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Biomedical subjects

E N Moore

Publications and source records attributed to E N Moore.

At least 55 records · Page 3Linked to original sources
PubMed1985

Cesium chloride-induced long QT syndrome: demonstration of afterdepolarizations and triggered activity in vivo.

The identification of afterdepolarizations and their relationship to arrhythmias in vivo is not available. Experiments were undertaken to determine whether afterdepolarizations could be detected in monophasic action potentials (MAPs) recorded in vivo and whether they were related to arrhythmias in an intact canine preparation of the long QT syndrome. Isolated cardiac tissues from six dogs were studied to validate the technique. In simultaneous MAP and transmembrane recordings, afterdepolarizations induced with barium (early) or acetylstrophanthidin (delayed) were detected in MAPs when present in microelectrode recordings. MAPs were then recorded in situ in eight dogs with cesium chloride-induced long QT syndrome associated with ventricular arrhythmias. Afterdepolarizations were identified in each of the dogs and were similar to early afterdepolarizations identified in vitro; they occurred during phase 3 and were attenuated during overdrive pacing. The afterdepolarizations were closely related to arrhythmias: (1) afterdepolarizations always preceded ventricular arrhythmias, (2) the coupling intervals (CI) of the afterdepolarizations (AD) and the ventricular premature beats (VPB) were nearly identical (VPB CI = 1.06 AD CI -10.24; r2 = .87), (3) the take-off potentials of the ventricular premature beats were nearly identical to the amplitude of the afterdepolarizations (take-off potential = 0.98 afterdepolarization amplitude +0.46, r2 = .87), and (4) afterdepolarizations and ventricular arrhythmias resolved concurrently during overdrive pacing and with time. Thus, a new catheter technique has been validated and has been used to directly identify afterdepolarizations and triggered activity in vivo.

Action Potentials↗
PubMed1985

The importance of the electrophysiologic substrates in the development of ventricular tachyarrhythmias.

Our electrophysiologic findings are summarized in Table 3. In our animal model of chronic myocardial infarction, induced sustained ventricular tachyarrhythmias occur from 3 days to months following the infarction procedure. Isolated tissues removed from the infarcted region in these animals and studied (table: see text) in vitro reveal regions of slow conduction and local conduction block. These characteristics also persist over this time period and appear to be the substrate responsible for the reentrant excitation at the basis of the ventricular tachyarrhythmias. Our cellular electrophysiologic studies indicate the mechanisms responsible for the abnormal conduction change with time. Up to approximately 2 weeks following the infarction procedure, cellular membrane depolarization is depressed and cell-to-cell electrical continuity is decreased. Both of these factors probably contribute to the slow conduction. Depression in membrane excitability does not seem to play a role. Although an increased dispersion in refractoriness probably contributes to the inducibility of ventricular reentry due to an enhanced propensity for a premature impulse to undergo functional block in one region while continuing to conduct in another region. At two weeks and beyond, action potential depolarization has returned to normal. At this time the sole contributor to the abnormal conduction appears to be cellular electrical uncoupling. Two possibilities for the cause of this cellular uncoupling are as follows: First, the low resistance gap junctions between cells may be modified in the infarcted region causing an increase in internal axial resistance. Another possibility is that the fibrotic matrix in which the surviving cells in the mottled infarct are distributed may contribute to an increase in extracellular resistance as compared to normal myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1985

Critical appraisal of programmed electrical stimulation for evaluating hearts prone to ventricular tachyarrhythmias.

Programmed electrical stimulation has provided a unique new opportunity to evaluate both mechanisms and treatment regimens aimed at preventing ventricular tachyarrhythmias. The variable results that have been reported from different laboratories, undoubtedly are due in part to the differences in programmed electrical stimulation protocols. Although it is unlikely that all laboratories will adapt the same programmed electrical stimulation protocol, it nevertheless is very important that the number of sites of stimulation, stimulus strength, stimulus duration, stimulus polarity, drive train length, and patient population all be listed in order for some comparison between laboratories to be made.

Animals↗
PubMed1985

Use of signal averaging to identify low level late potentials in hearts prone to developing tachyarrhythmias.

