Modulation of QT interval by cardiac sympathetic nerve sprouting and the mechanisms of ventricular arrhythmia in a canine model of sudden cardiac death.

INTRODUCTION: We previously reported that there is a high incidence of sudden cardiac death (SCD) in dogs with myocardial infarction (MI), complete AV block (CAVB), and nerve growth factor (NGF) infusion to the left stellate ganglion (LSG). Whether or not QT interval prolongation underlines the mechanism of SCD was unclear. METHODS AND RESULTS: We analyzed QT intervals in three groups of dogs. All dogs had CAVB and MI. The LSG group (n = 9) and right stellate ganglion (RSG) group (n = 6) received NGF infusion via the osmotic pumps over a 5-week period to LSG and RSG, respectively. The control group (n = 6) received no NGF. The dogs either died suddenly or were sacrificed within 2 to 3 months after MI. Heart rhythm and QT and RR intervals were monitored using implantable cardioverter defibrillator ECG recordings. There was a time-dependent increase of QTc intervals in the LSG group and a time-dependent decrease of QTc intervals in the RSG group. At the end of NGF infusion, QTc intervals in the LSG group (408 +/- 41 msec) were significantly longer than those in the control (350 +/- 41 msec; P < 0.05) and RSG groups (294 +/- 23 msec; P < 0.01). In the LSG group, 4 of 9 dogs died of SCD. There was no SCD in either the RSG or control group. Immunocytochemical staining showed NGF infusion to LSG and RSG resulted in left and right ventricular sympathetic nerve sprouting and hyperinnervation, respectively. CONCLUSION: NGF infusion to the LSG in dogs with MI and CAVB resulted in increased QT interval and incidence of ventricular tachycardia, ventricular fibrillation, and SCD, whereas NGF infusion to the RSG shortened QT interval and reduced the incidence of ventricular tachycardia. These findings indicate that QT interval prolongation is causally related to the occurrence of ventricular arrhythmia in dogs with nerve sprouting, MI, and CAVB.

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.

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.

Marked reduction of ventricular defibrillation threshold by application of an auxiliary shock to a catheter electrode in the left posterior coronary vein of dogs.

INTRODUCTION: For endocardial shocks near the defibrillation threshold (DFT), postshock activity originates from the lateral left ventricular apex, where the shock field is weak. This study tested the hypothesis that an auxiliary shock (AS) delivered between an electrode at this site and a superior vena cava (SVC) electrode before the primary endocardial shock (PS) would reduce the DFT. METHODS AND RESULTS: In six pentobarbital-anesthetized dogs (26 to 36 kg), catheter electrodes were placed in the right ventricular (RV) apex and the SVC. To simulate transvenous introduction, a small electrode was inserted into the posterior cardiac vein using an epicardial approach. For dual shock treatments, AS (2-msec monophasic) was applied to the coronary vein electrode at different time intervals before a biphasic PS (4 msec/3 msec) to the RV-SVC electrodes. The mean DFT energy for dual shocks treatments were significantly reduced (P < 0.05) in comparison to the control treatment (no AS, 26.5+/-8.8 J). Mean DFT energy after 10 seconds of electrically induced ventricular fibrillation for dual shocks, in which AS and PS were separated by 1, 5, 10, and 20 msec, were 10.2+/-4.1 J, 10.9+/-5.5 J, 11.3+/-6.3 J, and 15.4+/-7.2 J, respectively. These values were all significantly lower than the PS alone (26.5+/-8.8 J). CONCLUSION: Addition of an AS from the posterior cardiac vein before an endocardial PS reduces DFT energy by more than 50%. Such DFT reduction could improve therapeutic safety margin or permit reduction in volume of implantable cardioverter defibrillators.

Nerve sprouting and sudden cardiac death.

