Search PubMed⌕ Search

Biomedical subjects

E N Moore

Publications and source records attributed to E N Moore.

At least 37 records · Page 2Linked to original sources
PubMed1988

Interaction of metoprolol and lidocaine on the ventricular fibrillation threshold in the anesthetized dog.

In the present study, we evaluated the antiarrhythmic interaction (s) of metoprolol and lidocaine in 16 dogs using the ventricular fibrillation threshold (VFT) method. The right ventricle was stimulated with a 100 Hz train of 12.4 ms pulses delivered after every eighth atrial paced beat at a basic cycle length of 300 ms. Lidocaine dosage was 2 mg/kg followed by a 70 micrograms/kg/min infusion and metoprolol dosage was a 75 micrograms/kg bolus. In Group 1, lidocaine was followed by metoprolol; in Group 2, first lidocaine then metoprolol and again lidocaine were given; and in Group 3, dogs received first metoprolol, then lidocaine, and subsequently metoprolol. Drug dose intervals were 45 min. In Group 1, lidocaine elevated the VFT to 149% +/- 20% and metoprolol to 204% +/- 30% of control, (p less than 0.01). In group 2, the VFT remained elevated after the second lidocaine administration (p less than 0.05 vs. Group 1). In Group 3, the VFT was increased by metoprolol to 227% +/- 30% of control (p less than 0.01). Interestingly, defibrillation induced by the combination of metoprolol and lidocaine occurred after 3.2 +/- 0.5 s in four out of 16 animals (p less than 0.05). This "chemical" defibrillation never occurred when only metoprolol or lidocaine alone was administered. Fibrillation was often more organized in the presence of the combination of metoprolol plus lidocaine, which might relate to the observed defibrillation associated with metoprolol plus lidocaine. In conclusion, the combination of metoprolol and lidocaine has no proarrhythmic effects and may enhance the electrical stability of the ventricles as measured by the VFT method.

Anesthesia↗
PubMed1988

Inducible sustained ventricular tachycardia 4 years after experimental canine myocardial infarction: electrophysiologic and anatomic comparisons with early healed infarcts.

We studied a group of 17 dogs 4 to 6 years after infarction produced by 2 hr occlusion of the anterior descending coronary artery followed by reperfusion. Dogs in this "late" infarct group were compared with a group of 24 dogs with "early" healed infarcts (2 to 24 weeks old). With signal-averaging techniques body surface potentials were recorded during sinus rhythm. After thoracotomy epicardial electrograms were recorded from 45 standardized sites within the infarcted region and characteristics of selected electrograms were compared with anatomic features of underlying myocardium. Epicardial recordings from the late infarct group demonstrated earlier local activation (p less than .001) and shorter electrogram duration (p less than .001) when compared with recordings from the early infarct group. There was less temporal dispersion of activation and electrogram duration among the 45 sites in dogs with late infarcts as measured by respective coefficients of variance (p = .007 and less than .001). With programmed stimulation six dogs in the late and eight in the early infarct group exhibited inducible sustained ventricular tachycardia. Mean cycle length of the tachycardia in dogs with late infarcts was significantly shorter (p = .035). Late potentials were notably less prominent in dogs in the late infarct group with ventricular tachycardia than in dogs in the early infarct group. Fewer abnormal electrophysiologic characteristics of late infarcts coincided with relatively less scar in the underlying myocardium. Moreover, the strength of electrophysiologic-anatomic correlations differed in late as opposed to early infarcts. The latter findings suggest long-term evolution of infarct anatomy. We conclude that a substrate for reentrant tachycardia is present in dogs 4 to 6 years after reperfused infarction. Conduction characteristics are less abnormal in these late healed infarcts and are associated with a shorter ventricular tachycardia cycle length and less pronounced late potentials on the body surface.

Animals↗
PubMed1988

Autonomic modulation of ventricular arrhythmia in cesium chloride-induced long QT syndrome.

