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B H KenKnight

Publications and source records attributed to B H KenKnight.

18 recordsLinked to original sources

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.

Analysis of Variance↗

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.

Adrenergic beta-Antagonists↗

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.

Animals↗

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.

Algorithms↗

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.

Death, Sudden, Cardiac↗

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.

Bradycardia↗

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.

Animals↗

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.

Animals↗

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.

Animals↗

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.

Animals↗

The effects of ventricular fibrillation duration and a preceding unsuccessful shock on the probability of defibrillation success using biphasic waveforms in pigs.

INTRODUCTION: While the defibrillation threshold has been reported to increase with ventricular fibrillation (VF) duration for monophasic waveforms, the effect of VF duration for biphasic waveforms is unknown. METHODS AND RESULTS: The ED 50 requirements (the 50% probability of defibrillation success) for an endocardial lead system, which included a subcutaneous array, were determined by logistic regression using a recursive up-down algorithm for a biphasic waveform (6/6 msec). The study was performed in two parts, each with eight pigs. In part 1, ED 50 was compared for shocks delivered after 10 seconds of VF and for shocks delivered after 20 seconds of VF following a failed first shock at 10 seconds. Energy at ED 50 decreased from 6.5 +/- 0.9 J for shocks delivered after 10 seconds of VF to 4.9 +/- 0.8 J (P < 0.01) for shocks delivered after 20 seconds. To determine if improved second shock efficacy was a result of preconditioning by the failed first shock or a function of VF duration, part 2 of the study compared defibrillation efficacy between shocks delivered after 10 seconds of VF with shocks delivered after 20 seconds of VF with and without a failed first shock at 10 seconds. Mean energy at ED 50 decreased from 10.1 +/- 2.4 J for shocks delivered after 10 seconds of VF to 7.9 +/- 2.4 J (P < 0.01) and 7.5 +/- 3.2 J (P < 0.01) for shocks delivered after 20 seconds of VF with and without a failed first shock, respectively. The mean energy at ED 50 for shocks delivered after 20 seconds of VF with and without a failed first shock was not significantly different (P = 0.53). A strong linear correlation for energy at ED 50 was found between shocks delivered after 10 seconds of VF and shocks delivered after 20 seconds of VF following a failed first shock (r = 0.95, P < 0.01). CONCLUSION: (1) As opposed to monophasic shocks, ED 50 is significantly lower for biphasic shocks delivered after 20 seconds of VF compared with shocks delivered after 10 seconds of VF in pigs. (2) An unsuccessful biphasic shock in pigs does not affect the defibrillation efficacy for a subsequent shock. (3) ED 50 for a biphasic shock delivered after 20 seconds of VF is linearly related to ED 50 for a shock delivered after 10 seconds of VF.

Animals↗

Technological advances in implantable cardioverter-defibrillators before the year 2000 and beyond.

The implantable cardioverter-defibrillator (ICD) has evolved rapidly since its clinical introduction; product life cycles have been exceedingly short. This swift transition from early shock-only devices to small, programmable, tiered-therapy systems has been driven by 2 major factors: minimally invasive implant procedures and technological innovation. Yet, while many new ICD systems have been introduced recently, even more advanced products are on the horizon before the year 2000 and beyond. In general, devices will be smaller and smarter. Certainly, ICD volume will be further reduced without detrimentally affecting longevity. Endocardial lead systems will become smaller and more versatile. Rhythm discrimination algorithms will become more effective. New adaptive-rate pacing systems that limit the maximum paced rate based on hemodynamic indices will become features of tachyarrhythmia products. Pacing schemes for prevention of supraventricular tachyarrhythmias and improvement of hemodynamic function in patients with congestive heart failure will likely be introduced for clinical evaluation.

Cardiac Pacing, Artificial↗

Influence of malpositioned transvenous leads on defibrillation efficacy with and without a subcutaneous array electrode.

Some patients cannot receive a transvenous lead system because of high defibrillation thresholds (DFTs). We hypothesized that a right ventricular (RV) catheter electrode not extending as far as possible into the RV apex could cause high DFTs. Recently, a subcutaneous array (SQA) electrode has been shown to lower DFTs substantially. We compared the influence of a malpositioned RV catheter electrode on defibrillation efficacy for endocardial lead systems with and without a SQA. In eight anesthetized pigs, defibrillation catheters were placed in the RV apex and near the junction of the superior vena cava (SVC) and right atrium. SQA, formed by three elements, each 20 cm in length, was placed in the left thorax. DFTs were determined for a biphasic waveform using an up/down protocol with the RV catheter at the apex and with it repositioned 1-cm and 2-cm proximal to the apex. The mean DFT energies for the configurations with a SQA were less than those without a SQA for every catheter position. The placement of the RV catheter away from the apex caused an increase in defibrillation energy for the configurations without a SQA (apex: 17.1 +/- 3.8 J [mean +/- SD]; 1 cm: 20.1 +/- 4.6 J; 2 cm: 27.6 +/- 9.5 J; P < 0.05), but not for the configurations with a SQA (apex: 12.2 +/- 2.2 J; 1 cm: 12.3 +/- 2.9 J; 2 cm: 12.1 +/- 0.9 J: P = NS). These results suggest that a malpositioned RV catheter electrode, at the time of implantation or by late dislodgment, significantly elevates DFTs for a total endocardial system but not for a system that includes a SQA.