The factors that contribute to the occurrence of sudden cardiac death (SCD) in patients with chronic myocardial infarction (MI) are not entirely clear. The present study tests the hypothesis that augmented sympathetic nerve regeneration (nerve sprouting) increases the probability of ventricular tachycardia (VT), ventricular fibrillation (VF), and SCD in chronic MI. In dogs with MI and complete atrioventricular (AV) block, we induced cardiac sympathetic nerve sprouting by infusing nerve growth factor (NGF) to the left stellate ganglion (experimental group, n=9). Another 6 dogs with MI and complete AV block but without NGF infusion served as controls (n=6). Immunocytochemical staining revealed a greater magnitude of sympathetic nerve sprouting in the experimental group than in the control group. After MI, all dogs showed spontaneous VT that persisted for 5.8+/-2.0 days (phase 1 VT). Spontaneous VT reappeared 13.1+/-6.0 days after surgery (phase 2 VT). The frequency of phase 2 VT was 10-fold higher in the experimental group (2.0+/-2.0/d) than in the control group (0.2+/-0.2/d, P<0.05). Four dogs in the experimental group but none in the control group died suddenly of spontaneous VF. We conclude that MI results in sympathetic nerve sprouting. NGF infusion to the left stellate ganglion in dogs with chronic MI and AV block augments sympathetic nerve sprouting and creates a high-yield model of spontaneous VT, VF, and SCD. The magnitude of sympathetic nerve sprouting may be an important determinant of SCD in chronic MI.

Ventricular defibrillation with triphasic waveforms.

BACKGROUND: It has been reported that triphasic defibrillation waveforms cause less myocardial injury than biphasic waveforms. This study compared the defibrillation thresholds (DFTs) of triphasic and biphasic waveforms. METHODS AND RESULTS: ++DFTs were determined for a transvenous lead system and a 300-microF-capacitor defibrillator. In 8 pigs (group 1), DFTs were determined for 5 triphasic waveforms with tilts of 80%, 83%, and 86% and for 1 biphasic waveform. DFTs were determined in another 8 pigs (group 2) for 2 triphasic and 4 biphasic waveforms with tilts of 43%, 49%, and 56%. In both groups, a biphasic waveform from a 140-microF-capacitor defibrillator was also evaluated, and both shock polarities were tested for each waveform. In group 1, with the 300-microF-capacitor defibrillator, the leading-edge voltage and energy stored at DFT were significantly lower for triphasic waveforms with phase-duration ratios of 50/33/17 and an anode at the right ventricular electrode for phase 1 than for biphasic waveforms (P<0.001). In group 2, the stored energy of triphasic waveforms with 56% and 49% tilt was significantly lower than that of biphasic waveforms with the same tilts for anodal but not cathodal phase 1 at the right ventricular electrode. Electrode polarity significantly affected the DFT of triphasic waveforms for both studies. CONCLUSIONS: Some 80% tilt triphasic waveforms defibrillate more efficiently than biphasic waveforms with a 300-microF-capacitor defibrillator. The triphasic waveforms for both groups were not superior to 140-microF-capacitor biphasic waveforms. The efficacy of triphasic waveforms depends on phase durations and electrode polarity.

Detection of atrial arrhythmia for cardiac rhythm management by implantable devices.

Implantable atrial defibrillators (IAD) should provide pacing therapy whenever appropriate (ie, typical atrial flutter) to minimize shock-related patient discomfort. Additionally, IADs should provide diagnostics regarding atrial arrhythmia type and frequency of occurrence to enable improved physician management of atrial arrhythmia. To achieve this, IADs should accurately classify atrial arrhythmia such as atrial fibrillation (AF) and atrial flutter (AFL) This article evaluates the performance of an algorithm, atrial rhythm classification (ARC), designed to classify AF and AFL. The ARC algorithm uses maximum rate, standard deviation, and range of the 12 most recent atrial cycle lengths to plot a point in a three-dimensional space. A decision boundary divides the space into 2 regions--faster/unstable atrial cycle lengths (AF) or slower/stable cycle lengths (AFL). Classifications are made on a sliding window of 12 consecutive cycles until the end of the episode is reached. In this way, continuous episode feedback is provided that can be used to help guide device therapy, measure arrhythmia type and frequency of occurrence. Bipolar (1-cm) electrogram episodes of AF (n = 16) and AFL (n = 7) were acquired from 20 patients and retrospectively analyzed using the ARC algorithm. The sensitivity and specificity in this study was 0.993 and 0.982, respectively. The ARC algorithm would have appropriately guided atrial therapy and minimized discomfort associated with defibrillation shocks in this small patient data set warranting further studies. The ARC algorithm may also be beneficial as a diagnostic tool to assist physician management of atrial arrhythmia.

