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Jack M Rogers

Publications and source records attributed to Jack M Rogers.

18 recordsLinked to original sources

Panoramic optical mapping reveals continuous epicardial reentry during ventricular fibrillation in the isolated swine heart.

During ventricular fibrillation (VF), activation waves are fragmented and the heart cannot contract synchronously. It has been proposed that VF waves emanate from stable sources ("mother rotors"). Previously, we used new optical mapping technology to image VF wavefronts from nearly the entire epicardial surface of six isolated swine hearts. We found that VF was not driven by epicardial rotors, but could not exclude the presence of stable rotors hidden within the ventricular walls. Here, we use graph theoretic analysis to show that, in all 17 VF episodes we analyzed, it was always possible to trace sequences of wavefronts through series of fragmentation and collision events from the beginning to the end of the episode. The set of wavefronts that were so related (the dominant component) consisted of 92%+/-1% of epicardial wavefronts. Because each such wavefront sequence constitutes a continuous activation front, this finding shows that complete reentrant pathways were always present on the epicardial surface and therefore, that wavefront infusion from nonepicardial sources was not strictly necessary for VF maintenance. These data suggest that VF in this model is not driven by localized sources; thus, new anti-VF treatments designed to target such sources may be less effective than global interventions.

Action Potentials↗

Lifetimes of epicardial rotors in panoramic optical maps of fibrillating swine ventricles.

During ventricular fibrillation (VF), electrical activation waves are fragmented, and the heart cannot contract in synchrony. It has been proposed that VF waves emanate from stable periodic sources (often called "mother rotors"). The objective of the present study was to determine if stable rotors are consistently present on the epicardial surface of hearts comparable in size to human hearts. Using new optical mapping technology, we imaged VF from nearly the entire ventricular surface of six isolated swine hearts. Using newly developed pattern analysis algorithms, we identified and tracked VF wave fronts and phase singularities (PS; the pivot point of a reentrant wave front). We introduce the notion of a compound rotor in which the rotor's central PS can change and describe an algorithm for automatically identifying such patterns. This prevents rotor lifetimes from being inappropriately abbreviated by wave front fragmentation and collision events near the PS. We found that stable epicardial rotors were not consistently present during VF: only 1 of 17 VF episodes contained a compound rotor that lasted for the entire mapped interval of 4 s. However, shorter-lived rotors were common; 12.2 (SD 3.3) compound rotors with lifetime >200 ms were visible on the epicardium at any given instant. We conclude that epicardial mother rotors do not drive VF in this experimental model; if mother rotors do exist, they are intramural or septal. This paucity of persistent rotors suggests that individual rotors will eventually terminate by themselves and therefore that the continual formation of new rotors is critical for VF maintenance.

Algorithms↗

Quantification of activation patterns during ventricular fibrillation in open-chest porcine left ventricle and septum.

BACKGROUND: A single stationary mother rotor has been hypothesized to be responsible for maintenance of ventricular fibrillation (VF) in the guinea pig. Previous studies have pointed to the ventricular septum as a possible location for a mother rotor in the pig heart. OBJECTIVES: The purpose of this study was to test the hypothesis that a mother rotor is located in the septum. METHODS: In seven open-chest pigs, we mapped the first 20 seconds of electrically induced VF simultaneously from the posterior left ventricle (LV) and right side of the septum with two electrical arrays. Each array contained 504 electrodes (21 x 24) spaced 2 mm apart in the LV and 1.5 mm apart in the septum. RESULTS: The percentage of VF wavefronts that formed reentrant circuits was significantly lower in the septum (1% +/- 1% [mean +/- SD]) than in the LV (2% +/- 1%). The peak frequency during VF also was significantly smaller in the septum (8.6 Hz +/- 3.0 Hz) than in the LV (10.4 Hz +/- 3.4 Hz). The mean direction of spread of activation of VF wavefronts was away from the region where the posterior LV free wall intersects the posterior septum in both the LV and septum. CONCLUSIONS: The lower incidence of reentry and lower peak frequency in the mapped region of the septum than in the LV indicate that a mother rotor is not present in swine on the RV side of the septum. The mean directions of the VF activation sequences in the LV and septum suggest that if a mother rotor is present during the first 20 seconds of VF, it exists where the posterior LV free wall joins the septum, the region where the posterior papillary muscle inserts.

