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W M Smith

Publications and source records attributed to W M Smith.

At least 91 records · Page 5Linked to original sources
PubMed1995

Responses of the transmembrane potential of myocardial cells during a shock.

INTRODUCTION: The purpose of this investigation was to study the transmembrane potential changes (delta Vm) during extracellular electrical field stimulation. METHODS AND RESULTS: Vm was recorded in seven guinea pig papillary muscles in a tissue bath by a double-barrel microelectrode with one barrel in and the other just outside a cell while shocks were given across the bath. The short distance (15 to 30 microns) between the two microelectrode tips and alignment of the tips parallel to the shock electrodes eliminated the shock artifact. Following ten S1 stimuli, an S2 shock field created by a 10-msec square wave was delivered during the action potential plateau or during diastole through shock electrodes 1 cm on either side of the tissue. Four shock strengths creating field strengths of 1.7 +/- 0.1, 2.9 +/- 0.2, 6.1 +/- 0.6, and 8.8 +/- 0.9 V/cm were given for the same impalement. Both shock polarities were given at each shock strength. For shocks delivered during the action potential plateau, the magnitudes of the peak delta Vm caused by the above four potential gradients were 21.1 +/- 8.2, 33.6 +/- 13.6, 49.9 +/- 24.2, and 52.3 +/- 28.0 mV (P < 0.05 among the four groups) for the shocks causing depolarization and 37.9 +/- 14.2, 56.6 +/- 16.4, 83.1 +/- 19.4, and 92.9 +/- 29.1 mV (P < 0.05 among the four groups) for the shocks causing hyperpolarization. Though delta Vm increased as potential gradients increased, the relationship was not linear. The magnitude of hyperpolarization was 1.9 +/- 0.5 times that of depolarization when the shock polarity was reversed (P < 0.05). As potential gradients increased from 1.7 +/- 0.1 to 8.8 +/- 0.9 V/cm, the time constant of the membrane response decreased significantly from 3.5 +/- 1.8 to 1.6 +/- 0.7 msec for depolarizing shocks and from 6.0 +/- 3.1 to 3.4 +/- 1.9 msec for hyperpolarizing shocks (P < 0.01 vs depolarizing shocks). For shocks delivered during diastole, hyperpolarizing shocks induced triphasic changes in Vm during the shock, i.e., initial hyperpolarization, than depolarization, followed again by hyperpolarization. CONCLUSION: During the action potential plateau, the membrane response cannot be represented by a classic passive RC membrane model. During diastole, activation upstrokes occur even during hyperpolarization caused by shocks creating potential gradients between approximately 2 and 9 V/cm.

Animals↗
PubMed1995

Alteration of ventricular fibrillation by propranolol and isoproterenol detected by epicardial mapping with 506 electrodes.

INTRODUCTION: We hypothesized that drugs which alter ventricular refractoriness or excitability produce quantifiable changes in ventricular fibrillation. METHODS AND RESULTS: We used a 528-channel mapping system to quantify the effects of the beta-antagonist, propranolol, and the beta-agonist, isoproterenol, on activation patterns in ventricular fibrillation. A plaque of 506 (22 x 23) electrodes spaced 1.12 mm apart and covering about 5% of the ventricular epicardium was sewn to the anterior right ventricle in 18 pigs (30 kg). Propranolol (0.25 to 0.4 mg/kg) increased the refractory period at a right ventricular epicardial site while isoproterenol (3 to 5 micrograms/min) shortened it. Ventricular fibrillation was induced by programmed stimulation, and unipolar electrograms were recorded from the 506 plaque electrodes for 2 seconds beginning 1, 15, and 30 seconds after the onset of fibrillation. Active epicardial recording sites were identified from the first derivative of the unipolar potentials (dV/dt) detected at each electrode. Then, neighboring active sites were grouped into activation fronts by computer analysis. In six pigs the effect of repeated inductions of ventricular fibrillation was assessed by comparing ventricular fibrillation after saline with a preceding control episode of fibrillation. Each activation front excited 40% +/- 46% of the mapped region before blocking. No changes were observed with saline and multiple inductions of fibrillation. In another six pigs, ventricular fibrillation after propranolol was compared with a preceding control episode of fibrillation. Ventricular fibrillation after propranolol exhibited a decreased activation rate per epicardial recording site and fewer activation fronts per second. There was no change in the amount of tissue excited by each activation front or the number of reentry cycles per activation front compared with control. In addition, there was no change in the maximum negative dV/dt detected per activation at an epicardial site. In six pigs ventricular fibrillation during isoproterenol was compared with control episodes of ventricular fibrillation before and 45 minutes after washout of the drug. The control episodes of fibrillation were not different from each other. Compared with control, ventricular fibrillation during isoproterenol exhibited an increased activation rate per epicardial site, an increased amount of tissue excited by each activation front, and an increased maximum negative dV/dt for each activation. There was no change in the number of activation fronts per second or the number of reentry cycles per activation front compared with control. CONCLUSION: Quantitative analysis revealed that propranolol and isoproterenol do not have symmetrically opposite effects on ventricular fibrillation. Propranolol decreased the number of activation fronts while isoproterenol increased the amount of tissue excited by each activation front. Thus, drugs that alter ventricular refractoriness or excitability alter ventricular fibrillation.

