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Biomedical subjects

E N Moore

Publications and source records attributed to E N Moore.

At least 73 records · Page 4Linked to original sources
PubMed1981

Further electrophysiologic and anatomic correlates in a canine model of chronic myocardial infarction susceptible to the initiation of sustained ventricular tachyarrhythmias.

A canine model of chronic myocardial infarction has been studied in which animals are susceptible to the initiation of sustained ventricular tachyarrhythmias using routine methods of programmed stimulation. The pacing-induced arrhythmias in this model are similar to those observed in man in their mode of initiation and termination, as well as in their response to both pacing and pharmacologic interventions. Indirect evidence has suggested a localized protected reentrant mechanism for these arrhythmias. The susceptibility to arrhythmia initiation in this model has been related to both electrophysiologic and histopathologic findings. Consistently, animals have demonstrated a marked heterogeneity of local properties of excitability and refractoriness at sites within areas of infarction. Correspondingly, animals have shown a marked inhomogeneity of histopathologic findings within areas of infarction, with close interspersing of normal and abnormal myocardium. Remarkably, even animals with small mottled infarctions, often less than 1 cm x 2 cm and electrocardiographically silent, were highly susceptible to the initiation of ventricular tachyarrhythmias, and especially fibrillation. Thus, initial provocative studies in this model have suggested its potential importance both in studying arrhythmia mechanisms and in evaluating the efficiency of potential antiarrhythmic interventions. In addition, this should be an ideal model in which to correlate pathophysiologic and morphologic alterations in the setting of chronic myocardial infarction.

Animals↗
PubMed1981

Relation of the endocardial and epicardial ventricular fibrillation thresholds of the right and left ventricle.

Ventricular fibrillation thresholds were measured on the endocardium and epicardium of the right or left ventricle, or both, in 13 dogs. The electrodes, introduced through a right or left atriotomy to avoid injury to the ventricles, were aligned opposite and parallel to each other on the endocardium and epicardium. The ventricular fibrillation threshold was measured during atrial pacing by delivering a train of impulses to the ventricle during the vulnerable period after every 12th paced complex in 1 milliampere (mA) increments of current until fibrillation ensued. The mean (+/- standard deviation) right ventricular epicardial and endocardial fibrillation thresholds were 18.3 +/- 5.3 and 17.6 +/- 5.3 mA, respectively, (values not significantly different). However, the fibrillation threshold of 36.1 +/- 9.5 mA in the left ventricular epicardium was significantly higher than the value of 20.7 +/- 9.4 mA on the left ventricular endocardium. These data suggest that the proximity of the fibrillating electrodes and Purkinje network may be a factor in the measurement of ventricular vulnerability.

Animals↗
PubMed1981

Stability of an experimental atrioventricular reentrant tachycardia in dogs.

The factors leading to spontaneous block and instability of a reentrant tachycardia were studied with a computer model and in eight anesthetized dogs with an electronically simulated atrioventricular (AV) bypass tract. The bypass tract delay could be changed in a programmed sequence. AV nodal refractoriness in the dogs was increased with verapamil. Stability of the reentrant tachycardia was assessed by noting how rapidly cycle-length changes from a transient alteration in the bypass-tract delay time would dampen out and the tendency of the reentrant tachycardia to spontaneously block. There was close agreement between computer model predictions and experimental results. After a transient change in bypass tract delay time, dampened oscillations of the cycle length were noted. The degree of dampening was related to the slope of the AV nodal refractory curve. When the reentrant tachycardia operated on a steep portion of the refractory curve (slope steeper than -1), spontaneous oscillations and block developed. In the dog, the reentrant tachycardias terminated spontaneously either by an increase in amplitude of oscillations or by an increase in AV nodal refractoriness. We conclude that, for stable reentry, a reentrant circuit must have no conduction block and must be able to dampen out transient perturbations.

Animals↗
PubMed1981

Detection of delayed ventricular activation on the body surface in dogs.

