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Biomedical subjects

R E Ideker

Publications and source records attributed to R E Ideker.

At least 19 recordsLinked to original sources
PubMed1992

Correlation of the complete version of the Selvester QRS scoring system with quantitative anatomic findings for multiple left ventricular myocardial infarcts.

The correlation between myocardial infarct size estimated by the complete version of the Selvester QRS scoring system and that documented by pathoanatomic studies has been reported for single anterior, inferior and posterolateral infarcts. Although previous studies described electrocardiographic changes in patients with multiple infarcts, no quantitative documentation of the ability of such changes to estimate the total amount of left ventricular infarction has been reported. This study of 32 patients with anatomically documented multiple infarcts shows a significant correlation between QRS-estimated and anatomically documented sizes (r = 0.44; p = 0.01), which is less than that previously reported for single infarcts in the anterior, inferior and posterolateral locations. Several of the 54 electrocardiographic criteria were never satisfied. Criteria for posterior infarction were seldom present, suggesting "cancellation effect" of coexisting anterior infarction. These results will be the basis for future modification of QRS criteria for estimating myocardial infarct size.

Adult↗
PubMed1992

Defibrillation electrode configurations developed from cardiac mapping that combine biphasic shocks with sequential timing.

Previous canine mapping studies of the transvenous defibrillation lead configuration of right ventricle (RV) to left R2 patch (P) revealed regions of low potential gradient in the left ventricular apex (A) and the right ventricular outflow tract (O). Thus 16 new lead configurations were tested in eight dogs, which incorporated electrodes in A and O to raise the gradient. When used in conjunction with two sequential biphasic shocks, the average defibrillation threshold energy from these configurations was 57% lower than that produced by a single biphasic shock delivered through RV-->P (phase 1 cathode-->anode, p < 0.001). Of the 16 configurations tested, the most effective was RV-->P followed by A-->O. When the shocking order of this configuration was reversed in another eight dogs, no difference in defibrillation efficacy was noted. In individual configurations of RV-->P and A-->O that used a single biphasic shock, defibrillation was not effective. Finally, when two sequential biphasic shocks were delivered to the same two electrodes in seven other dogs, the defibrillation efficacy was low. Thus configurations that use two sequential biphasic shocks can produce low defibrillation thresholds when the shocks are delivered to two different sets of electrodes. The high efficacy may be caused by one shock increasing the potential gradient in regions of low potential gradient that are produced by the other shock.

Animals↗
PubMed1992

Evaluation of a QRS scoring system for estimating myocardial infarct size. VIII. Specificity in a control group with left ventricular hypertrophy and proposal of a new scoring system for use with this confounding factor.

Electrocardiographic differentiation between left ventricular hypertrophy (LVH) and myocardial infarction (MI) is often difficult because both diagnoses are based primarily on QRS changes on the electrocardiogram (ECG). The specific goal of this study was the development of ECG criteria that could be used with the complete Selvester QRS scoring system for MI size in patients with LVH. A study population of 127 patients had significant aortic valve disease verified by cardiac catheterization. Inclusion in the study required no significant coronary artery disease, no focal contraction abnormality on the left ventriculogram, and no documented MI. Quantitative criteria for LVH developed by Bonner (IBM) and also those developed by the Cornell group were used to determine the ECG evidence for LVH in each patient. One or both sets of criteria were met in 110 (87%) of the 127 patients. This group was compared to a previously evaluated control population of 500 normal subjects. The complete 54-criteria, 32-point QRS MI size scoring system was applied to the 12-lead ECG of both groups. The score was 98% specific in the normal controls and 73% specific in the LVH group using a score of greater than 3 points as diagnostic for MI. Of the 54 individual QRS criteria, 16 failed to achieve 95% specificity in the LVH population: 13 were for anterior (and apical), 2 for inferior, and 1 for posterior locations. Of these 16, minor modifications to 11 were sufficient to achieve the 95% specificity standard.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiomegaly↗
PubMed1992

Rigid and flexible thin-film multielectrode arrays for transmural cardiac recording.