To evaluate autonomic influence on arrhythmogenesis in an animal preparation of triggered activity, we gave increasing doses of cesium chloride (0.125 to 5.0 mmol/kg iv) to 24 dogs distributed equally among four protocols of autonomic intervention: control, total denervation, beta-blockade, and left stellate stimulation. All dogs underwent atrioventricular node ablation followed by ventricular pacing. A left ventricular endocardial monophasic action potential (MAP) catheter allowed for detection of "MAP early afterdepolarizations" (mEAD). mEAD amplitude was measured relative to MAP amplitude. Cesium chloride (CsCl) increased both MAP duration (132% after 0.125 mmol/kg to 188% after 1.0 mmol/kg; p less than .001) and mEAD amplitude (20% after 0.125 mmol/kg to 49% after 1.0 mmol/kg; p less than .001) in a dose-dependent fashion. All dogs exhibited ventricular ectopy at roughly equivalent doses (0.88 +/- 0.5 mmol/kg). Cesium's peak effect on MAP characteristics, sinus node automaticity, and systolic blood pressure coincided with the onset of sustained ventricular tachycardia (VT). Whereas control and denervated dogs developed VT after similar doses of CsCl (1.21 +/- 0.1 vs 1.12 +/- 0.14 mmol/kg; p = NS), none of the six beta-blocked dogs developed sustained VT. Conversely, those dogs having undergone stellate stimulation developed VT after smaller doses (0.58 +/- 0.34 mmol/kg; p less than .001) and with earlier onset (12 vs 30 sec; p less than .025). After 0.5 mmol/kg of CsCl, left stellate stimulation augmented relative mEAD amplitude compared with control (51% vs 38%; p less than .001), whereas beta-blockade had little effect (39% vs 38%; p = NS). Autonomic intervention as such can affect the arrhythmogenicity of CsCl and similarly alter MAP characteristics. Furthermore, as beta-blockade can prevent sustained arrhythmia without eliminating mEADs, autonomic tone appears to modulate the expression of mEADs as sustained VT.

Action Potentials↗
PubMed1988

Mechanisms of depressed conduction from long-term amiodarone therapy in canine myocardium.

Amiodarone therapy leads to a significant impairment in myocardial conduction, yet it causes only a modest decrease in the maximum rate of depolarization of the action potential (dV/dT). To determine whether the decrease in dV/dT solely accounts for the impaired myocardial conduction or whether passive membrane properties may also be involved, we studied 21 ventricular epicardial tissues from 14 beagles; six dogs received long-term treatment (3-6 weeks) of amiodarone orally, and the remaining dogs served as controls. Amiodarone therapy was associated with a decrease in conduction velocity (0.41 +/- 0.15 vs. 0.56 +/- 0.05 m/sec; p less than 0.01). There was a trend toward a decrease in dV/dT and a significant decrease in the space constant (0.69 +/- 0.27 vs. 1.05 +/- 0.25 mm; p = 0.01), of which the latter correlated closely with the decrease in conduction velocity measured in the amiodarone-treated tissues (r = 0.85, p less than 0.05). These data indicate that the decrease in myocardial conduction velocity caused by amiodarone is primarily due to effects on overall resistance to passive current flow rather than effects on the inward sodium current.

Action Potentials↗
PubMed1988

Interaction of fiber orientation and direction of impulse propagation with anatomic barriers in anisotropic canine myocardium.

We developed a computer model of the interaction of impulse propagation with anatomic barriers in uniformly anisotropic tissue. Its predictions were confirmed experimentally by using an in vitro cut to create a 6 X 1-mm anatomic barrier in 12 canine epicardial strips. The model predicted that long, thin barriers located parallel to the direction of impulse propagation would have little effect in delaying conduction regardless of the arrangement of cardiac fibers. In this situation, the mean experimental ratio of postcut to control conduction times across the barrier was 1.05:1.00 in 10 tissues. When impulses were proceeding perpendicular to an anatomic barrier, significant distal conduction delay was predicted and found to occur only when the conduction from pacing to recording sites was initially longitudinal to fiber orientation (mean experimental ratio, 2.34:1.00 in five tissues) but not transverse to fiber orientation (ratio, 1.08:1.00 in five tissues). We conclude that the direction of initial impulse propagation and the orientation of myocardial fibers have large effects on the degree to which anatomic barriers delay activation in cardiac tissue. These findings may have implications for the participation of anatomic barriers in reentrant circuits.

Animals↗
PubMed1988

Effects of cellular uncoupling on conduction in anisotropic canine ventricular myocardium.