A preview of implantable cardioverter defibrillator systems in the next millennium: an integrative cardiac rhythm management approach.

The implantable cardioverter defibrillator (ICD), a primary therapeutic option for preventing sudden cardiac death, has rapidly evolved since being introduced clinically in 1980. Technologic advances in several key areas have enabled ICDs to provide more sophisticated rhythm management. Recent emphasis has been placed on dual-chamber ICDs possessing adaptive-rate pacing capabilities. Adoption of dual-chamber ICD systems has been rapid. The capabilities of future ICD systems will be governed by an integrative strategy that brings together sets of features specifically targeted at multifaceted rhythm disorders. The addition of atrial therapy will require more sophisticated rhythm discrimination algorithms. ICD technology will improve on several fronts including leads, integrated circuits, batteries, and capacitors. Additionally, state-of-the-art pacemaker technology will continue to be incorporated into ICDs. As these new ICD systems become increasingly sophisticated from an engineering viewpoint, tremendous emphasis will be placed on decreasing the complexity of programming, device interrogation, and patient monitoring during routine patient follow-up. Vast improvements in ICD programming systems may ultimately permit the 1-minute follow-up.

Future of bradyarrhythmia therapy systems: automaticity.

Since the first fixed-rate ventricular pacemaker was introduced in the late 1950s, pacing systems have evolved rapidly. Current developments focus on making devices more sophisticated and less complex--a challenging combination. Automaticity features such as beat-by-beat capture verification, sensitivity threshold adaptation, and algorithms to govern dynamically the maximum sensor rate have either recently been introduced or are likely to be introduced in the near future. Technologic advances are likely to allow meaningful improvements in current drain, battery performance, memory capacity, signal processing, telemetry, and programmer interface. Bradyarrhythmia therapy devices of the future promise to go beyond the pacemaker. Ultimately, pacing systems will become part of integrated cardiac rhythm management systems.

Defibrillation efficacy of different electrode placements in a human thorax model.

The objective of this study was to measure the defibrillation threshold (DFT) associated with different electrode placements using a three-dimensional anatomically realistic finite element model of the human thorax. Coil electrodes (Endotak DSP, model 125, Guidant/CPI) were placed in the RV apex along the lateral wall (RV), withdrawn 10 mm away from the RV apex along the lateral wall (RVprox), in the RV apex along the anterior septum (RVseptal), and in the SVC. An active pulse generator (can) was placed in the subcutaneous prepectoral space. Five electrode configurations were studied: RV-->SVC, RVprox-->SVC, RVSEPTAL-->SVC, RV-->Can, and RV-->SVC + Can. DFTs are defined as the energy required to produce a potential gradient of at least 5 V/cm in 95% of the ventricular myocardium. DFTs for RV-->SVC, RVprox-->SVC, RVseptal-->SVC, RV-->Can, and RV-->SVC + Can were 10, 16, 7, 9, and 6 J, respectively. The DFTs measured at each configuration fell within one standard deviation of the mean DFTs reported in clinical studies using the Endotak leads. The relative changes in DFT among electrode configurations also compared favorably. This computer model allows measurements of DFT or other defibrillation parameters with several different electrode configurations saving time and cost of clinical studies.

Evolution of the organization of epicardial activation patterns during ventricular fibrillation.