Thin-film transmural cardiac multielectric arrays were fabricated using integrated-circuit processing techniques. Several substantial improvements were achieved over conventional handmade arrays such as a smaller cross-sectional area, a larger number of recording sites per needle, more accurately controlled size and spacing of the recording sites, smaller bipolar spacings, and higher throughout yield. These advantages allow for a higher density of closely spaced bipolar electrodes capable of monitoring complex voltage and gradient fields present during ventricular fibrillation and defibrillation. Both rigid and flexible arrays were fabricated and used in the acquisition of transmural electrical signals. The rigid multielectrode arrays were made of gold electrodes on a molybdenum substate, and the flexible arrays of silver and gold electrodes on a polyimide substrate. In vitro and in vivo testing of the thin-film transmural cardiac multielectrode arrays indicates that there are no adhesion or delamination problems observed during acute studies, no implantation difficulties, and that unipolar and bipolar recordings during normal sinus rhythm and injury potentials in unipolar recordings are similar to those obtained using the handmade electrodes.

Animals↗
PubMed1992

A comparison of measured and calculated intracavitary potentials for electrical stimuli in the exposed dog heart.

The objective of this paper is to test the feasibility of using a multielectrode, intracavitary probe to solve a forward problem in which measured intracavitary potentials are compared to those calculated from subendocardial potentials and left ventricular (LV) cavity geometry. Intracavitary potentials and subendocardial potentials are measured simultaneously during electrical pacing stimuli from the LV apex, LV anterior base, LV posterior base, and right ventricular (RV) outflow tract of three exposed dog hearts. The LV cavity geometry is measured from postmortem magnetic resonance microscopy images of fixed hearts. Boundary integrals are approximated using a boundary element method and solved for intracavitary potentials. Correlation coefficients for LV apical pacing episodes are 0.989 +/- 0.002 while those for nonapical pacing episodes are 0.873 +/- 0.092. These results indicate that for electrical pacing from the apex, intracavitary stimulus potentials can be calculated with a high degree of accuracy. For nonapical pacing locations, the accuracy decreases since the calculations are more sensitive to errors in measuring probe position and LV cavity geometry near the septum. These results show that accurate geometric measurements of the intracavitary probe position and subendocardial surface are the primary concerns in solving future forward and inverse problems using an intracavitary probe.

Animals↗
PubMed1992

Calculating endocardial potentials from epicardial potentials measured during external stimulation.

This paper presents a boundary integral method for calculating the potential field generated by external stimulation at locations within the heart using realistic heart geometry and samples of the potential taken from the epicardial surface. This method assumes the heart is homogeneous and isotropic. To test the method we made epicardial and endocardial measurements in dogs during transthoracic pacing stimuli. From the epicardial potential measurements we predicted the endocardial potential values and compared them with the measured data. Despite the seemingly gross assumptions, the mean correlation coefficient between the measured and predicted potentials for three dogs and eleven stimulation electrode configurations was 0.985, and the mean rms error was 17%.

Action Potentials↗
PubMed1992

Propagation versus delayed activation during field stimulation of cardiac muscle.

This modeling study seeks to explain the experimentally detected delay between the application of an electric field and the recorded response of the transmembrane potential. In this experiment, conditions were deliberately set so that the field should excite all cells at once and so that no delay should be caused by a propagating wave front. The explanation of the observed delay may lie in the intrinsic properties of the membrane. To test this hypothesis, the strength latency curves were determined for three cases: (1) for a membrane patch model, in which the membrane is uniformly polarized and its intrinsic properties can be studied; (2) for the cardiac strand directly excited by the electric field; and (3) for the cardiac strand excited by a propagating wave front. The models of the membrane patch and the directly excited strand yield excitation delays that are comparable to those observed experimentally in magnitude and in the overall shape of the strength latency curves. The delays resulting from propagation are, in general, dependent on the position along the strand, although for some positions the strength latency curves for propagation are similar to those obtained from the directly activated strand and from the patch model. Therefore, the delay in excitation does not necessarily imply the presence of propagating wave fronts and can be attributed to intrinsic membrane kinetics.