Animals↗

Mechanisms for the maintenance of ventricular fibrillation: the nonuniform dispersion of refractoriness, restitution properties, or anatomic heterogeneities?

INTRODUCTION: The relative importance of nonuniform dispersion of refractoriness, steep restitution slopes, and anatomic heterogeneities in causing conduction block during ventricular fibrillation (VF) remains unknown. METHODS AND RESULTS: In six open-chest pigs, ventricular refractoriness and restitution curves were estimated from activation recovery intervals (ARIs) calculated from 504 (21 x 24) unipolar electrode recordings 2 mm apart in a plaque sutured to the left ventricular (LV) free wall. A steady-state restitution protocol was performed twice at each of two pacing sites: the LV base and near the left anterior descending artery. VF was electrically induced four times and the incidence of conduction block at each electrode during the first 20 seconds was determined by an automated algorithm. The gradient of the ARI was calculated at each electrode to estimate the spatial dispersion of refractoriness. An exponential curve was fit to the restitution plots of ARIs versus the corresponding diastolic intervals (DIs) for all pacing cycle lengths at each electrode. The locations of epicardial blood vessels were noted after the study. Spatial patterns of conduction block were significantly correlated between the four VF episodes in the same animal (r = 0.66 +/- 0.07, P < 0.05). At the shortest pacing cycle length, the spatial distribution of ARIs, ARI gradients, and restitution slopes was not random but formed clusters of similar values. However, none of these variables was significantly correlated with the incidence of conduction block, even though ARI gradients >2 msec/mm were present between many clusters and approximately 90% of restitution slopes were >1. Instead, conduction block frequently appeared to cluster along epicardial vessels. CONCLUSION: Neither the dispersion of refractoriness nor action potential duration restitution determined during rapid pacing by itself is the major determinant of the location of conduction block during early VF in normal pigs. It may be that these factors interact synergistically with each other as well as with other factors, including anatomic heterogeneities such as those caused by blood vessels, which may be particularly important for the formation of conduction block and maintenance of VF.

Animals↗

Epicardial organization of human ventricular fibrillation.

OBJECTIVE: The objective of this study was to test the hypothesis that on the epicardium of the in vivo human heart, ventricular fibrillation (VF) consists of chaotic small wavefronts that constantly change paths. BACKGROUND: Despite the significance of VF to cardiovascular mortality, little is known about the wavefronts that constitute VF in humans. METHODS: In 9 patients undergoing cardiac surgery, a single VF episode was induced by rapid pacing immediately after institution of cardiopulmonary bypass while recordings were made from 504 electrodes spaced 2 mm apart in a 20 cm(2) plaque held against the anterior left ventricle epicardium. A total of 26 segments of VF, each 2 s long, were analyzed. A computer algorithm identified individual wavefronts and classified them into groups that followed similar activation sequences. RESULTS: The mean activation rate was 5.8 +/- 1.8 (mean +/- SD) cycles/s. The wavefronts during each epoch were grouped into 9.4 +/- 7.1 different activation pathways, and 8.3 +/- 2.3 wavefronts followed each pathway. Individual wavefronts spread to activate an area of 5.1 +/- 3.0 cm(2) in the mapped region. The majority of the wavefronts propagated into the mapped region and/or propagated out of the mapped region into adjacent tissue, suggesting that the wavefronts were larger than 5.1 cm(2). Reentry was identified in only 16 of the 26 (62%) 2-s segments, always completed <2 cycles, and lasted for 9.5 +/- 6.6% of these 16 epochs, which is 5.8% of the total duration of all the segments analyzed. CONCLUSION: VF wavefronts on the human epicardium are usually large, repeatedly follow distinct pathways, and only occasionally reenter. If these results for the left ventricular epicardium are representative of those for the entire ventricular mass, they do not support the hypothesis that human VF consists of small, constantly changing wavefronts, but rather suggest that there is significant organization of human VF.

Action Potentials↗

Comparison of conventional and biventricular antitachycardia pacing in a geometrically realistic model of the rabbit ventricle.