Animals↗
PubMed1995

Choosing the optimal monophasic and biphasic waveforms for ventricular defibrillation.

INTRODUCTION: The truncated exponential waveform from an implantable cardioverter defibrillator can be described by three quantities: the leading edge voltage, the waveform duration, and the waveform time constant (tau s). The goal of this work was to develop and test a mathematical model of defibrillation that predicts the optimal durations for monophasic and the first phase of biphasic waveforms for different tau s values. In 1932, Blair used a parallel resistor-capacitor network as a model of the cell membrane to develop an equation that describes stimulation using square waves. We extended Blair's model of stimulation, using a resistor-capacitor network time constant (tau m), equal to 2.8 msec, to explicitly account for the waveform shape of a truncated exponential waveform. This extended model predicted that for monophasic waveforms with tau s of 1.5 msec, leading edge voltage will be constant for waveforms 2 msec and longer; for tau s of 3 msec, leading edge voltage will be constant for waveforms 3 msec and longer; for tau s of 6 msec, leading edge voltage will be constant for waveforms 4 msec and longer. We hypothesized that the best phase 1 of a biphasic waveform is the best monophasic waveform. Therefore, the optimal first phase of a biphasic waveform for a given tau s is the same as the optimal monophasic waveform. METHODS AND RESULTS: We tested these hypotheses in two animal experiments. Part I: Defibrillation thresholds were determined for monophasic waveforms in eight dogs. For tau s of 1.5 msec, waveforms were truncated at 1, 1.5, 2, 2.5, 3, 4, 5, and 6 msec. For tau s of 3 msec, waveforms were truncated at 1,2,3,4,5,6, and 8 msec. For tau s of 6 msec, waveforms were truncated at 2,3,4,5,6,8, and 10 msec. For waveforms with tau s of 1.5, leading edge voltage was not significantly different for the waveform durations of 1.5 msec and longer. For waveforms with tau s of 3 msec, leading edge voltage was not significantly different for waveform durations of 2 msec and longer. For waveforms with tau s of 6 msec, there was no significant difference in leading edge voltage for the waveforms tested. Part II: Defibrillation thresholds were determined in another eight dogs for the same three tau s values. For each value of tau s, six biphasic waveforms were tested: 1/1, 2/2, 3/3, 4/4, 5/5, and 6/6 msec. For waveforms with tau s of 1.5 msec, leading edge voltage was a minimum for the 2/2 msec waveform. For waveforms with tau s of 3 msec, leading edge voltage was a minimum for the 3/3 msec waveform. For waveforms with tau s of 6 msec, leading edge voltage was a minimum and not significantly different for the 3/3, 4/4, 5/5, and 6/6 msec waveforms. CONCLUSIONS: The model predicts the optimal monophasic duration and the first phase of a biphasic waveform to within 1 msec as tau s varies from 1.5 to 6 msec: for tau s equal to 1.5 msec, the optimal monophasic waveform duration and the optimal first phase of a biphasic waveform is 2 msec, for tau s equal to 3.0 msec, the optimal duration is 3 msec, and for tau s equal to 6 msec, the optimal duration is 4 msec. For both monophasic and biphasic waveforms, optimal waveform duration shortens as the waveform time constant shortens.