Animals↗
PubMed1992

High and low strength nonsynchronized shocks given during canine ventricular tachycardia.

UNLABELLED: Cardioversion shocks given during ventricular tachycardia may cause ventricular fibrillation or acceleration of ventricular tachycardia, or arrest the tachycardia. A recently proposed theory may explain why the former two phenomena may occur. Briefly, this theory states that potential gradient shock fields of a critical strength delivered to tissue with a critical degree of refractoriness will cause circulating wave fronts of ventricular activation ("rotors") manifest as ventricular arrhythmia. We tested this theory by delivering nonsynchronized shocks 50% higher than defibrillation threshold or 50% lower than defibrillation threshold during 275 episodes of ventricular tachycardia in eight dogs with 5- to 7-day-old myocardial infarcts. Shocks stronger than the defibrillation threshold are likely to create shock fields in the ventricles everywhere stronger than this critical value, and therefore would not generate rotors. Shocks less strong than the defibrillation threshold may create shock fields within the ventricles that include the critical value, and therefore cause rotors if given when critically refractory tissue is present. Nonsynchronized shocks were used to increase the likelihood of encountering tissue with a critical degree of refractoriness. Ventricular fibrillation or acceleration of ventricular tachycardia occurred following 83 of 138 (60%) low strength shocks and following 20 of 137 (14.6%) high strength shocks. The pooled odds ratio for induction of ventricular fibrillation or accelerated ventricular tachycardia after low strength shocks as compared to high strength shocks was 8.9. CONCLUSION: when given during ventricular tachycardia, low strength shocks are much more likely to cause ventricular fibrillation or accelerated ventricular tachycardia than are high strength shocks (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

High-current stimuli to the spared epicardium of a large infarct induce ventricular tachycardia.

BACKGROUND: Previous studies have demonstrated that both ventricular tachycardia (VT) and ventricular fibrillation (VF) may begin as figure-eight reentry: VT with a longer cycle length from spared tissue adjacent to an infarct by programmed stimulation and VF with a shorter cycle length from noninfarcted tissue by a large premature S2 stimulus. These results suggest that the type of tissue or cycle length of the arrhythmia rather than the mode of induction determines whether the figure eight becomes sustained VT or degenerates into VF. Thus, a protocol similar to that by which a VF threshold is determined may induce VT rather than VF when performed in the spared tissue over an infarct. METHODS AND RESULTS: In 10 dogs, 4 days after occlusion-reperfusion of the left anterior descending coronary artery, 10 S1 stimuli were delivered from a total of 34 right and left ventricular sites outside the infarct. An epicardial S2 stimulus over the infarct was increased in 10-mA steps and introduced in diastole at decreasing cycle lengths of 5 msec until VT or VF was induced. Sustained monomorphic figure-eight VT was induced from 24 S1 sites and VF from nine (p = 0.03). The mean cycle lengths for the initial six arrhythmic cycles was 152 +/- 33 msec for VT and 115 +/- 13 msec for VF (p less than 0.001). Mean transmural infarct extent was 80% in five dogs with only VT, 63% in three dogs with both VT and VF, and 15% in two dogs with only VF. Different morphologies of VT were induced by changing the S1 site, the S2 strength, or the S1S2 coupling interval. In 25 of the 34 arrhythmias, the central part of the initial figure-eight pathway was oriented opposite the S1 activation sequence in that region. CONCLUSIONS: A large S2 stimulus over a nontransmural infarct induces VT if the spared myocardium is thin. This study introduces a useful technique for inducing sustained monomorphic VT in which the location and direction of the figure-eight pathway are known a priori and in which different morphologies of sustained VT can be produced by changing the S1 site.

Animals↗
PubMed1992

Cardiac potential and potential gradient fields generated by single, combined, and sequential shocks during ventricular defibrillation.