INTRODUCTION: ICDs often are programmed with antitachycardia pacing (ATP) as the first response to ventricular tachycardia (VT). Many ICDs have an additional lead available for ventricular pacing. We hypothesized that using the additional lead for ATP would improve therapy by advancing the orthodromic wavefront, thereby reducing the size of the excitable gap and inducing block of all reentrant activity. METHODS AND RESULTS: Monomorphic VT was initiated in a thin-walled model of rabbit ventricular myocardium that included an apical infarct and anatomically realistic dimensions. ATP with up to eight pulses was delivered at 90% of VT cycle length to one (conventional) or two (biventricular) stimulation areas. Stimulation areas were adjusted from 0.017 cm2 to 0.169 cm2 to modulate interactions between the antidromic and VT wavefronts, and between the orthodromic wavefront and the VT's refractory region. During conventional ATP, we found that larger stimulation areas terminated the VT in three pulses. Continued pacing after termination caused VT reinitiation in the reversed direction in some instances. With smaller stimulation areas, conventional ATP simply reset the circuit. During biventricular ATP, larger stimulation areas terminated VT in one pulse. There were no instances of reinitiation with reversal. However, with smaller stimulation areas, prolongation of refractoriness near the additional stimulation area facilitated induction of functional reentry with pathways modified by continued pacing. CONCLUSION: Our modeling suggests that biventricular ATP is superior to conventional ATP under conditions where the additional ventricular lead effectively advances the orthodromic wavefront. Failure to achieve this advancement poses a risk of VT acceleration.

Animals↗

Combined phase singularity and wavefront analysis for optical maps of ventricular fibrillation.

Much of the research into the mechanisms of ventricular fibrillation (VF) employs high-resolution mapping of electrical activation and recovery patterns. We previously developed a method for analyzing electrically mapped VF patterns that was based on identifying individual VF wavefronts. We now introduce a related method designed to take into account the information on repolarization that is present in optically mapped VF data. The new method first converts raw fluorescence data to an angular variable that tracks the phase of the mapped tissue through the depolarization-repolarization cycle. We define wavefronts in this context as isolines of phase that terminate either at boundaries or at singular points within the phase field. These singularities are the pivots of functional reentry and are important determinants of VF patterns. We parameterize VF by constructing data structures that describe wavefronts and singularities and also maintain wavefront-wavefront, wavefront-singularity, and singularity-singularity relationships. We describe one important application of this parameterization, which is to identify, localize, and characterize the importance of occurrences of propagation block during VF.

Action Potentials↗

Three-dimensional surface reconstruction and panoramic optical mapping of large hearts.

Optical mapping of electrical activity from the surface of the heart is a powerful tool for studying complex arrhythmias. However, a limitation of traditional optical mapping is that the mapped region is restricted to the field of view of the sensor, which makes it difficult to track electrical waves as they drift in and out of view. To address this, we developed an optical system that panoramically maps epicardial electrical activity in three dimensions. The system was engineered to accomodate hearts comparable in size to human hearts. It is comprised of a surface scanner that measures epicardial geometry and a panoramic fluorescence imaging system that records electrical activity. Custom software texture maps the electrical data onto a reconstructed epicardial surface. The result is a high resolution, spatially contiguous, mapping dataset. In addition, the three-dimensional positions of the recording sites are known, making it possible to accurately measure parameters that require geometric information, such as propagation velocity. In this paper, we describe the system and demonstrate it by mapping a swine heart.

Algorithms↗

Evolution of activation patterns during long-duration ventricular fibrillation in dogs.

Although resuscitation for sudden cardiac arrest attempts are frequently not instituted for several minutes after the onset of ventricular fibrillation (VF), previous mapping studies have examined only the first 40 s of VF or have involved isolated perfused hearts that did not become ischemic during VF. We applied quantitative pattern analysis to mapping data throughout the first 10 min of VF acquired from a 21 x 24 unipolar electrode array located on the ventricular epicardium of six open-chest dogs. The following twelve descriptors were continuously quantified: 1) number of wavefronts, 2) incidence of reentry, 3) wavefront propagation velocity, 4) incidence of breakthrough/focus, 5) incidence of block, 6) mean area activated by the wavefronts, 7) wavefront fractionations, 8) wavefront collisions, 9) multiplicity index, 10) repeatability, 11) negative peak rate of voltage change, and 12) peak frequency of activation. Cluster analysis of these descriptors divided VF into five stages (stages i-v). The values of most descriptors (except block and breakthrough incidence) increased during stage i (1-11 s after VF induction) and maintained high values with rapid dynamic fluctuations during stage ii (12-62 s). Descriptors changed quickly to values indicating greater organization during stage iii (63-86 s), decreased steadily during stage iv (87-310 s), and approached zero during stage v (311-600 s). There was a high incidence of reentry just before, during, and after stage iii. In conclusion, during the first 10 min, VF can be divided into five stages according to the evolution of electrophysiological characteristics. All of the parameters show a rapid deterioration during VF, except for a temporary reversal approximately 1 min after induction when activation briefly became more organized. Thus a quantitative description of activation does not uniformly decrease as VF progresses, but undergo rapid changes and exhibit a brief interval of increased organization after approximately 1 min of VF. Further studies are warranted to determine whether these changes, particularly the increased organization of stage iii, have clinical consequences, such as an alteration in defibrillation efficacy.