INTRODUCTION: This study quantified how the organization of epicardial activation changes during the first 40 seconds of ventricular fibrillation (VF). METHODS AND RESULTS: Unipolar potentials were mapped from a 504 (24 x 21) electrode array (2-mm interelectrode spacing) on the anterior right ventricle (RV) and left ventricle (LV) epicardium. The array covered approximately 20% of the epicardial surface. In each of seven pigs, six episodes of VF were induced by premature stimulation. One-half second epochs of VF were analyzed, starting 0, 10, 20, 30, and 40 seconds post induction and using novel pattern analysis algorithms. Eight parameters were quantified: (1) the number of wavefronts; (2) the epicardial area activated by wavefronts; (3) the fraction of wavefronts arising from epicardial breakthrough or from a focus; (4) the fraction of wavefronts terminated by conduction block; (5) the multiplicity index (number of distinct activation pathways in the rhythm); (6) the repeatability index (number of times activation pathways are traversed); (7) the activation rate; and (8) the wavefront propagation velocity. The results showed that VF patterns were less organized at 10 than at 0 seconds, with more, smaller wavefronts traversing a larger variety of pathways for fewer repetitions. VF activation patterns then gradually reorganized up to 40 seconds, but by a different mechanism: the spatial size of subpatterns grew, but the dynamics otherwise appeared unchanged. During both transitions, both activation rate and propagation velocity slowed monotonically. CONCLUSION: Thus, changes in organization during VF can occur by multiple mechanisms.

The effects of ventricular fibrillation duration and site of initiation on the defibrillation threshold during early ventricular fibrillation.

OBJECTIVES: The purpose of this study was to determine if the defibrillation threshold (DFT) is lower during the first few cycles of ventricular fibrillation (VF) than after 10 s of VF and, if so, if the effect is caused by local or global factors. BACKGROUND: The DFT may be low very early during VF because: (1) for the first few cycles VF arises from a localized region close to a defibrillation electrode where the shock field is strong (local factors), or (2) during early VF the effects of ischemia and sympathetic discharge have not yet fully developed and the heart has not yet completely dilated (global factors). METHODS: Protocol 1 included seven pigs in which a defibrillation electrode and a pacing catheter were both placed in the right ventricular apex. VF was induced by delivering a high current premature stimulus from the pacing catheter that should have caused reentry confined to the right ventricular apex for the first few cycles of VF. A bipolar electrogram was recorded from the tip of the defibrillation catheter. Using a three reversal up-down protocol, the DFT was determined for biphasic shocks delivered after 1, 2, 3, 4, 5, 7, 10, 15, 20 and 25 activations in this electrogram and after 10 s (control). Protocol 2 included seven pigs undergoing the same procedure as in protocol 1 except that an additional pacing catheter was placed in the left ventricle. Defibrillation thresholds were determined after 1, 2, 3, 4 and 5 VF activations following VF induction from the right ventricle (RV) or the left ventricle (LV) and after 10 s (control). RESULTS: In protocol 1, the mean +/- SD DFrs were lower during the first three cycles than after 10 s of VF (3.0 +/- 4.1 J for the first VF cycle vs 15.8 +/- 6.6 J after 10 s of VF, p < 0.05). In protocol 2, the DFF for the first few cycles of VF induced away from the defibrillation electrode in the LV (6.9 +/- 1.4 J for the first VF cycle) was significantly lower than that after 10 s of VF (16.0 +/- 2.2 J), whereas the DFF for the first few cycles induced near the defibrillation electrode in the right ventricular apex was significantly lower (2.3 +/- 2.7 J for the first VF cycle) than that induced from the LV. CONCLUSIONS: This study demonstrates that the DFT is significantly lower during the first few VF cycles of VF than after 10 s of VF and that this decrease may be caused by both local factors and global factors. These results provide an impetus for exploring earlier shock delivery in implantable devices.