BACKGROUND: Potential gradient field determination may be a helpful means of describing the effects of defibrillation shocks; however, potential gradient field requirements for defibrillation with different electrode configurations have not been established. METHODS AND RESULTS: To evaluate the field requirements for defibrillation, potential fields during defibrillation shocks and the following ventricular activations were recorded with 74 epicardial electrodes in 12 open-chest dogs with the use of a computerized mapping system. Shock electrodes (2.64 cm2) were attached to the lateral right atrium (R), lateral left ventricular base (L), and left ventricular apex (V). Four electrode configurations were tested: single shocks of 14-msec duration given to two single anode-single cathode configurations, R:V and L:V, and to one dual anode-single cathode configuration, (R+L):V; and sequential 7-msec shocks separated by 1 msec given to R:V and L:V (R:V----L:V). Defibrillation threshold (DFT) current was significantly lower for R:V----L:V than for the other configurations and markedly higher for L:V. Despite these differences, the minimum potential gradients measured at DFT were not significantly different (approximately 6-7 V/cm for each electrode configuration). Potential gradient fields generated by the electrode configurations were markedly uneven, with a 15-27-fold change from lowest to highest gradient, with the greatest decrease in gradient occurring near the shock electrodes. Although gradient fields varied with the electrode configuration, all configurations produced weak fields along the right ventricular base. Early sites of epicardial activation after all unsuccessful shocks occurred in areas in which the field was weak; 87% occurred at sites with gradients less than 15 V/cm. Ventricular tachycardia originating in high gradient areas near shock electrodes followed 11 of 67 successful shocks. CONCLUSIONS: These data suggest that 1) defibrillation fields created by small epicardial electrodes are very uneven; 2) achievement of a certain minimum potential gradient over both ventricles is necessary for ventricular defibrillation; 3) the difference in shock strengths required to achieve this minimum gradient over both ventricles may explain the differences in DFTs for various electrode configurations; and 4) high gradient areas in the uneven fields can induce ectopic activation after successful shocks.

Animals↗
PubMed1992

Three-dimensional potential gradient fields generated by intracardiac catheter and cutaneous patch electrodes.

BACKGROUND: Defibrillation may be improved if electrode configurations can be found that create a larger and more even voltage gradient field across the heart. This study determined the magnitude of the shock gradient fields generated by four nonthoracotomy electrode configurations for defibrillation. METHODS AND RESULTS: In six dogs, a catheter was inserted containing a right ventricular apical electrode (V) and a right atrial electrode (A). A cutaneous patch electrode (P) was placed on the left lateral thorax. Shock potentials were recorded simultaneously from 128 electrodes in the left ventricular and right ventricular subepicardium and subendocardium, ventricular septum, and atria. With the chest closed, 50-mA shocks were given during diastole via the following lead configurations: V----A (V, cathode; A, anode); V----P; V----A+P; and V+A----P. Potential gradients were calculated at the subepicardium and subendocardium in millivolts per centimeter per volt of shock. In most dogs, the V----A+P configuration produced higher gradients throughout the ventricles than did V----A, V----P, or V+A----P. The maximum potential gradient was smaller for the V+A----P configuration than for V----A, V----P, or V----A+P. The gradient fields for the configurations with the catheter alone or combined with P were uneven. CONCLUSIONS: It is possible to estimate shock gradient fields in three dimensions. Of the four configurations tested, V----A+P produced the highest gradients and V+A----P produced the lowest high gradient. The gradient fields were uneven throughout the ventricles.

Animals↗
PubMed1992

Effect of pulse separation between two sequential biphasic shocks given over different lead configurations on ventricular defibrillation efficacy.