Animals↗
PubMed1995

Interventional cardiology in New Zealand.

Death rates from coronary heart disease in New Zealand are among the highest in the world although they have steadily fallen since a peak in 1968. The health care system is largely publicly funded with most cardiologists being salaried, although there has been a growth in fee-for-service private practice. Waiting times in public hospitals for bypass surgery can be years for chronic stable angina. The publicly funded health care system is being reformed. In 1993 there were in New Zealand, for a population of just less than 3.5 million: 6,227 coronary angiograms; 1,365 percutaneous interventions; and 1,513 coronary artery bypass only operations. The percutaneous intervention rate was 391 per million. There has been an increase in new device use so that in Auckland 11% of percutaneous interventions involved new devices.

Angioplasty, Balloon, Coronary↗
PubMed1995

Predicting the potential gradient field in ventricular fibrillation from shocks delivered in paced rhythm.

A method of defibrillation threshold determination that utilizes low-strength shocks delivered in a benign rhythm would be desirable. Because the two-dimensional epicardial potential gradient (PG) is a shock parameter that is linked to defibrillation, we examined whether the epicardial PG measured for shocks delivered in paced rhythm could be used to predict the PG for defibrillation-strength shocks delivered in ventricular fibrillation (VF). In six open-chest pentobarbital-anesthetized pigs with left ventricular apex and right atrial internal defibrillation patches, we measured the epicardial PG field for shocks delivered in paced rhythm and during VF. We determined that there was a linear relationship between epicardial PG and shock strength for shocks delivered in paced rhythm. However, prediction of the PG measured for shocks in VF from those measured in paced rhythm resulted in a statistically significant overestimation of the PG in VF. We conclude that, for equivalent strength shocks, the epicardial PG field is weaker for shocks delivered in VF. This change in the potential gradient field can have an effect on defibrillation threshold estimates that are based on shocks delivered in paced rhythm.

Animals↗
PubMed1995

Optical transmembrane potential measurements during defibrillation-strength shocks in perfused rabbit hearts.

To study the optical transmembrane potential change (delta F) induced during shocks, optical recordings were obtained in 15 isolated perfused rabbit hearts treated with the potentiometric dye di-4-ANEPPS and diacetyl monoxime. Shock electrodes were sutured on the right and left ventricles. A laser beam 30 microns in diameter was used to optically excite di-4-ANEPPS. Fluorescence from a region 150 microns in diameter was recorded during a shock. In the macroscopic study (six animals), there were nine recording spots that were 3 mm apart between the two shock electrodes. In the microscopic study, there were three recording regions that were 3 mm away from either shock electrode and midway between them, with nine recording spots that were 30 microns (three animals), 100 microns (three animals), and 300 microns (three animals) apart in each region. After 20 S1 stimuli, a 10-ms truncated exponential S2 shock of defibrillation-threshold strength was given during the plateau of the last S1 action potential. In the microscopic study, shocks were also given during diastole, with delta F recordings at the three recording regions. Shocks of both polarities were tested. delta F during the shock was expressed as a percentage of the fluorescence change during the S1 upstroke action potential amplitude (the S1 Fapa), ie, delta F/Fapa%. In the macroscopic study, the magnitudes of delta F/Fapa% from recording spots 1 to 9, numbered from the left to the right ventricular electrodes, were 77 +/- 41%, 46 +/- 32%, 32 +/- 27%, 28 +/- 20%, 37 +/- 25%, 24 +/- 20%, 33 +/- 22%, 37 +/- 25%, and 59 +/- 29%, respectively (P < .05 among the nine spots). Depolarization or hyperpolarization could occur near either shock electrode with both shock polarities, but the magnitude of hyperpolarization was 1.8 +/- 0.9 times that of depolarization at the same recording spot when the shock polarity was reversed (P < .01). In the microscopic study, the change in delta F/Fapa% varied significantly over the microscopic regions examined. The maximum values of delta F/Fapa% for hyperpolarizing shocks during diastole reached only 7 +/- 10% of those for shocks during the plateau (P < .01). During diastole, the time until a new action potential occurred after the beginning of the shock was shorter when the membrane was depolarized (1.1 +/- 0.5 ms) than when it was hyperpolarized (12.8 +/- 9.1 ms, P < .01). Conclusions are as follows: (1) A shock can induce either hyperpolarization or depolarization. (2) Hyperpolarization or depolarization during a shock can occur near either the anodal or cathodal shock electrode. (3) Variation of delta F/Fapa% exists within a microscopic region.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1995