Our studies have shown that infarcted dogs which exhibit inducible sustained ventricular tachycardia had late potentials and could be distinguished from those with no arrhythmias by the following QRS characteristics. A QRS duration greater than 63 msec and a duration of late activity below 30 microvolts greater than 18 msec. In addition, delayed and fractionated epicardial activation in the infarcted region correlates with late potentials on the body surface. Finally, induced ventricular fibrillation in this animal model appears to have mixed causes and is a non-specific end point.

Action Potentials↗
PubMed1984

Electrophysiologic substrate for ventricular tachycardia: correlation of properties in vivo and in vitro.

Cardiac electrophysiologic studies were performed in three control dogs and in nine dogs with previous (8 to 22 days) anterior myocardial infarction. During programmed stimulation, no control dog had more inducible ventricular fibrillation (VF) or tachycardia (VT), three dogs with infarcts had inducible VF and six had inducible VT. Recordings in vivo were made via a plaque electrode containing 10 bipolar electrodes (3.0 x 1.5 cm) placed on the epicardial surface of the anteroapical left ventricle. Subsequently, epicardial strips (2 mm thick) from beneath the plaque were prepared for studies in vitro. Electrogram durations were significantly greater in dogs with infarcts than in control dogs both in vivo (p less than .05) and in vitro (p less than .001). Electrogram amplitudes were significantly lower in dogs with VT in vivo (p less than .05) and in vitro (p less than .001). In control animals activation was continuous and most rapid in the direction of fiber orientation; there were areas of slow and/or discontinuous conduction in all dogs with infarcts. In one case, sustained reentrant beating in vitro was caused by functional unidirectional block and microreentry at a site of continuous electrical activity during VT in vivo. Reentrant beating in vitro persisted in 0.5 cc of isolated tissue. We conclude that broad low-amplitude electrograms in vivo and in vitro depict local areas of slow and/or discontinuous conduction, that the intrinsic asymmetry of cardiac activation due to fiber orientation is accentuated by infarction and may predispose to intraventricular reentry, and that intraventricular reentrant circuits that may be present on the epicardial surface may persist in a volume of myocardial tissue as small as 0.5 cc.

Animals↗
PubMed1984

Evaluation of arrhythmogenicity of surgically induced endocardial versus ischemic myocardial damage.

Ventricular tachyarrhythmias are common sequelae of ischemic myocardial damage. To assess the susceptibility to sustained ventricular tachycardia in a canine model in which endocardial excision was performed, 30 adult mongrel dogs were divided into three groups and studied in an open-chest condition, anesthetized under pentobarbital anesthesia, 7 to 14 days after undergoing one of three alternative procedures: (Group A) sham-operated controls, 10 dogs; (Group B) left ventricular endocardial excision, 10 dogs; and (Group C) myocardial infarction produced by a 2-hour occlusion and subsequent reperfusion of the left anterior descending coronary artery, 10 dogs. Using programmed ventricular pacing with two extrastimuli via plunge electrodes at 10 normal sites in the distribution of the left anterior descending coronary artery in each dog, sustained ventricular tachycardia was induced in 0/10 Group A dogs at 0/100 sites and in 0/10 Group B dogs at 0/100 sites; in contrast, in Group C, 7/10 (70%, p less than 0.01) dogs had inducible sustained ventricular tachycardia and at 39/70 (56%, p less than 0.001) sites. Thus, 7 to 14 days following endocardial excision, dogs are no more susceptible to the initiation of sustained ventricular tachycardia than are sham-operated control animals. This is in contrast to dogs with chronic heterogeneous infarctions (Group C) due to coronary occlusion and reperfusion, which are highly susceptible to ventricular tachycardia initiation.

Animals↗
PubMed1983

Cellular electrophysiologic characteristics of chronically infarcted myocardium in dogs susceptible to sustained ventricular tachyarrhythmias.