Experiments were performed on canine superfused ventricular epicardial tissue slices to determine the effects of 1.0-2.0 mM heptanol, an uncoupling agent, on conduction longitudinal and transverse to myocardial fiber orientation. Conduction velocities were measured between proximal and distal pairs of epicardial electrodes oriented transverse and longitudinal to the direction of a conducted wavefront evoked by pacing at a basic cycle length of 2,000 msec from one margin of the tissue before and after the addition of heptanol. In a separate group of tissues, the dual bipolar orthogonal electrode was used to sequentially map epicardial activation at 40 to 45 sites in a 1 cm x 2 cm area before and 30 minutes after the introduction of heptanol. In a third group of tissues, transmembrane potentials were recorded with standard microelectrode techniques to determine the effects of heptanol on action potential characteristics. Heptanol did not significantly effect action potential amplitude or maximum rate of depolarization. After 1.0 mM heptanol, conduction velocity began to decrease in 1-2 minutes and reached a steady state in 15-20 minutes. Conduction velocity in the longitudinal direction decreased from a control value of 0.56 +/- 0.13 to 0.46 +/- 0.10 M/sec (+/- SD) at 30 minutes after heptanol (p = 0.005). In the transverse direction, it decreased from 0.24 +/- 0.09 to 0.17 +/- 0.05 M/sec (p = 0.002). The ratio of longitudinal to transverse conduction velocities increased from 2.54 +/- 1.00 to 2.94 +/- 0.82 (p = 0.042). Thus, heptanol preferentially slowed conduction in the transverse direction. Because heptanol did not greatly influence active membrane properties, we used cable equations to calculate the time course of the change in effective junctional resistivity, which rose from 133.2 omega.cm before heptanol to 312.2 omega.cm 30 minutes after heptanol administration. We conclude that heptanol slows conduction velocity by selectively increasing junctional resistivity. The preferential slowing of conduction in the transverse direction is most likely due to the fact that more junctional resistances are encountered per unit distance in the transverse than in the longitudinal direction.

Action Potentials↗
PubMed1988

A model of conduction through the N region of the AV node.

A computer model of the AV node was developed in order to study mechanisms of conduction delay in the AV node. Three cells were used corresponding to the AN, N, and NH region. The basic mechanisms for delay were a high intercellular resistance and a delayed, time dependent recovery of excitability in the center cell. The action potentials for all cells were held constant. The model reproduces antegrade conduction characteristics of the AV node and the waveform of the center cell resemble the two component action potentials of N cells. The model suggests that the conduction properties of the AV node may be due to subthreshold phenomenon.

Atrioventricular Node↗
PubMed1987

The cellular electrophysiologic changes induced by ablation: comparison between argon laser photoablation and high-energy electrical ablation.

The cellular electrophysiologic effects of myocardial ablation performed in vitro with argon laser energy were compared with those of high-energy electrical shocks. A border zone of injured but nonnecrotic tissue surrounding the site of energy delivery was present after tissue ablation by both energy modalities. A decrease in resting membrane potential, action potential amplitude, and maximum rate of upstroke velocity was noted in each tissue sample, was greatest nearest the site of energy delivery, and was of graded severity at increasing distances from the crater edge. The extent of injury, as indexed by changes in action potential variables and necrosis, histologically determined, was greater for tissues exposed to high-energy shocks. The relatively focal injury after argon laser photoablation may explain the lower incidence of arrhythmias and hemodynamic dysfunction noted with the use of this method of ablation in vivo.

Action Potentials↗
PubMed1987

Depression of action potential characteristics and a decreased space constant are present in postischemic, reperfused myocardium.

Brief periods of ischemia and reperfusion may lead to arrhythmias and delayed epicardial activation. To determine the nature of the electrophysiologic substrate and to gain insight into potential mechanisms underlying the electrophysiologic and hemodynamic abnormalities that develop in this setting, standard microelectrode techniques were used to measure action potential characteristics, conduction velocity, and space constants in canine isolated epicardial preparations removed after a 15-min anterior descending artery occlusion and 20-min reflow period in vivo. Our results demonstrate a significant reduction in conduction velocity (0.78 +/- 0.38 vs. 0.31 +/- 0.12 m/s, P less than 0.001), space constant (1.05 +/- 0.42 vs. 0.45 +/- 0.12 mm, P = 0.004), resting membrane potential (81.3 +/- 2.5 vs. 61.7 +/- 7.8 mV, P less than 0.001), action potential amplitude (94.1 +/- 4.2 vs. 64.1 +/- 1.5 mV, P less than 0.001), and dV/dT (164.7 +/- 37.3 vs. 52.6 +/- 19.7 V/s, P less than 0.001) in postischemic reperfused myocardium. The space constant and dV/dT each correlated with conduction velocity; in addition, the space constant was an independent predictor of conduction velocity in these tissues. These electrophysiologic abnormalities may play a role in the arrhythmias and abnormalities of contraction present in postischemic, reperfused myocardium.