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

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

Animals↗
PubMed1994

An automated technique for identification and analysis of activation fronts in a two-dimensional electrogram array.

Cardiac activation sequences are normally determined by (i) the detection and timing of local activations in cardiac electrograms, (ii) the grouping together of activations in different electrodes that are generated by the same activation fronts, and (iii) the construction by interpolation of isochronal maps showing the pathways of the activation fronts. This process is typically carried out by manual or semiautomated methods. These methods are usually adequate for stable, repeatable rhythms in normal hearts. However, in situations in which the electrograms are distorted, as in those recorded from abnormal myocardium, or the mapped rhythms are rapidly changing, as in ventricular fibrillation, they are tedious and time-consuming and yield results that are subjective and not repeatable from one investigator to another. Therefore, we developed a computer-based method for automating the identification and analysis of activation fronts recorded from a large array of electrodes. The electrodes are closely spaced (1 mm) so that interpolation is not required. Electrodes are identified as recording an activation when the temporal derivative of the potential is more negative than a user-specified value. Activations occurring less than a user-specified distance apart in time and space are identified as part of the same activation front. Characteristics of the activation fronts, such as their number, size, and the presence of reentry or collision, are then quantified. The differences between the results obtained by this automated method and those obtained by four human investigators was no greater than the differences in results among the four investigators themselves. Because the method is automated and algorithmic, it is both rapid and repeatable.

Algorithms↗
PubMed1994

Acute treatment of paroxysmal tachycardia by adenosine.

BACKGROUND: Adenosine has proven efficacy in clinical trials and in the electrophysiological laboratory for the treatment of paroxysmal tachycardia. AIMS: To evaluate the efficacy and safety of adenosine administered in a clinical setting by non-consultant staff. METHODS: Incremental doses of adenosine were administered intravenously to five children and 32 adults during 39 episodes of paroxysmal tachycardia in a clinical setting. Structural heart disease was present in 43% of patients. RESULTS: Of 35 episodes of narrow complex tachycardia, adenosine terminated 26 of 28 episodes of supraventricular re-entrant tachycardia (SVRT), one episode of ectopic atrial tachycardia, and induced transient atrioventricular block to reveal atrial arrhythmias in four. Termination of SVRT occurred at a mean (SD) dose of 9.2 (4.0) mg in adults and 0.09 (0.04) mg/kg in children, but two patients had later spontaneous reinitiation of SVRT. Two patients with narrow complex tachycardia who failed to respond to adenosine were subsequently found to have ventricular tachycardia. Adenosine was therapeutic or diagnostic in three of four episodes of broad complex tachycardia. Overall, by intention to treat by the clinician, adenosine was therapeutic or diagnostic in 34 of 39 episodes (87%). Breathlessness (26%), chest tightness (18%) and flushing (18%) occurred transiently. There were no episodes of hypotension. Adenosine was given safely to 15 patients in whom verapamil was considered contraindicated. CONCLUSIONS: Adenosine is a safe treatment for both narrow and broad complex tachycardias; usually effective for the former and diagnostic for the latter.

Acute Disease↗
PubMed1994

Strength-interval curves in canine myocardium at very short cycle lengths.