Action Potentials↗

Sustained reentry in the left ventricle of fibrillating pig hearts.

It has been proposed that ventricular fibrillation (VF) is driven by sustained reentry. However, mapping studies have not detected such "mother rotors" in large mammalian hearts. We mapped VF from three 21x12 unipolar electrode arrays in 6 pigs. Two of the arrays were adjacent to each other on the left-ventricular epicardium. Electrode spacing was 2 mm. The third array consisted of 21 needles (0.5-mm diameter, 12 electrodes, 1-mm spacing) inserted in a row (2-mm spacing) between the epicardial arrays. A total of 88 5-second VF epochs were analyzed with automatic reentry detection algorithms. Although intramural reentry was sporadically present (29 total occurrences), it was always short-lived with a mean life span of 127+/-57 ms. However, in 3 of the 6 animals, sustained epicardial reentry (ie, reentry persisting for more than a few cycles) was consistently present, often lasting for several seconds. For each epoch, we computed indices characterizing (1) the relative duration of reentry on the two epicardial arrays (R), (2) the flow of wavefronts between epicardial arrays (W), and (3) the relative activation rates of the two epicardial arrays (F). R did not correlate with either W or F indicating that rotor-containing regions did not produce a net outflow of wavefronts and were not faster than neighboring regions. Thus, sustained epicardial, but not intramural, rotors were consistently present in some large animal hearts during VF. However, we found no evidence that these rotors were responsible for sustaining VF through the mechanisms outlined in the mother rotor hypothesis.

Animals↗

Effects of heart isolation, voltage-sensitive dye, and electromechanical uncoupling agents on ventricular fibrillation.

We tested whether the interventions typically required for optical mapping affect activation patterns during ventricular fibrillation (VF). A 21 x 24 unipolar electrode array (1.5 mm spacing) was sutured to the left ventricular epicardium of 16 anesthetized pigs, and four episodes of electrically induced VF (30-s duration) were recorded. The hearts were then rapidly excised and connected to a Langendorff perfusion apparatus. Four of the hearts were controls, in which 24 additional VF episodes were then mapped. In the remaining 12 hearts, four VF episodes were mapped after isolation, four more episodes were mapped after exposure to the voltage-sensitive dye di-4-ANEPPS, and six more episodes were mapped after exposure to the electromechanical uncoupling agents diacetyl monoxime (DAM; 20 mmol/l, n = 6) or cytochalasin D (CytoD; 10 micromol/l, n = 6). VF episodes were separated by 4 min. VF activation patterns were quantified using custom pattern analysis algorithms. From comparisons with time-corrected control data, all interventions significantly changed VF patterns. Most changes were broadly consistent with slowing and regularization due to loss of excitability. Heart isolation had the largest effect on VF patterns, followed by CytoD, DAM, and dye.

Animals↗

Regional differences in ventricular fibrillation in the open-chest porcine left ventricle.

It has been hypothesized that during ventricular fibrillation (VF), the fastest activating region, the dominant domain, contains a stable reentrant circuit called a mother rotor. This hypothesis postulates that the mother rotor spawns wavefronts that propagate to maintain VF elsewhere and implies that the ratio of wavefronts propagating off a region to those propagating onto it (propoff/propon) should be >1 for the dominant domain but <1 elsewhere. To test this prediction in the left ventricular (LV) epicardium of a large animal, most of the LV free wall was mapped with 1008 electrodes in 7 pigs. VF activation rate was faster in the posterior than in the anterior LV (10.0+/-1.3Hz versus 9.3+/-1.3Hz; P<0.001). The anterior LV had a higher fraction of wavefronts that blocked than did the posterior LV and had a propoff/propon ratio <1 (P<0.001). The mean conduction velocity vectors of the VF wavefronts pointed in the direction from the posterior to the anterior LV. Although these findings favor a dominant domain in the posterior LV, the facts that the anterior LV had a higher incidence of reentry than did the posterior LV and that the posterior LV did not have propoff/propon significantly different from 1 do not. Thus, quantitative regional differences are present over the porcine LV epicardium during VF. Although these differences are not totally consistent with the presence of a dominant domain within the LV free wall, the mean conduction velocity vector is consistent with one in the septum.