Action Potentials↗
PubMed1987

Electrophysiological studies on atrial fibrillation.

We tested the multiple-wavelet hypothesis by studying the initiation and maintenance of atrial fibrillation in normal mules, horses, cows, calves, and goats. Persistence of atrial fibrillation in animals with a large atrial mass was compared with results in adult goats and calves having a smaller atrial mass. Atrial stimulation in clinically normal cows, mules, calves, and goats was accomplished using an intra-atrial stimulating catheter with rapid atrial pacing (30/s). Once initiated, atrial fibrillation persisted for 95,120,125 min, 3 days, and 8 weeks in five adult cows, respectively. In contrast, in five calves, atrial fibrillation failed to persist for more than a few minutes. Similar results were found in the small atria of adult goats, indicating that atrial size rather than maturity of the atrial myocardium was responsible. In addition, to demonstrate that this was not a species-dependent phenomenon, it was shown in adult mules that atrial fibrillation could persist for 24 h or more once initiated. These studies are consistent with the multiple-wavelet hypothesis for initiation and maintenance of atrial fibrillation. We also studied the ventricular response in atrial fibrillation. We found that as many as nine consecutive atrial responses can be concealed within the atrioventricular (AV) node associated with a long R-R interval during atrial fibrillation. Although concealment of rapid atrial activity normally occurred in the AV node, one case of infranodal block was observed. It has also been suggested that subsidiary AV junctional pacemakers may be the cause of the ventricular irregularity. However, our experimental studies using microelectrodes in isolated tissue and extracellular bundle of His recordings in intact animals failed to demonstrate that this mechanism was responsible for the irregularity of the ventricular response in atrial fibrillation.

Animals↗
PubMed1986

The cellular electrophysiologic changes induced by high-energy electrical ablation in canine myocardium.

High-energy electrical ablation is a new experimental approach to control arrhythmias. In this study, the cellular electrophysiologic effects of high-energy shocks (5 to 40 J) delivered in vitro to 14 epicardial tissues from 11 dogs were studied in an attempt to understand the nature and extent of injury as well as potential arrhythmogenic mechanisms. In addition, this preparation was used to test the importance of cathode-anode configuration, current density, and fiber orientation in the induction of tissue injury in vitro. Electrophysiologic abnormalities were noted up to 10 mm from the electrode wall, and their extent was determined in part by current density and the cathode-anode orientation. A decrease in resting membrane potential, action potential amplitude, and dV/dT occurred in all tissues after high-energy shocks, which was worst nearest the cathode and of graded severity at increasing distances from the cathode. The most severe effects were noted with high current densities and in tissues located between the cathode and anode. In addition, impaired impulse conduction and abnormal repolarization were documented. Histologic study demonstrated contraction band necrosis immediately after delivery of high-energy shocks. The extent and distribution of the contraction bands was in part dependent on the energy delivered and the cathode-anode configuration. These findings suggest potential mechanisms for arrhythmogenesis and altered regional hemodynamic abnormalities that occur in vivo.

Action Potentials↗
PubMed1986

Vector mapping of myocardial activation.