While ventricular electrophysiological properties have been intensively studied at normal heart rates, little is known about these properties at the very short cycle lengths (approximately 100 msec), which are present in ventricular fibrillation. We examined refractoriness in the right ventricles of six dogs at stimulation intervals of 80 to 300 msec. Starting at 300 msec, the basic (S1) cycle length was decremented by 10 msec each beat to 200, 150, or 125 msec. A 1-msec premature (S2) stimulus of 1, 5, 10, or 20 mA was then introduced. The S1-S2 interval was decremented until capture was lost. The refractory period was considered to be the shortest interval that captured the heart for each S2 strength. Only pacing episodes that did not induce fibrillation were included. Strength-interval curves maintained the same hyperbolic shape but shifted to very short refractory periods as the S1-S1 interval was decreased. At the shortest S1-S1 intervals, premature stimuli were capable of capturing the heart without inducing ventricular fibrillation for S1-S2 intervals as short as 83 +/- 3 msec. Thus, decremental rapid pacing can produce refractory periods shorter than the cycle length during ventricular fibrillation. This finding suggests that there is no need to postulate a discontinuous jump to new electrophysiological properties or relationships at the onset of fibrillation, but that the capability for fibrillation is an integral part of normal electrophysiological parameters when they are pushed to values that do not occur normally. The results of this study should be useful in the further development of active membrane models and cellular automata models of cellular electrical behavior.

Animals↗
PubMed1994

The probability of defibrillation success and the incidence of postshock arrhythmia as a function of shock strength.

The effects of high voltage defibrillation shocks given to six swine were studied to determine if there is a limit to the advantage gained from increasing the shock strength. An endocardial electrode was placed in the right ventricle, and a 114-cm2 cutaneous patch was placed on the left lateral thorax. Monophasic (10 msec) and single capacitor biphasic (5/5 msec) shocks with leading edge voltages of 200, 400, 600, 800, and 990 volts (approximately 2.3-59 J) were tested. For monophasic shocks, the probability of successful defibrillation ranged from 0% at 200 V to 90% at 990 V. The incidence of postshock arrhythmia increased from 0% for successful shocks at 600 V to 67% for successful shocks at 990 V. For biphasic shocks, the probability of success peaked at 97% for the 600-, 800-, and 990-V shocks. The incidence of postshock arrhythmia increased from 8% at 400 V to 55% at 990 V. Although more postshock arrhythmias occurred at lower strengths for biphasic than for monophasic shocks, an efficacy criterion, quantifying the probability of defibrillation success and the probability that a postshock arrhythmia will not occur, was always higher for biphasic shocks. The probability of success never reached 100% for either waveform while the incidence of postshock arrhythmia increased as the shock strength increased. In conclusion, for the catheter-patch electrode configuration, increasing the shock strength does not always improve the probability of success and may increase the incidence of postshock arrhythmia.

Animals↗
PubMed1994

Prolongation and shortening of action potentials by electrical shocks in frog ventricular muscle.

Effects of electrical shocks on myocardium are important for defibrillation. We measured effects of shocks (5 ms, 1-40 V/cm) in isolated frog ventricular strips. We recorded contraction strength and intracellular action potential (AP) with a shock-voltage cancellation technique to allow recordings immediately after shocks. Shocks of > or = 5 V/cm produced a dose- and latency-dependent prolongation of the AP ongoing during the shock. Stronger shocks of 28-40 V/cm decreased the duration, maximum diastolic potential, amplitude, and maximum rate of rise of the phase zero depolarization of paced APs that began after the shock. The contraction strength increased 43 and 59% during the 10 s after the stronger shocks. The transmembrane potential was shifted toward 0 mV immediately after the stronger shocks. We concluded that weak or strong shocks prolong the AP ongoing during the shock, whereas sufficiently strong shocks also shorten APs that begin after the shock. AP prolongation and shortening may be important for defibrillation and acceleration of tachycardia after failed cardioversion shocks.

Action Potentials↗
PubMed1994

Effects of peroneal nerve stimulation on hypothalamic stimulation-induced ventricular arrhythmias in rabbits.