Standard microelectrode techniques were used to record transmembrane potentials and determine conduction characteristics in regions of mottled infarcts of canine epicardium, 3 to 5 days or 8 to 15 days after left anterior descending coronary artery occlusion and reperfusion. At 3 to 5 days, resting potential, action potential amplitude, maximal rate of depolarization and action potential duration at 30% repolarization were significantly reduced in the infarcted region. Cells on the epicardial surface showed improvement in resting potential, action potential amplitude and rate of depolarization between 3 to 5 days and 8 to 15 days after infarction. In normal noninfarcted tissues, conduction velocity parallel to fiber orientation was 0.54 +/- 0.06 m/s (mean +/- standard deviation). Slow conduction in infarcted regions ranged from 0.015 to 0.2 m/s. Action potentials recorded from slowly conducting regions tended to include cells with more depressed amplitude and rate of depolarization than other cells in infarcted regions; they also had inappropriately depressed overshoot relative to their resting potential. Action potentials in slowly conducting areas where local conduction block occurred were associated with prepotentials and notches on their depolarization and repolarization phases. The prepotentials and notches appeared to be caused by electrotonic interactions resulting from microcircuitous conduction around or across inexcitable areas. These findings demonstrate that areas of slow conduction are heterogenously distributed in the mottled infarct and suggest that disruptions in cell to cell electrical continuity and decreased excitability may contribute to this slow conduction.

Action Potentials↗
PubMed1983

Effect of coronary occlusion on arrhythmias and conduction in the ovine heart.

The proximal left circumflex coronary artery was occluded for 1 h in 16 open-chest sheep anesthetized with pentobarbital sodium. Epicardial conduction was monitored at three or four sites within the ischemic zone and one site in the normal zone. Eight of the sheep developed ventricular fibrillation within the first 15 min of occlusion; the remaining sheep survived the 1-h observation period. In the sheep that developed spontaneous ventricular fibrillation, the circumflex perfused a significantly greater amount of the left ventricle (44 +/- 3 vs. 39 +/- 3%; P = 0.008). The occurrence of spontaneous ventricular fibrillation was invariably preceded by a period of sustained (0.5-4 min) ventricular tachycardia. Six of the surviving sheep developed episodes of sustained (2-10 min) tachycardia that were self-terminating. The ischemic zone electrograms showed continuous fractionated electrical activity during both self-terminating tachycardias and tachycardias ending in fibrillation. The continuous epicardial electrical activity did not appear to cause the tachycardias but rather occurred as a result of the tachycardias. The genesis of ventricular tachycardia and fibrillation in this model may involve mechanisms different from ischemia-induced ventricular tachycardia and fibrillation in canine and porcine hearts.

Animals↗
PubMed1983

Reduced space constant in slowly conducting regions of chronically infarcted canine myocardium.

Experiments were performed to test the hypothesis that a reduction in the space constant contributes to slow conduction in the infarcted myocardium of dogs 5-8 days after coronary artery occlusion and reperfusion. Standard microelectrode techniques were used to measure action potential characteristics and conduction velocity parallel to fiber orientation in normal and infarcted ventricular epicardial strips superfused in a tissue bath. The space constants were determined by measuring the decay of the transmembrane steady state electrotonic potential with distance from a suction electrode current source. In eight normal epicardial preparations, conduction velocity ranged between 0.305 and 0.603 m/sec, and the space constant was between 0.712 and 1.202 mm. In 10 infarcted epicardial preparations, in regions of slow conduction (0.032-0.299 m/sec), the space constant was reduced to values between 0.281 and 0.917 mm. Action potential amplitude and maximum rate of depolarization were also reduced in infarcted myocardium. There was a direct relationship between conduction velocity and space constant and maximum rate of depolarization. In infarcted tissues, two types of slow conduction occurred. Slow conduction was uniform down to a velocity of approximately 0.181 m/sec, and a space constant of 0.523 mm. Below these values, conduction was discontinuous with prepotentials associated with the action potential upstroke. Indirect evidence from our studies suggests that a depression in action potential depolarization and an increase in effective axial resistance contribute approximately equally to uniform slow conduction in the infarcted myocardium.

Action Potentials↗
PubMed1983

Surgical therapy for ventricular tachyarrhythmias.