A custom-made probe, consisting of four electrodes arranged so that two orthogonal bipolar electrograms could be recorded from a single site, was used to record epicardial activity during atrial and ventricular pacing in five normal and five anesthetized open-chest mongrel dogs with myocardial infarction. Unfiltered bipolar electrograms recorded with a 2 mm interelectrode distance averaged 36 +/- 15 mV in amplitude and 16 +/- 5 msec in duration in normal areas and 14 +/- 11 mV and 23 +/- 12 msec in infarcted areas (p less than .01 infarct vs normal). The bipolar electrograms were vector summed so that a vector loop could be generated at each site. The direction of epicardial impulse propagation as determined by multipoint isochronal activation mapping was compared with that indicated by maximum x,y deflection of the vector loop. At 203 sites (141 normal and 62 infarcted) there was a median error of only 13 degrees and an excellent correlation by linear regression (r2 = .95). In normal myocardium vector loops were straight (60%), open (21%), or hooked (19%). In infarcted myocardium, notched and irregular loops were occasionally seen. However, a clear maximum x,y deflection was still obtained from 98% of infarcted sites. During ventricular pacing in normal dogs, uniform epicardial conduction was observed for up to 4 cm longitudinal to fiber orientation but only 1 cm transverse to it. At selected sites longitudinal to fiber orientation conduction velocity was 0.618 m/sec, electrogram duration 12 msec, and vector amplitude 76 mV compared with 0.304 m/sec, 18 msec, and 38 mV during conduction transverse to fiber orientation (p less than .05 for all comparisons). Vector mapping of epicardial activation was performed during ventricular tachycardia induced by programmed stimulation in two of five 2-week-old canine myocardial infarcts. Aside from minor irregularities caused by impulse spread around areas of block, vector loops indicated when impulses were spreading away from the area of early epicardial activity and thus directed mapping to the region of earliest activation. We conclude that vector loops generated by summing orthogonal local bipolar electrograms accurately represent the direction of epicardial activation in both normal and infarcted myocardium. Such loops may prove useful in mapping tachycardias and in clarifying details about cardiac activation processes.

Animals↗
PubMed1986

The effects of procainamide on conduction in anisotropic canine ventricular myocardium.

Although conduction velocity in cardiac tissue is dependent on fiber orientation, the influence of commonly used antiarrhythmic agents on conduction longitudinal and transverse to such fibers is unknown. We evaluated the effects of procainamide on conduction velocity and intracellular potentials in vitro during conduction longitudinal and transverse to fiber orientation in epicardial strips obtained from areas of uniform fiber orientation from 15 adult mongrel dogs. Ventricular epicardial strips demonstrated marked anisotropy. At a pacing cycle length of 1000 msec, mean conduction velocity longitudinal to fiber orientation averaged 0.602 +/- 0.051 m/sec and mean conduction velocity transverse to fiber orientation was 0.186 +/- 0.024 m/sec, resulting in a ratio of longitudinal to transverse conduction velocities of (theta L/T) 3.27 +/- 0.38. After the addition of procainamide, conduction velocity decreased to 0.532 +/- 0.062 m/sec longitudinal to fiber orientation and to 0.174 +/- 0.023 m/sec transverse to fiber orientation resulting in a decrease of theta L/T to 3.09 +/- 0.37 (p less than .05 vs control). Before the addition of procainamide, when pacing at progressively shorter cycle lengths, conduction velocity longitudinal to fiber orientation was relatively unchanged, whereas conduction velocity transverse to fiber orientation decreased resulting in an increase in theta L/T. After the addition of procainamide, conduction velocity at shorter pacing cycle lengths decreased both longitudinal and transverse to fiber orientation demonstrating the well-known use-dependent effect of procainamide. However, in contrast to control conditions, conduction velocity longitudinal to fiber orientation was slowed by a greater extent than the conduction transverse to fiber orientation, resulting in an even greater decrease in theta L/T. To investigate the effect of differences in drug binding during propagation in different directions, we examined conduction velocity during alternations in pacing direction and compared it with velocity during steady-state pacing. At a pacing cycle length of 1000 msec, no difference was observed between the initial conduction velocity after changing pacing directions and the steady-state conduction velocity. At pacing cycle lengths shorter than 1000 msec, when changing from transverse to longitudinal conduction, there was an initial drop in normalized conduction velocity that was present on the first beat of longitudinal conduction; however, with continued pacing in a longitudinal direction there was a further decrease in conduction velocity.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1986

The monophasic action potential upstroke: a means of characterizing local conduction.