We tested the hypothesis that peripheral afferent nerve stimulation decreases the incidence of ventricular arrhythmias induced by central nervous system stimulation. The hypothalamus in each of 24 anesthetized rabbits (12 with anterior myocardial ischemia) was electrically stimulated for 10 s with 10-min intervals between each of six consecutive stimulation episodes. The left peroneal nerves were electrically stimulated for 15 min beginning 5 min after the second hypothalamic stimulation episode in six ischemic and six nonischemic rabbits. Cardiac rhythm was monitored with the electrocardiogram lead I and atrial and ventricular electrograms. Hypothalamic stimulation alone induced ventricular arrhythmias [mean no. of arrhythmic beats occurring during 3rd and 4th hypothalamic stimulation episodes: nonischemic animals, 20 +/- 8; ischemic animals, 62 +/- 41 (P < 0.05 by unpaired t-test)]. Peroneal nerve stimulation reduced the number of arrhythmic beats induced by hypothalamic stimulation in nonischemic animals (6 +/- 5; P < 0.05 vs. without peroneal stimulation) and prevented an increase in arrhythmic beats during ischemia (21 +/- 16). Thus peripheral nerve stimulation decreased the number of ventricular arrhythmic beats induced by repeated hypothalamic stimulation in both ischemic and normal rabbit hearts and may be important in the prevention of arrhythmias in patients.

Afferent Pathways↗
PubMed1994

Magnetic resonance imaging of chronic myocardial infarcts in formalin-fixed human autopsy hearts.

BACKGROUND: In post-myocardial infarction patients, three-dimensional structure of the infarct as well as infarct size are likely to be important factors affecting mortality, cardiac function, and arrhythmias. Current morphological methods for determining three-dimensional infarct structure in autopsied hearts are inexact and time consuming. The cardiac magnetic resonance imaging techniques used in living patients have shown potential in determining infarct size and structure but have limited resolution for morphometric postmortem studies. The recent development of magnetic resonance microscopy raises the possibility that three-dimensional infarct structure can be quantified at microscopic levels in autopsied hearts. The purpose of this study was to determine the ability of magnetic resonance imaging at different spatial resolutions to differentiate infarcted from noninfarcted myocardium. METHODS AND RESULTS: Magnetic resonance imaging was performed at 2.0 T on cross sections taken from 10 autopsied hearts containing old myocardial infarcts. T1 was derived from six images with repetition times (TRs) for each image ranging from 100 to 3200 milliseconds. T2 was derived from multi-echo images with echo times (TEs) ranging from 10 to 60 milliseconds. Resolution was approximately 400 x 400 microns in 2-mm-thick slices. Sites of infarcted and noninfarcted tissue were identified from histological sections taken from each slice, and the T1 and T2 values of these sites were obtained. Microscopic images were acquired with voxels of 100 x 100 x 625 microns, representing tissue volumes more than 1000-fold smaller than conventional clinical images. In all cases, T1 of infarcted tissue (459 +/- 266 milliseconds, mean +/- SD) was greater than that of noninfarcted tissue (272 +/- 163 milliseconds). Also, in all cases, T2 of infarcted tissue (49 +/- 14 milliseconds) was greater than that of noninfarcted tissue (35 +/- 8 milliseconds). CONCLUSIONS: T1 and T2 values for infarcted tissue are significantly different from those of noninfarcted tissue (P < .001). Based on these findings, it should be possible to develop techniques to perform three-dimensional imaging and quantitation of infarcts with a resolution of 400 microns or less. When volumetric three-dimensional imaging was performed using a T1-weighted sequence, the resulting 256(3) arrays supported isotropic resolution at 400 microns (voxel volume, 0.064 mm3). Subsequent volume rendering using a compositing algorithm clearly shows the infarcted areas in three dimensions. The techniques demonstrate the potential for quantitative three-dimensional cardiac morphometry using magnetic resonance imaging.

Algorithms↗
PubMed1993

Evaluation of an automatic cardiac activation detector for bipolar electrograms.