Estimation of conduction velocity vector fields from epicardial mapping data.

An automated method to estimate vector fields of propagation velocity from observed epicardial extracellular potentials is introduced. The method relies on fitting polynomial surfaces T(x, y) to the space-time (x, y, t) coordinates of activity. Both speed and direction of propagation are computed from the gradient of the local polynomial surface. The components of velocity, which are total derivatives, are expressed in terms of the partial derivatives which comprise the gradient of T. The method was validated on two-dimensional (2-D) simulations of propagation and then applied to cardiac mapping data. Conduction velocity was estimated at multiple epicardial locations during sinus rhythm, pacing, and ventricular fibrillation (VF) in pigs. Data were obtained via a 528-channel mapping system from 23 x 22 and 24 x 21 arrays of unipolar electrodes sutured to the right ventricular epicardium. Velocity estimates are displayed as vector fields and are used to characterize propagation qualitatively and quantitatively during both simple and complex rhythms.

Locally propagated activation immediately after internal defibrillation.

BACKGROUND: Electrical mapping studies indicate an interval of 40 to 100 ms between a defibrillation shock and the earliest activation that propagates globally over the ventricles (globally propagated activation, GPA). This study determined whether activation occurs during this interval but propagates only locally before being blocked (locally propagated activation, LPA). METHODS AND RESULTS: In five anesthetized pigs, the heart was exposed and a 504-electrode sock with 4-mm interelectrode spacing was pulled over the ventricles. Ten biphasic shocks of a strength near the defibrillation threshold (DFT) were delivered via intracardiac catheter electrodes, and epicardial activation sequences were mapped before and after attempted defibrillation. Local activation was defined as dV/dt < or =-0.5 V/s. Postshock activation times and wave-front interaction patterns were determined with an animated display of dV/dt at each electrode in a computer representation of the ventricular epicardium. LPAs were observed after 40 of the 50 shocks. A total of 173 LPA regions were observed, each of which involved 2+/-2 (mean+/-SD) electrodes. LPAs were observed after both successful and failed shocks but occurred earlier (P<.0001) after failed (35+/-8 ms) than successful (41+/-16 ms) shocks, although the times at which the GPA appeared were not significantly different. On reaching the LPA region, the GPA front either propagated through it (n=135) or was blocked (n=38). The time from the onset of the LPA until the GPA front propagated to reach the LPA region was shorter (P<.01) when the GPA front was blocked (32+/-12 ms) than when it propagated through the LPA region (63+/-20 ms). CONCLUSIONS: LPAs exist after successful and failed shocks near the DFT. Thus, the time from the shock to the GPA is not totally electrically silent.

Spatial organization, predictability, and determinism in ventricular fibrillation.

The degree of spatial organization of ventricular fibrillation (VF) is a fundamental dynamical property of the arrhythmia and may determine the success of proposed therapeutic approaches. Spatial organization is closely related to the dimension of VF, and hence to its predictability and controllability. We have explored several techniques to quantify spatial organization during VF, to predict patterns of activity, and to see how spatial organization and predictability change as the arrhythmia progresses. Epicardial electrograms recorded from pig hearts using rectangular arrays of unipolar extracellular electrodes (1 mm spacing) were analyzed. The correlation length of VF, the number of Karhunen-Loeve modes required to approximate data during VF, the number, size and recurrence of wavefronts, and the mean square error of epicardial potential fields predicted 0.256 seconds into the future were all estimated. The ability of regularly-timed pacing stimuli to capture areas of fibrillating myocardium during VF was confirmed by a significant increase in local spatial organization. Results indicate that VF is neither "low-dimensional chaos" (dimension <5) nor "random" behavior (dimension= infinity ), but is a high-dimensional response with a degree of spatial coherence that changes as the arrhythmia progresses. (c) 1998 American Institute of Physics.

A quantitative framework for analyzing epicardial activation patterns during ventricular fibrillation.