The upstrokes of monophasic action potentials (MAPs) recorded with an extracellular pressure electrode were characterized in isolated canine tissue preparations in vitro. The characteristics of the MAP upstroke were compared with those of the local action potential foot as well as with the characteristics of approaching electrical activation during uniform and asynchronous conduction. The upstroke of the MAP was exponential during uniform conduction. The time constant of rise of the MAP upstroke (TMAP) correlated with that of the action potential foot (Tfoot): TMAP + 1.01 Tfoot + 0.50; r2 = .80. Furthermore, changes in Tfoot with alterations in cycle length were associated with similar changes in TMAP: Tfoot = 1.06 TMAP - 0.11; r2 = .78. In addition, TMAP and Tfoot both deviated from exponential during asynchronous activation; the inflections that developed in the MAP upstroke correlated in time with intracellular action potential upstrokes that were asynchronous in onset in these tissues. Finally, the field of view of the MAP was determined and was found to be dependent in part on tissue architecture and the space constant. Specifically, the field of view of the MAP was found to be greater parallel compared with transverse to fiber orientation (6.02 +/- 1.74 vs 3.03 +/- 1.10 mm; p less than .01). These data suggest that the MAP upstroke may be used to define and characterize local electrical activation. The relatively large field of view of the MAP suggests that this technique may be a sensitive means to record focal membrane phenomena in vivo.

Action Potentials↗
PubMed1985

Effect of sympathetic tone on ventricular arrhythmias during circumflex coronary occlusion.

To determine if the sympathetic nervous system exerts an arrhythmogenic effect on the ischemic myocardium independent of heart rate, the proximal circumflex coronary artery was occluded for 1 h in 62 open-chest, anesthetized dogs. The atrial rate was maintained at 200/min, and the vagosympathetic trunks were transected in all dogs. The total incidence of ventricular fibrillation was 35% in 20 dogs with intact stellates and not significantly different from the incidence of ventricular fibrillation (15%) in another 20 dogs in which both stellate ganglia had been decentralized. Electrical stimulation of the left ansae subclavia (3 Hz, 2 ms, 6-8 V) in the remaining 22 dogs significantly increased the incidence of ventricular fibrillation to 73% (P less than 0.05). The magnitude of S-T segment elevation in the lead II electrocardiogram 90 s after occlusion was 0.69 +/- 0.08 mV in the group with left ansae stimulation and significantly elevated (P less than 0.01) compared with dogs with intact stellates (0.35 +/- 0.06 mV) and with the denervated dogs (0.19 +/- 0.05 mV). The data indicate that the sympathetic nervous system is capable of a direct arrhythmogenic influence on the ischemic myocardium independent of heart rate. The rate-independent arrhythmogenic effects of the sympathetic nervous system may be mediated by an increase in severity of the ischemic insult.

Animals↗
PubMed1985

The effects of premature stimulation of the His bundle on epicardial activation and body surface late potentials in dogs susceptible to sustained ventricular tachyarrhythmias.

Experiments were performed on 20 anesthetized dogs to determine the effects of premature stimulation of the His bundle on epicardial conduction and late potentials recorded on the body surface. Fifteen dogs underwent occlusion of the left anterior descending coronary for 2 hr followed by reperfusion, and five that did not undergo operation served as controls. Animals were studied 2 to 52 weeks after the induction of infarction, and four animals with infarction and four control animals exhibited no sustained arrhythmias in response to programmed ventricular extrastimulation. Five dogs with infarction and one control dog had ventricular fibrillation while the six remaining dogs had inducible sustained ventricular tachycardia. All animals with ventricular tachycardia had late potentials in the terminal portion of the signal-averaged body surface QRS complexes during sinus rhythm and QRS durations in the animals were 64 msec or greater. The voltage in the last 20 msec of the QRS complex was 13.5 microV or less and the duration of late activity below 30 microV was 18.2 msec or more. These values did not overlap values in animals with no inducible arrhythmias. Ventricular fibrillation was a nonspecific end point in these experiments and values overlapped those in animals with no arrhythmias and those with ventricular tachycardia. All animals with infarction and late potentials associated with their QRS complexes also had delayed and prolonged epicardial electrograms that extended into the time of the late potentials recorded from 45 standard sites in the infarcted regions. A single premature beat evoked by His bundle pacing (coupling interval of 192 to 270 msec) had no significant effect on late potentials or their relationship to epicardial activation in the area of infarct. However, changes in the durations of electrograms in response to premature beats were different in animals with infarction and ventricular tachycardia than in those with ventricular fibrillation. In animals with ventricular tachycardia, electrograms at 15 of 210 sites increased in duration by more than 10 msec while those at 61 of 210 sites decreased in duration. In animals with ventricular fibrillation, electrograms at 40 of 207 sites were of increased duration while those at 26 of 207 decreased. The decreases in duration were usually due to components of fractionated electrograms "dropping out" and likely represent local conduction block near the recording electrode.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