Recurrent sustained ventricular tachyarrhythmias unresponsive to medical therapy are associated with a one year mortality of 70 to 85 per cent. Patients who are susceptible to these re-entrant arrhythmias usually have a history of previous myocardial infarction or chronic myocardial ischemic disease. More specifically, these patients demonstrate both anatomic and electrophysiologic derangements. Experimental work suggests that regions of non-uniform damage render the ventricle most susceptible to ventricular tachyarrhythmias, and even relatively large areas of homogeneous myocardial ischemic damage may not display the same susceptibility to these arrhythmias. Surgical techniques are being devised to treat patients with ventricular tachyarrhythmias refractory to medical management. These have provided control of arrhythmias in patients whose disease was previously resistant to all medical treatment. The evolving surgical therapies presently employed share either of two physiopathologic consequences which render them successful: the homogeneous ablation of previous heterogeneous myocardial ischemic damage or the delimiting of an arrhythmogenic focus by excluding conduction to surrounding myocardium. Finally, antitachycardia and defibrillating devices have also been developed to facilitate the management of patients not controlled satisfactorily with either conventional or investigative drugs. The surgeon will need to be familiar with these devices as well.

Animals↗
PubMed1982

Inotropic, chronotropic and dromotropic effects of prenalterol, a new cardiostimulant drug.

Prenalterol (H 133/22) is an adrenergic beta-receptor stimulator which unlike isoproterenol is both orally active and has a long duration of action. The inotropic, chronotropic and dromotropic effects of prenalterol were investigated in pentobarbital anaesthetized dogs. Prenalterol was found to increase left ventricular maximum dP/dt in a dose-dependent manner up to a dose level of 50 micrograms/kg. Additional doses resulted in only small further increases in cardiac contractility. Electrophysiological studies were done to compare the effects of prenalterol and isoproterenol on sinus node and ventricular pacemaker function. Complete AV block was produced by electrocauterization of the His bundle. Prenalterol accelerated both ventricular and sinus node pacemakers at doses up to 50 micrograms/kg. The increase in ventricular rate was greater than the increase in sinus rate following supramaximal inotropic doses of prenalterol yet no ventricular extrasystoles were ever observed. Similar acceleration of the ventricular and sinus node pacemakers were observed by infusion of isoproterenol. Prenalterol and isoproterenol accelerated AV nodal conduction and ventricular conduction but had little effect upon His-Purkinje conduction. Sinus node reset time was abbreviated as was the functional and effective refractory periods of the atrium and AV nodes.

Animals↗
PubMed1982

Initiation of ventricular tachyarrhythmia with programmed stimulation: sensitivity and specificity in an experimental canine model.

Programmed stimulation (PS) is used in the catheterization laboratory and operating room to initiate and study malignant ventricular tachyarrhythmia (VT). The purpose of this study was to evaluate the specificity and sensitivity of PS in short-term studies of 10 normal animals (group A), 10 sham-operated controls (group B), and 10 dogs with chronic myocardial infarction susceptible to inducible VT by an occlusion-reperfusion method (group C). Groups B and C were studied 7 to 14 days after the initial procedure. the pH, PaO2, and PaCO2 were determined and corrected every 30 minutes during the procedure. When bipolar ventricular pacing with three ventricular extrastimuli was used, VT initiation was attempted at 10 normal intramyocardial sites in groups A and B and in close proximity (less than or equal to 1 cm) to areas of infarction in group C. When one ventricular extrastimulus was used during ventricular pacing, VT was induced in dogs with chronic infarctions (3 of 10, 30%, group C). Using two extrastimuli, however, VT was inducible in 4 of 10 (40%) of group A, 6 of 10 60%) of group B, and all 10 (100%) of group C. With three extrastimuli, all 30 dogs had inducible VT. Overall, PS with one extrastimulus was highly specific in 100% but insensitive in 30%. With two extrastimuli the sensitivity increased to 100%, but the specificity fell to 50%. Finally, with three extrastimuli the sensitivity was also 100%, but the specificity decreased to 0%. PS remains an invaluable technique in diagnosing and assessing therapy for patients with VT. The diagnostic implications of this test await more precise pathophysiologic elucidation of arrhythmic mechanisms.

Animals↗