Few techniques have been developed for deriving quantitative measures of activation patterns during ventricular fibrillation (VF). Such measures have many potential applications, for example, assessing the effects of time, drugs, or electrical interventions. We have developed a new framework for quantifying VF patterns as mapped from an array of approximately 500 unipolar electrodes. Individual activation wavefronts are isolated from one another using an algorithm that groups together adjacent active electrogram samples (dV/dt < -0.5 V/sec). Contacts between wavefronts are detected: these include fractionations, in which a single wavefront breaks into multiple wavefronts, and collisions, in which multiple wavefronts coalesce to form a new wavefront. The timing and contact relationships between wavefronts are summarized as a directed graph. From this model of the VF episode, we derive several parameters: number of wavefronts, number of fractionations, number of collisions, mean wavefront size, mean area swept out, and mean duration. As an example of this analysis, we computed these parameters in six open-chest pigs at 5, 10, 15, and 20 sec after electrical induction of VF. The number of wavefronts and the number of collisions decreased, whereas the mean wavefront size and mean area swept out increased during this period. These results are consistent with previous studies showing a recovery of organization during the first minute of VF.

Recurrent wavefront morphologies: a method for quantifying the complexity of epicardial activation patterns.

We have developed a method for quantifying the complexity of activation patterns observed during ventricular fibrillation (VF) that is based on our previously reported methodology for decomposing epicardial mapping data into a set of isolated wavefronts. One-half second datasets are acquired from a 21 x 24 array of unipolar electrodes (1 mm spacing), and the wavefronts are isolated. A correlation technique is used to compute the similarity between all possible pairs of the isolated wavefronts. From these data, the wavefronts are sorted into clusters, each of which represents a recurring wavefront morphology. We define multiplicity (M) as the number of clusters needed to account for 90% of the total activations in the VF episode. M measures the complexity of the rhythm. In repetitive patterns (e.g., sinus rhythm), M = 1, indicating that the same morphology repeatedly activates the mapped region. Typically, in VF, M > 1, with larger numbers representing more complex, disorganized patterns. As an example, we computed M at 5, 10, 15, and 20 sec after electrical induction of VF in six pigs. M decreased significantly (p < 0.001), suggesting increasing organization during this period.

Effects of transvenous electrode polarity and waveform duration on the relationship between defibrillation threshold and upper limit of vulnerability.

BACKGROUND: The upper limit of vulnerability (ULV) hypothesis for defibrillation predicts that maneuvers that alter the ULV will cause a similar alteration in the defibrillation threshold (DFT). The purpose of this study was to test this prediction by evaluating the effects of electrode polarity and waveform duration on the relationship between the DFT and the ULV. METHODS AND RESULTS: Platinum spring electrodes were placed in the right ventricular (RV) apex and the superior vena cava in 12 pigs. Strength-duration curves were constructed for the DFT and ULV for each electrode polarity with monophasic waveforms (6 pigs) of different durations (2 to 14 ms) and biphasic truncated exponential waveforms (6 pigs) having phase 1 equal to 4 ms and phase 2 of different durations (0 to 10 ms). ULV data were gathered by scanning of the T wave. The ventricular pacing threshold (VPT) and ventricular fibrillation threshold (VFT) were also determined with these same waveforms. For the RV electrode as a cathode for monophasic and the first phase of biphasic stimuli, VPTs for the same waveform duration were significantly lower than for the configuration with the RV electrode as an anode. VFTs were not significantly different for the two electrode polarities with either monophasic or biphasic waveforms. The DFT changed in a fashion similar to the ULV with changes in electrode polarity and phase duration for both monophasic and biphasic waveforms. The ULV and DFT for each waveform duration for each polarity were strongly correlated (r=.83 to .99). CONCLUSIONS: The almost identical changes in ULV and DFT with changes in electrode polarity and waveform duration provide new evidence to support the ULV hypothesis of defibrillation.

Effect of a passive endocardial electrode on defibrillation efficacy of a nonthoracotomy lead system.