Animals↗

The effects of acute and chronic amiodarone on activation patterns and defibrillation threshold during ventricular fibrillation in dogs.

OBJECTIVES: The goal of this study was to evaluate the effects of acute and chronic amiodarone on activation patterns during ventricular fibrillation (VF), ventricular effective refractory period (VERP) and defibrillation threshold (DFT). BACKGROUND: Acute and chronic amiodarone may act through different mechanisms. METHODS: The VERP, VF activation patterns and DFT were determined in 24 dogs. Twelve dogs received acute intravenous amiodarone (10 mg/kg, n = 6) or saline (n = 6), and 12 dogs received chronic oral amiodarone (20 mg/kg/day, n = 6) or placebo (n = 6). Epicardial VF activation patterns were recorded with 504 electrodes. Quantitative descriptors of VF were calculated. RESULTS: The DFT was unchanged by acute or chronic amiodarone. Although chronic amiodarone significantly extended the VERP, acute amiodarone did not. In the mapped region, acute and chronic amiodarone decreased the number of VF wavefronts by 42% and 60%. Acute amiodarone decreased conduction block by 22%, while chronic amiodarone increased block by 41% but decreased wave fractionation by 50%. Both chronic and acute amiodarone increased the size of the core of re-entrant circuits and decreased the incidence of re-entry by 44% and 57%; however, chronic amiodarone increased wavelength, while acute amiodarone did not. CONCLUSIONS: Neither acute nor chronic amiodarone change the DFT. While both acute and chronic amiodarone decrease the number of wavefronts, decrease the incidence of re-entry and increase the size of re-entrant cores in the mapped region during VF, they achieve these antiarrhythmic effects through different electrophysiologic mechanisms. Chronic amiodarone prolonged the VF cycle length and slowed conduction velocity, indicating it increased the wavelength and/or the excitable gap.

Amiodarone↗

Endocardial wave front organization during ventricular fibrillation in humans.

OBJECTIVES: This study was designed to characterize the organization of ventricular fibrillation (VF) on the endocardium of humans. BACKGROUND: Most proposed mechanisms for the maintenance of VF postulate the propagation of a number of activation wave fronts that reenter to maintain the arrhythmia. We tested the hypothesis that, in patients undergoing internal cardioverter-defibrillator implantation, VF consists primarily of a few large wave fronts on the endocardium. METHODS: Electrograms were recorded from a 36-electrode catheter in the left ventricle of 16 patients during VF. Activation times were chosen for a 2-s epoch for each fibrillation episode, and a two-dimensional Kolmogorov-Smirnov test was performed to determine if activation occurred randomly along the catheter over that time interval. The maximum cross-correlation was found for all possible pairs of electrodes on the catheter, and these values were plotted relative to the distance between the two electrodes. An exponential curve was then fit to the data, and a length constant was determined. Activation times were grouped into wave fronts along the catheter, and the lengths of the wave fronts were estimated. RESULTS: The Kolmogorov-Smirnov test showed that activation was not random along the catheter in any of the patients studied. The correlation length determined was 9 +/- 2 cm. The number of wave fronts recorded by the catheter was 9.2 +/- 2.9 wave fronts/s. The length of the pathway of each wave front along the catheter was 6.5 +/- 4.5 cm. CONCLUSIONS: Ventricular fibrillation is well organized on the endocardial surface of humans, consisting primarily of a few large wave fronts on the order of 6 to 9 cm.

Adult↗

Fiberglass needle electrodes for transmural cardiac mapping.

We developed a new method for fabricating plunge needle electrodes for use in cardiac mapping. The needles have 12 electrodes with 1-mm spacing, are 0.5 mm in diameter, and are fabricated from fiberglass reinforced epoxy. They are stiff enough to be easily inserted into beating hearts and durable enough to be reused many times. We found that these new needles elicit smaller, more quickly resolving injury potentials, and when inserted in a row with 2-mm spacing, disrupt ventricular fibrillation activation patterns less than traditional steel needles.

Animals↗