This study describes a noninvasive method for detecting delayed ventricular activation, caused by ischemia, on the body surface. Signal averaging and a newly developed high-pass digital filter were used. The filter has the property that it does not create an artifact or ring after the QRS complex ends, thereby allowing the detection of microvolt-level potentials that occur immediately after the QRS complex. Eleven dogs were studied before and during acute ischemia induced by coronary artery ligation and latex embolization. The ischemic region was mapped with bipolar electrodes and, after the chest was rapidly closed, signal-averaged recordings were made from the body surface. Repeated cycles of ventricular mapping and signal averaging were performed. In each dog, delayed and fractionated electrograms were recorded directly from the ischemic epicardium that lasted a maximum of 118 +/- 18 ms after QRS onset. The duration of the ventricular electrograms varied with time. Whenever delayed epicardial electrograms were recorded, filtered signal-averaged leads showed microvolt-level potentials early in the S-T segment that were continuous with the QRS complex. The duration of ventricular activation, as measured from the bipolar electrograms and from the filtered signal-averaged leads, correlated well (r = 0.93, P less than 0.001). Because of the absence of filter ringing, low-level potentials could be detected less than 40 ms after the QRS complex ended. This study demonstrates that microvolt-level potentials arising from delayed ventricular activation can be reliably detected on the body surface, even when they occur just after the QRS complex.

Animals↗
PubMed1981

Autonomic control of ventricular refractoriness.

The effects of vagal and sympathetic stimulation on canine ventricular refractoriness were studied in vivo. Sympathetic stimulation reduced the left ventricular refractory period to an extent linearly related to the logarithm of nerve stimulation frequency. Vagal stimulation had no effect in the absence of sympathetic stimulation but produced a frequency-dependent attenuation of sympathetic effects when the two systems were stimulated simultaneously. The effects of combined vagal and sympathetic stimulation were best described by a multilinear regression model using the logarithm of vagal and sympathetic frequency as covariates. The magnitude of vagal attenuation of sympathetic effects did not show any regional variation at the five widely spaced sites (2 right ventricular, 3 left ventricular) studied.

Animals↗
PubMed1981

Initiation of sustained ventricular tachyarrhythmias in a canine model of chronic myocardial infarction: importance of the site of stimulation.

The importance of the site of stimulation to the initiation of sustained ventricular tachyarrhythmias was determined in 24 adult mongrel dogs. Studies were performed 3-30 days after two-stage occlusion of the mid- or distal left anterior descending coronary artery, modified by a reperfusion stage. Unipolar cathodal stimuli of twice-threshold intensity and 2 msec duration were introduced at five to 24 sites in each dog in the distribution of occluded and nonoccluded vessels. Strength-interval curves were constructed from 232 measurements at these sites and local properties of excitability and refractoriness were correlated with the ability to initiate arrhythmias. All dogs had sustained ventricular tachyarrhythmias inducible from at least one site. Intramyocardial sites with normal excitability and refractoriness within 2 cm of an area of infarction were most often successful (27 of 44, 61%) in the initiation of sustained arrhythmias. Less successful sites included normal left ventricular plunge electrode sites less than 2 cm from an area of infarction (eight of 32, 25%) (p = 0.002), left ventricular plunge electrode sites within an area of infarction (20 of 103, 19%) (p less than 0.001), normal right ventricular sites (five of 24, 21%) (p less than 0.001), and endocardial catheter sites (six of 29, 21%), (p less than 0.001). These findings suggest that local properties of excitability and refractoriness at the site of stimulation, as well as anatomic and geometric factors, may be critical in the initiation of sustained ventricular tachyarrhythmias using the technique of programmed electrical stimulation.

Animals↗
PubMed1981

Strength-interval relations in a chronic canine model of myocardial infarction. Implications for the interpretation of electrophysiologic studies.

Fifteen adult mongrel dogs underwent two-stage occlusion of the mid- or distal left anterior descending coronary artery and then a reperfusion stage. The dogs were studied 3-30 days later to determine strength-interval relations in a canine model of chronic myocardial infarction. These dogs were susceptible to the initiation of sustained ventricular tachyarrhythmias with the introduction of one, two or three ventricular extrastimuli. Using unipolar cathodal stimuli with a pulse width of 2 msec, strength-interval curves were constructed from measurements made at multiple sites in the distribution of occluded and nonoccluded vessels during drive pacing at a cycle length of 300 msec. At 56 normal sites, ventricular refractory periods measured at twice-diastolic-excitability threshold approximated the relative refractory periods (mean absolute difference 3 msec), but were variably longer than effective refractory periods (mean difference 18 msec, range 4-29 msec). At 51 infarct sites, differences between ventricular refractory periods measured at twice-diastolic-excitability threshold and both relative refractory periods (mean difference 13 msec, range -60 to +18 msec) and effective refractory periods (mean difference 28 msec, range 1-60 msec) were markedly disparate. These differences were further exaggerated after administration of i.v. procainamide. These findings suggest limitations in interpreting the results of programmed pacing studies performed using stimuli of twice-threshold intensity.