OBJECTIVES: We investigated the impact of an inactive endocardial lead on the 50% effective dose (ED50%) for successful ventricular defibrillation. BACKGROUND: The presence of abandoned epicardial mesh patch electrodes detrimentally affects the defibrillation efficacy of an endocardial lead system. It is not known whether abandoned endocardial electrodes produce a similar effect. METHODS: An endocardial lead system (ENDOTAK, model 0062, Cardiac Pacemakers, Inc.) was implanted in eight dogs (mean +/- SD weight 23.7 +/- 1.0 kg). The ED50% for each of seven lead configurations was determined by a three-reversal point protocol in a balanced-randomized order with and without a second electrically passive endocardial lead system in the right ventricle (power 0.97 to detect a 50-V difference). Biphasic shocks with 80% tilt were delivered 10 s after the induction of ventricular fibrillation. In one configuration the active electrode made contact with the passive electrode in the right ventricular (RV) apex. In another configuration the active electrode was placed in a more proximal position to avoid contact. Additionally, the ED50% was determined for the endocardial lead system with a passive pacing lead positioned in the RV apex. RESULTS: ED50% values for peak voltage, peak current and delivered energy were not significantly different with or without a passive RV electrode, and this was true whether or not the active electrode touched the passive electrode. However, ED50% values were significantly higher when the active electrode was slightly proximal than when it was positioned at the apex. CONCLUSIONS: Physical contact between active and passive endocardial electrodes does not significantly alter defibrillation efficacy in this dog model. An increase in ED50% energy was caused by a slightly proximal position. Therefore, a good electrode position within the right ventricle is a more important determinant of defibrillation efficacy than is avoidance of the electrode touching a passive electrode.

Effect of electrode polarity on internal defibrillation with monophasic and biphasic waveforms using an endocardial lead system.

INTRODUCTION: To test the hypothesis that the effect of shock polarity on defibrillation depends on waveform duration, this study determined strength-duration defibrillation curves of monophasic and biphasic truncated exponential waveforms for both polarities. METHODS AND RESULTS: Defibrillation thresholds (DFTs) were obtained in 32 pigs for catheter electrodes in the right ventricle (RV) and superior vena cava (SVC) using a modified Purdue technique. Both electrode polarities were tested in five different protocols. In part 1, DFTs were determined with 1- to 14-msec monophasic waveforms. In parts 2, 3, and 4, DFTs were determined with two different sizes of SVC electrodes for biphasic waveforms with a phase 1 of 4 or 6 msec and a phase 2 ranging from 1 to 10 msec. In part 5, DFTs were tested for monophasic waveforms ranging from 2 to 11 msec and for biphasic waveforms with a phase 1 duration corresponding to each monophasic waveform and a phase 2 held constant at 1 msec. Mean DFTs for monophasic waveforms were significantly lower when the RV electrode was an anode than when it was a cathode for waveform durations > or = 3 msec. For biphasic waveforms in which phase 2 was < or = phase 1 in duration, no significant difference in mean DFT was observed when polarity was reversed. Even a phase 2 as short as 1 msec could eliminate the DFT difference between polarities observed with monophasic shocks. When phase 2 was > or = 2 msec longer than phase 1, polarity did affect the DFT of biphasic waveforms; it affected the DFT similarly to a monophasic waveform of the same polarity as phase 2. Phase 1 duration and electrode size also affected the difference in DFT produced by changing the electrode polarity. CONCLUSIONS: For phase durations most commonly used clinically because of their low DFTs, reversing polarity changed defibrillation efficacy for monophasic but not biphasic shocks. For inefficient biphasic waveforms with phase 2 > or = 2 msec longer than phase 1, the DFT was lower when the RV electrode was an anode during phase 2, similar to the polarity difference for monophasic waveforms, suggesting that a long second phase of biphasic waveforms defibrillates in a similar fashion to monophasic waveforms.