The identification of local activation events in bipolar cardiac electrograms, the first step of isochronal map construction, is a time-consuming and difficult process. Owing to the variability among bipolar activation complexes and the lack of practical knowledge concerning the relationship of the bipolar waveform to action potential characteristics, a set of empirical rules to guide the assignment of local activation times have been adopted. A computer program, called AP, has been designed, which implements these rules in the form of a syntactic analyser. Canine epicardial recordings were used to evaluate AP by comparing local activation times, assigned by AP, with times assigned independently by three investigators. The Hermes-Cox model for detector evaluation and a bootstrap statistical method were used in conjunction with ROC analysis to evaluate the ability of AP to detect events. Analysis of discrepancies among investigator-assigned times showed that the reliabilities of AP event detection and AP-assigned times were comparable to those of the investigators. The methods used in system design and evaluation are applicable to a broad range of problems in the detection and localisation of waveform components.

Animals↗
PubMed1993

Efficient electrode spacing for examining spatial organization during ventricular fibrillation.

Spatial organization has been observed during episodes of ventricular fibrillation (VF) by recording epicardial unipolar electrograms on a grid of electrodes. In such studies, the choice of spacing between electrodes is an important decision, affecting the resolution and the size of the domain to be studied. A basic tenet of sampling theory, the Nyquist criterion, states that an electrode spacing smaller than half the smallest significant wavelength is required to capture the important details of a spatially sampled process. In this paper, we suggest a method to choose a practical interelectrode spacing by examining wavenumber power spectra of high-resolution VF data recorded from a square 11 x 11 array of electrodes spaced 0.28 mm apart. The plaque was sutured on the epicardium near the left ventricular apex in seven anesthetized pigs. VF was induced with ac simulation. Unipolar extracellular electrograms were simultaneously recorded from each channel for 2 s after the induction of VF. Each signal was sampled in time at 1000 Hz. Wavenumber power spectra were calculated for 100 ms segments using the zero-delay wavenumber spectrum method, for a total of 140 power spectra. All spectra had dominant peaks at the origin and fell off rapidly with increasing wavenumber (decreasing wavelength). In all the spectra, every wavelength shorter than 1.4 mm contributed insignificant power. Furthermore, in 134 of 140 spectra (96%), insignificant power levels were associated with every wavelength shorter than 2.8 mm. These results suggest that, for unipolar extracellular electrodes, an intersensor spacing on the order of 1 mm is appropriate to study organization during early VF.

Animals↗
PubMed1993

Effective defibrillation in pigs using interleaved and common phase sequential biphasic shocks.

Previous studies have shown that low internal defibrillation thresholds (DFTs) can be attained by using two pairs of electrodes and combining biphasic shocks with sequential timing. The purpose of this two-part study was to test the defibrillation efficacy of two new shock sequences, an interleaved biphasic, and a common phase sequential biphasic, that utilized two pairs of electrodes and were developed from the concept of sequential biphasic shocks. In the first part, defibrillation catheters were placed in the right ventricle and the superior vena cava of six anesthetized pigs. A small patch electrode was placed on the LV apex through a subxiphoid incision and a cutaneous patch was placed on the left thorax. The mean DFT energies for the interleaved biphasic (5.2 +/- 0.4 J) and the common phase sequential biphasic waveforms (5.4 +/- 0.4 J) were substantially less (P < 0.0001) than those for either the sequential monophasic (10.6 +/- 1.0 J) or single biphasic waveforms (9.0 +/- 1.0 J). In the second study, which used nine anesthetized pigs, the importance of phase reversal was demonstrated by the finding that the DFT energy of a common phase sequential biphasic shock (6.2 +/- 0.4 J) was much less than a common phase sequential monophasic shock (17.9 +/- 1.3 J, P < 0.0001); furthermore, the average DFT for four common phase sequential biphasic configurations (5.7 +/- 0.2 J) was much less than for a configuration that was similar except that current flow was not reversed in one phase so that no biphasic effect was present (19.7 +/- 1.2 J). The efficacy of common phase sequential biphasics was comparable to that of sequential biphasics. The effectiveness of sequential biphasics, interleaved biphasics, and common phase sequential biphasics is possibly due to two mechanisms: (A) an increase in the potential gradient during a later phase in regions that were low during the first phase, and (B) the exposure of most of the myocardium to a biphasic shock that reduces the minimum extracellular potential gradient needed to defibrillate.

Animals↗