cava/right ventricular configuration. AF was induced by burst pacing and maintained with acetyl beta-methylcholine (2 to 42 microL/min). ADFTs were obtained before and after a linear RFA lesion was created in the left atrium (LAL; n = 6), right atrium (RAL; n = 6), or neither atrium as a control (n = 6). In animals receiving an LAL, a 504-unipolar-electrode plaque was sutured to the LA. For animals receiving an RAL, two 504-electrode plaques were placed, one each on the LA and RA. From each plaque, activations were recorded before and after ADFT shocks, and organizational characteristics of activations were analyzed using algorithms that track individual wavefronts. In sham-treated controls, the ADFT did not change. In contrast, LAL reduced ADFT energy 29%, from 4.5 +/- 2.3 J to 3.2 +/- 2.0 J (P < 0.05). RAL reduced ADFT energy 25%, from 2.0 +/- 0.9 J to 1.5 +/- 0.7 J (P < 0.05). AF activation was substantially more organized after RFA than before RFA for both the RAL- and LAL-treated animals. CONCLUSION: A single RFA lesion in either the RA or LA reduces the ADFT in this sheep model. This decrease is associated with an increase in fibrillatory organization.

Improvement of defibrillation efficacy and quantification of activation patterns during ventricular fibrillation in a canine heart failure model.

BACKGROUND: Little is known about the effects of heart failure (HF) on the defibrillation threshold (DFT) and the characteristics of activation during ventricular fibrillation (VF). METHODS AND RESULTS: HF was induced by rapid right ventricular (RV) pacing for at least 3 weeks in 6 dogs. Another 6 dogs served as controls. Catheter defibrillation electrodes were placed in the RV apex, the superior vena cava, and the great cardiac vein (CV). An active can coupled to the superior vena cava electrode served as the return for the RV and CV electrodes. DFTs were determined before and during HF for a shock through the RV electrode with and without a smaller auxiliary shock through the CV electrode. VF activation patterns were recorded in HF and control animals from 21x24 unipolar electrodes spaced 2 mm apart on the ventricular epicardium. Using these recordings, we computed a number of quantitative VF descriptors. DFT was unchanged in the control dogs. DFT energy was increased 79% and 180% (with and without auxiliary shock, respectively) in HF compared with control dogs. During but not before HF, DFT energy was significantly lowered (21%) by addition of the auxiliary shock. The VF descriptors revealed marked VF differences between HF and control dogs. The differences suggest decreased excitability and an increased refractory period during HF. Most, but not all, descriptors indicate that VF was less complex during HF, suggesting that VF complexity is multifactorial and cannot be expressed by a scalar quantity. CONCLUSIONS: HF increases the DFT. This is partially reversed by an auxiliary shock. HF markedly changes VF activation patterns.

Pacing during ventricular fibrillation: factors influencing the ability to capture.

INTRODUCTION: Recent studies showed that pacing atrial and ventricular fibrillation (VF) is possible. The studies presented here determined which parameters influence the efficacy of a pacing train to capture fibrillating ventricular myocardium. Electrode type, current strength, order of pacing trains, polarity, and VF morphology preceding the pacing trains were investigated. METHODS AND RESULTS: A 504-electrode recording plaque sutured to the right ventricle of pig hearts was used to record the activations of VF and those resulting from the pacing stimulation. Capture of VF by pacing was determined by observing an animated display of the first temporal derivative of the electrograms. A series of electrodes in a line captured the heart more frequently during VF than did a point electrode. Increasing the current strength to 10 x diastolic pacing threshold increased the incidence of capture, but increasing this strength further did not. The second or third train of 40 stimuli had greater capture rates than did the first train during the same VF episode. Anodal and cathodal unipolar, and bipolar stimulation were equally efficacious in capturing VF. VF activation during the 1-second interval preceding pacing was more organized for pacing trains that captured than those that did not. The highest incidence of capture, 46% to 61% of pacing trains, occurred with a line of electrodes at 10 x diastolic pacing threshold delivered by the second or third train. CONCLUSION: The probability of a pacing train capturing fibrillating myocardium can be influenced by the pacing protocol parameters.

Reduction of atrial defibrillation threshold with an interatrial septal electrode.