BACKGROUND: Two sequential biphasic shocks delivered over separate lead configurations markedly improve defibrillation efficacy compared with a single shock alone. We investigated the effect of varying the intershock interval between sequential biphasic shocks on defibrillation. METHODS AND RESULTS: Defibrillation thresholds (DFTs) were obtained in six dogs for shock separations ranging from 0.2 to 125 msec. The first shock was given from a catheter electrode in the right ventricular apex to a patch on the left lateral thorax; the second was from a small patch on the left ventricular apex to a catheter electrode in the right ventricular outflow tract. When the interval between shocks was less than or equal to 10 msec or greater than or equal to 75 and less than or equal to 125 msec, the mean DFTs were less than that previously found for the first shock by itself (4.2 versus 7.4 J, p = 0.002). At a separation of 50 msec, however, there was a marked rise in the DFT to 27 J. The mean DFT for the second shock at a delay of 50 msec was not different from the mean DFT previously found for the second shock by itself (7.2 versus 7.0 J). These results were confirmed in another six dogs using defibrillation probability-of-success curves. In 12 other dogs, probability-of-success curves were generated for delays between shocks as a percentage of the activation interval during ventricular fibrillation. Minimum defibrillation energy requirements were at two separations, 0.2 msec and 90% of the activation interval. CONCLUSIONS: The optimal intershock interval between two sequential biphasic shocks is either less than or equal to 10 msec or greater than or equal to 75 and less than or equal to 125 msec. The marked rise in the DFT at a shock separation of 50 msec, requiring more energy than that for the first shock alone, suggests that the second shock at this time delay is likely to reinduce fibrillation after it is halted by the first shock until the second shock is strong enough to defibrillate independently of the first shock.

Animals↗
PubMed1992

Effect of field stimulation on cellular repolarization in rabbit myocardium. Implications for reentry induction.

We have investigated the effects of electric field stimulation on membrane repolarization in rabbit papillary muscles and assessed the consequences of these effects for the dispersion of intracellular potentials and the production of a propagation wave front or unidirectional block in relatively refractory tissue. The stimuli studied had electric field strength of 0.25-14 V/cm, duration of 2 msec, and field orientation along or across the myocardial fibers. The field strengths to excite the muscles in diastole were 0.68 or 1.23 V/cm for stimuli oriented along or across the fibers, respectively (p less than 0.01, along versus across). A 2.5-V/cm stimulus given near the end of the action potential (AP) produced either no response or, after increasing the stimulus delay only 2-3 msec, a full response with almost no AP durations that were intermediate. For stimulation along and across the fibers, respectively, given at 70% of the AP duration, a 4-V/cm stimulus produced AP prolongation (measured at 90% repolarization) of 20% and 4% (p less than 0.05), an 8-V/cm stimulus produced AP prolongation of 36% and 20% (p less than 0.05), and a 14-V/cm stimulus produced AP prolongation of 36% and 30% (p = NS). For either orientation, AP prolongation by stimuli of 8 V/cm or 14 V/cm increased gradually as the stimulus delay was increased. The different effects in relatively refractory tissue of stimuli of 2.5 V/cm compared with 8 V/cm can explain the propagation wave front and block that occur with electrically induced functional reentry in the heart.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1992

Existence of both fast and slow channel activity during the early stages of ventricular fibrillation.

Although sodium channels have been reported to be inactive after 5-10 minutes of ventricular fibrillation (VF), their state during early VF is unknown. In 12 open-chest dogs, a floating glass microelectrode was used to record intracellular action potentials from the right ventricle during pacing and during electrically induced VF. Before any drug was administered, an initial episode of VF was continuously recorded for at least 20 seconds followed by defibrillation. Recordings were made during VF episodes after superfusion for 15 minutes around the microelectrode site by low (2.8 x 10(-5) M) and high (10(-4) M) concentrations of tetrodotoxin (TTX) in five dogs, or by low (4 microM) and high (100 microM) concentrations of verapamil in another four dogs. In three dogs, VF was induced without drugs three times to determine if the effects observed in the previous dogs were caused by the drugs or by successive episodes of VF. Ten consecutive action potentials were analyzed at the onset and after 5, 10, 15, and 20 seconds of VF. Action potential amplitude and duration during paced rhythm or VF were not changed by the local perfusion of either TTX or verapamil. In the TTX group, the maximum upstroke rate of depolarization of an action potential (Vmax) during paced rhythm was 104 +/- 14 V/sec for control cycles before any drug was given, 86 +/- 15 V/sec for the low TTX concentration, and 55 +/- 14 V/sec for the high TTX concentration (p less than 0.05 versus other two). Vmax decreased from 55 +/- 32 V/sec at the beginning of VF to 37 +/- 27 V/sec after 20 seconds of VF for predrug VF, from 39 +/- 20 V/sec to 18 +/- 11 V/sec for low-dose TTX VF, and from 18 +/- 13 V/sec to 12 +/- 7 V/sec for high-dose TTX VF (p less than 0.05 among the three groups). In the dogs receiving verapamil, VF was still inducible with Vmax not significantly different from predrug VF at the onset and after 5 or 20 seconds of VF but with Vmax smaller (p less than 0.05) for verapamil than for predrug VF after 10 or 15 seconds of VF. In three dogs, Vmax was not significantly different during three successive episodes of VF when no drug was given between the episodes.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1991