Animals↗
PubMed1980

Continuous fractionated electrical activity after stimulation of the ventricles during the vulnerable period: evidence for local reentry.

Ventricular multiple extrasystoles and fibrillation were induced in open chest dogs by the delivery of either a single electrical pulse or a train of pulses to the right ventricle during the vulnerable period of the cardiac cycle. Bipolar epicardial electrodes delivered current while bipolar plunge electrodes recorded the activation complexes at various distances from the stimulation site. At stimulus intensities below the threshold for multiple ventricular responses, the electrograms recorded from muscle adjacent to the stimulation site showed fragmented activation complexes that lasted considerably longer than the control complexes. At stimulus intensities that evoked multiple ventricular extrasystoles or fibrillation, the fragmented electrical activity became continuous and bridged the diastolic interval between successive ectopic complexes. The continuous fractionated electrical activity that preceded the appearance of multiple extrasystoles and fibrillation was recorded only from electrodes placed within a few millimeters of the stimulating electrodes and could be evoked only by stimulation during the vulnerable period. Disappearance of the fractionated local electrical activity during a run of extrasystoles was followed immediately by the resumption of a normal rhythm. In addition, the fractionated continuous electrical activity that appeared after delivery of a single stimulus during the vulnerable period could be abolished by the delivery of a second stimulus during the protective zone. The presence of continuous local electrical activity before the development of multiple extrasystoles and fibrillation provides strong evidence that the ventricular fibrillation threshold technique operates by producing local reentrant activity.

Animals↗
PubMed1980

Supernormal conduction in the canine bundle of His and proximal bundle branches.

We used close bipolar intramural electrodes and catheter electrodes to study the characteristics of conduction in the bundle of His and proximal bundle branches during premature atrial beats in 17 open-chest anesthetized dogs. The electrophysiological properties of the proximal conducting system were heterogenous. The shortest interval between a normal His bundle response and a premature response that was not accompanied by changes in conduction time (the total recovery time) was 258.8 +/- 23.9 (SD) ms for the proximal His and 310.7 +/- 30.6 ms for the distal His and proximal bundle branches. A period of supernormal conduction, in which the conduction times of premature beats were faster than during earlier or later beats, was localized to the distal portion of the bundle of His and proximal bundle branches. The minimal conduction time during the supernormal period was decreased by 9.6 +/- 4.6% below control diastolic conduction times, and the supernormal period was 61.0 +/- 25.7 ms in duration. The characteristics of the period of supernormal conduction in the distal bundle of His and proximal bundle branches were very similar to those previously found in the peripheral bundle branch-Purkinje system. The mechanism of supernormal conduction in the bundle of His is most probably due to a period of supernormal excitability.

Animals↗
PubMed1979

Cellular electrophysiology of human myocardial infarction. 1. Abnormalities of cellular activation.

Ventricular tissues were obtained at the time of operation from 12 patients who underwent aneurysmectomy or mitral valve replacement. The electrophysiologic characteristics of these tissues were determined in a tissue bath using microelectrodes. Normal-appearing action potentials were recorded from surviving Purkinje fibers and ventricular muscle cells within infarcted ventricular tissues. Normal muscle action potential recordings from infarcted tissues were similar to action potentials from noninfarcted papillary muscles, except that the duration of the action potential was significantly longer in the former. In other areas slow response potentials were recorded. These action potentials conducted slowly and were eliminated by verapamil. We observed verapamil-sensitive slow response automaticity, but this did not correlate with ventricular tachycardias, present in three patients. Variable amplitude responses arising from normal resting potentials and characterized by stimulus intensity-dependent changes in action potential amplitude were recorded in tissues from two patients. These potentials had many characteristics similar to the slow response, but were not eliminated by verapamil. We also saw inexcitable cells with both normal and abnormal resting potentials. The heterogeneous electrophysiologic characteristics of these tissues provide a likely substrate for arrhythmias and may be the source of the ectopic ventricular rhythms observed in these patients.