Animals↗

Impedance to defibrillation countershock: does an optimal impedance exist?

Defibrillation is thought to occur because of changes in the transmembrane potential that are caused by current flow through the heart tissue. Impedance to electric countershock is an important parameter because it is determined by the magnitude and distribution of the current that flows for a specific shock voltage. The impedance is comprised of resistive contributions from: (1) extra-tissue sources, which include the defibrillator, leads, and electrodes; (2) tissue sources, which include intracardiac and extra-cardiac tissue; and (3) the interface between electrode and tissue. Tissue sources dominate the impedance and probably contribute to the wide range of impedance values presented to the defibrillation pulse. Because impedance is not constant within or between subjects, defibrillators must be designed to accommodate these differences without compromising patient safety or therapeutic efficacy. Experimental investigations in animals and humans suggest that impedance changes at several different time scales ranging from milliseconds to years. These alterations are believed to be a result of both electrochemical and physiological mechanisms. It is commonly thought that impedance is optimized when it has been decreased to a minimum, since this allows the most current flow for a given voltage shock. However, if the impedance is lowered by changing the location or size of the electrodes in such a way that current flow is decreased in part of the heart even though current flow is increased elsewhere, then the total voltage, current, and energy needed for defibrillation may increase, not decrease, even though impedance is decreased. A simple boundary element computer model suggests that the most even distribution of current flow through the heart is achieved for those electrode locations in which the impedance across the heart is at or near the maximum cardiac impedance for any location of these particular electrodes. Thus, the optimum shock impedance is achieved when impedance is minimized for extra-tissue and extra-cardiac tissue sources and is at or near a maximum for intracardiac tissue sources.

Animals↗

Position of epicardial patch electrodes for implantable defibrillation significantly affects shock strength requirements.

OBJECTIVE: To assess the impact of epicardial patch electrode position on internal defibrillation efficacy. METHODS: Two mesh patch electrodes (13 cm2) were positioned on the epicardium of acute, isoflurane-anesthetized pigs (n = 7, 40-47 kg). Defibrillation efficacy was determined for three different patch positions: P1 = anterior-basal right ventricle (RV) and lateral-apical left ventricle (LV); P2 = lateral RV and lateral LV; and P3 = anterior-basal septal region and posterior-apical septal region. To quantify defibrillation efficacy, single capacitor discharge, fixed-tilt (68%) biphasic waveforms were delivered to the heart 10 seconds after initiation of ventricular fibrillation. Initial shock intensities were selected using an up/down protocol. Conversion data were used to construct sigmoidal curves relating probability of defibrillation to energy delivered, peak voltage, and peak current in each animal. RESULTS: Mean peak voltage and current at 50% defibrillation probability were 40% higher for P2 than they were for either P1 or P3 (p < 0.05). Similarly, mean energy delivered was 75% higher for P2. In this pig model, position of epicardial patch electrodes affects defibrillation efficacy. CONCLUSION: Apical-to-basal shock vectors (P1 and P3) yielded significantly lower defibrillation shock strength requirements than did a lateral-wall-to-lateral-wall vector (P2), which was perpendicular to the intraventricular septum. These data may help explain the disparity in defibrillation thresholds observed in the human population of patients undergoing implantable cardioverter defibrillator testing with epicardial patch electrodes.

Animals↗

Regional capture of fibrillating ventricular myocardium. Evidence of an excitable gap.

Previous investigations have suggested that during ventricular fibrillation (VF) pacing stimuli are incapable of evoking propagated ventricular activations. To determine whether regional myocardial capture could be achieved during rapid pacing in VF, extracellular unipolar potentials were sampled (2 kHz) and recorded from 506 Ag-AgCl electrodes arranged in a rectangular grid (22 x 23, 1.12-mm spacing) embedded in a plaque overlying two pacing electrodes in the epicardium of the anterobasal right ventricle in pentobarbital-anesthetized pigs (25 to 30 kg, n = 6). During separate episodes of electrically induced VF, two bursts of 40 monophasic stimuli (10 mA, 2-millisecond duration) were asynchronously applied to the stimulating electrodes in either a bipolar, unipolar anodal, or unipolar cathodal mode. Evidence of regional capture was provided by (1) animating the first temporal derivative of the extracellular potentials, (2) analyzing inter-beat interval patterns, and (3) employing the Karhunen-Loeve decomposition method to quantify the repetitiveness of spatio-temporal patterns of activation. Regional capture of ventricular myocardium during VF was observed when pacing stimuli fell late in the local myocardial activation interval and when the pacing cycle length was 80% to 115% of the mean subplaque activation cycle length. When myocardial activations became phase locked to the pacing stimuli, repeatable spatiotemporal patterns of activation followed each stimulus. Poincaré sections at the plaque border revealed that during VF prior to pacing, interbeat intervals were irregular but were driven by pacing to stable fixed values at times corresponding to our qualitative declaration of regional capture. A similar correspondence was demonstrated between the time of capture, defined by direct observation of the activation patterns, and a rise in the power contained in the first two spatial modes of a Karhunen-Loeve decomposition. These data demonstrate that appropriately timed stimuli produce regional capture of fibrillating right ventricular myocardium in the pig and support the existence of an excitable gap during VF in this model.

Animals↗

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.

Algorithms↗

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.

Algorithms↗