BACKGROUND: The standard lead configuration for internal atrial defibrillation consists of a shock between electrodes in the right atrial appendage (RAA) and coronary sinus (CS). We tested the hypothesis that the atrial defibrillation threshold (ADFT) of this RAA-->CS configuration would be lowered with use of an additional electrode at the atrial septum (SP). METHODS AND RESULTS: Sustained atrial fibrillation was induced in 8 closed-chest sheep with burst pacing and continuous pericardial infusion of acetyl-ss-methylcholine. Defibrillation electrodes were situated in the RAA, CS, pulmonary artery (PA), low right atrium (LRA), and across the SP. ADFTs of RAA-->CS and 4 other lead configurations were determined in random order by use of a multiple-reversal protocol. Biphasic waveforms of 3/1-ms duration were used for all single and sequential shocks. The ADFT delivered energies for the single-shock configurations were 1.27+/-0.67 J for RAA-->CS and 0. 86+/-0.59 J for RAA+CS-->SP; the ADFTs for the sequential-shock configurations were 0.39+/-0.18 J for RAA-->SP/CS-->SP, 1.16+/-0.72 J for CS-->SP/RAA-->SP, and 0.68+/-0.46 J for RAA-->CS/LRA-->PA. Except for CS-->SP/RAA-->SP versus RAA-->CS and RAA-->CS/LRA-->PA versus RAA+CS-->SP, the ADFT delivered energies of all of the configurations were significantly different from each other (P:<0. 05). CONCLUSIONS: The ADFT of the standard RAA-->CS configuration is markedly reduced with an additional electrode at the atrial SP.

Signal averaging in Wolff-Parkinson-White syndrome: evidence that fractionated activation is not necessary for body surface high-frequency potentials.

It is commonly assumed that the presence of high frequency components in body surface potentials implies that fractionated activation fronts, caused by heterogeneously viable tissue, are present in the heart. However, it is possible that non-fractionated activation fronts can also give rise to high frequency surface potentials and that the relative amount of high frequency power is related to the complexity of the activation sequence. In a test of this idea, averaged body surface potentials were recorded during the entire QRS complex of nine Wolff-Parkinson-White (WPW) patients in situations in which fractionated activation fronts should not have been present, but which represent increasing degrees of complexity of ventricular activation: (1) postoperative ectopic pacing from subepicardial wires placed during surgery, when a single coherent activation front was present throughout most of the QRS; (2) Preoperative preexcited rhythm, when a single coherent activation front was present for one portion of the QRS (the delta wave); and (3) postoperative normal rhythm, when two or more activation fronts were present in the ventricles throughout most of the QRS. For comparison, averaged body surface potentials were also analyzed during the last 40 ms of the QRS complex and the ST segment of 14 postinfarction patients with chronic ventricular tachycardia. In the patients with WPW syndrome, relatively high frequency content increased (attenuation -36.7 vs -27.2 vs -18.3 dB) and QRS width decreased (160.7 vs 125.9 vs 94.1 ms) significantly from paced to preoperative to postoperative beats. Significant high frequency content was present in all cases, showing that coherent activation fronts can give rise to high frequencies. Interestingly, the postoperative QRS of WPW patients contained a larger proportion of high frequency power than did the late potentials of the patients with ventricular tachycardia. Thus, while the presence of late fractionated body surface potentials may be a marker for ventricular tachycardia, these potentials by themselves do not necessarily signify that the underlying cardiac activation giving rise to these signals is fractionated.

Prediction of defibrillation outcome by epicardial activation patterns following shocks near the defibrillation threshold.

INTRODUCTION: Ventricular defibrillation is probabilistic and shock strength dependent. We investigated the relationship between defibrillation outcome and postshock activation patterns for shocks of the same strength (approximately 50% probability of success for defibrillation [ED50] to yield an equal number of successful and failed shocks). METHODS AND RESULTS: In five pigs, 10 shocks of approximately ED50 strength (right ventricle-superior vena cava, biphasic, 6/4 msec) were delivered after 10 seconds of ventricular fibrillation (VF). Epicardial activation sequences following shocks were mapped with a 504-electrode shock and analyzed by animating dV/dt of the electrograms. Intercycle interval (ICI, time between the onset of successive postshock cycles), wavefront conduction time (WCT, time between the earliest and latest activation of a cycle), and overlapping index (WCT of cycle[n]/ICI of cycle[n+1]) were determined for the first five postshock cycles. An overlapping index >1 indicates overlap between successive cycles. Of 50 defibrillation attempts, 25 were successes. There was no difference between successful and failed episodes for both ICI (68 +/- 9 msec vs 62 +/- 10 msec) and WCT (97 +/- 24 msec vs 100 +/- 14 msec) of cycle 1. However, starting at cycle 2, the ICI was longer, and the WCT was shorter for successful than failed episodes (P < 0.01). Overlapping cycles (index > 1) were found during the transition from cycles 2 through 5 in all failed (index >1) and in no successful episodes. CONCLUSIONS: (1) Defibrillation outcome cannot be determined during the first postshock cycle. (2) At least three rapid successive cycles with overlap of cycles 2 and 3 are present in all failed and in no successful episodes. (3) The overlapping index is a marker to predict defibrillation outcome.