Action Potentials↗
PubMed1979

The mechanism of apparent right bundle branch block after transatrial repair of tetralogy of Fallot.

The electrocardiographic pattern of right bundle branch block (RBBB) is routinely observed after transatrial repair of tetralogy of Fallot even though no ventriculotomy has been performed. The mechanism of this conduction disturbance was studied in 16 patients with tetralogy of Fallot and one patient with infundibular pulmonic stenosis. Preoperative ECGs and vectorcardiograms showed right ventricular hypertrophy and no RBBB. Epicardial activation maps were obtained before and after total surgical repair in all patients and after infundibular resection but before closure of ventricular septal defect (VSD) in four of these patients. After infundibular resection, RBBB appeared and activation was markedly delayed (greater than 30 msec) over the pulmonary outflow tract, but was unchanged over the body of the right ventricle. No further changes in ventricular activation occurred after closure of the VSD. This study shows that RBBB after transatrial repair of tetralogy of Fallot is usually produced by infundibular resection, but not by VSD closure, and is associated with delayed activation of the pulmonary outflow tract and base of the right ventricle which results from damage to portions of the right ventricular conduction system.

Adolescent↗
PubMed1979

The effects of coronary artery disease on the ventricular fibrillation threshold in man.

The ventricular fibrillation threshold (VFT) was measured in 28 patients at the time of cardiac surgery. The VFT was measured with a 100 Hz train of 24 rectangular pulses positioned across the ST segment and T wave. Current was applied to the epicardial surface of either ventricle with a bipolar electrode probe. In six patients, the normal right VFT was 24.3 +/- 5.2 mA, and in 10 patients the normal left VFT was 33.6 +/- mA (p less than 0.05). In 12 patients with greater than or equal to 75% obstruction of the left anterior descending coronary artery, the left VFT was 18.6 +/- 6.9 mA. This value was significantly less than the left VFT in patients without coronary artery disease (p less than 0.001). This study shows that the VFT can be measured in man and that coronary artery disease reduces this parameter.

Adult↗
PubMed1979

The relationship between atrioventricular nodal refractoriness and the functional refractory period in the dog.

We studied the relationship between the atrioventricular nodal functional refractory period (FRP) and refractoriness by mathematical analysis and by measurement during antegrade Wenckebach cycles in 16 dogs. The FRP relates directly to the conduction time of the control beat, and inversely to the coordinates of the point on the A'-H' vs. A-A refractory curve where the slope is -1. The FRP can vary without any change in refractoriness as measured by the effective refractory period (ERP) or the refractory curve. In 16 dogs the ERP and the FRP were measured during 4:3 Wenckebach cycles. Because of changes in the control conduction times, the FRP declined and did not reflect the progressive increase in refractoriness recorded during Wenckebach cycles. The FRP is a complex parameter and does not reliably measure refractoriness.

Analog-Digital Conversion↗
PubMed1979

The effect of brief vagal stimulation on the isolated rabbit sinus node.

We developed an isolated rabbit atrial preparation which responds consistently and reproducibly to brief, submaximal stimulation of the autonomic nerves contained in it. In 6 of 11 preparations in the presence of propranolol (1 mg/liter), the time course of changes in the atrial rate following 120 msec vagal stimulation was bimodal. The maximal slowing occurred at 0.64 +/- 0.16 second, and the peak secondary slowing occurred at 2.3 +/- 1.0 seconds. An acceleratory component occurred between the first and second peaks between 0.8 and 1.6 seconds. The total time course of vagal effect lasted for 5.0 +/- 2.0 seconds. These changes in rate could not be explained by shifts in the location of the primary pacemaker. The acceleratory component was due to a 4.7 +/- 2.0 (SD) mV depolarization of the maximum diastolic membrane potential of the primary pacemaker of the sinus node which lasted for 1.8 +/- 0.3 seconds. Following vagal stimulation, there was an increase of 0.2 mM in the activity of potassium in the extracellular space recorded with a potassium-sensitive electrode; this peaked between 1.4 and 2.5 seconds and cleared with an exponential time course. The halftimes for recovery ranged between 2.8 and 4.6 seconds. The initial peak slowing of the bimodal time course and the acceleratory component therefore appear to be direct effects of acetylcholine. The secondary slowing occurs after acetylcholine presumably has been inactivated and occurs coincidently with the accumulation of potassium in the extracellular space.

Acetylcholine↗