An assessment of variable thickness and fiber orientation of the skeletal muscle layer on electrocardiographic calculations.

This paper assesses the effectiveness of including variable thickness and fiber orientation characteristics of the skeletal muscle layer in calculations relating epicardial and torso potentials. A realistic model of a canine torso which includes extensive detail about skeletal muscle layer thickness and fiber orientation is compared with two other uniformly anisotropic models: one of constant thickness and the other of variable thickness. First, transfer coefficients are calculated from the model data. Then torso potentials for each model are calculated from the transfer coefficients and measured epicardial potentials. The comparison of calculated and observed torso potentials indicates that a simple model consisting of a uniformly anisotropic skeletal muscle layer of 1.0-1.5 cm constant thickness significantly improves the model. However, if photographic slices of the canine torso are used to introduce more detailed data about the variation in skeletal muscle thickness and fiber orientation into the model, the agreement and between calculated and measured torso potentials decreased, although a finite element mesh of over 5000 nodes was used to describe the skeletal muscle in the more detailed model. One source of error increase was considered to be due to numerical discretization and could be reduced with a much finer mesh or by utilizing higher order polynomials to represent the potential distribution within each finite element. However, the results presented in this paper show that high precision computation (64-bit word length) on the mainframe IBM 3081 with an attached FPS-164 gives a slow rate of improvement with reduced discretization intervals and that utilizing higher order polynomials within each finite element gives an even slower rate of improvement.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Dispersion of repolarization induced by a nonuniform shock field.

Dispersion of repolarization may contribute to arrhythmias. To determine whether an electrical field stimulus (S2) with a nonuniform potential gradient can induce a dispersion of repolarization, we applied 5 ms rectangular S2 that had a nonuniform or uniform potential gradient during the action potential (AP) of bathed frog ventricular strips. One group had a partitioned bath to produce a nonuniform S2 of 39 +/- 11 V/cm (mean +/- SD) in one half of the 1 x 6 mm strip (H) and 0.3 +/- 0.2 V/cm in the other half (L), and simultaneous intracellular AP recordings in H and L with glass microelectrodes positioned 1.4 +/- 0.4 mm apart. Another group had uniform S2 and an AP recorded near the center of the strip. S1 pacing at 0.5 Hz was performed at one end of the strip and conduction along the strip was monitored. In each experiment, the S2 trials had an S1-S2 interval of 300 ms so that S2 was given during an AP (shocked AP). In both H and L, nonuniform S2 produced cumulative shortening of paced APs and lengthening of each shock AP compared with the paced AP preceding it. Uniform S2 of 1 V/cm did not shorten the paced APs or lengthen the shocked APs indicating that the AP changes in L were not due to the small potential gradient in L. Before beginning nonuniform S2 trials, the AP duration determined at the maximum repolarization rate was 601 +/- 72 ms in H and 602 +/- 71 ms in L (P = ns). During 13-20 nonuniform S2 trials over a 60-80 minute period, paced APs were shortened to 490 +/- 51 ms in H and 515 +/- 39 ms in L while each shocked AP was lengthened, compared with the paced AP preceding it, to 636 +/- 40 ms in H and 561 +/- 21 ms in L (P less than 0.05). Therefore, paced APs after shocks repolarized 25 ms earlier in H than in L and shocked APs repolarized 75 ms later in H than in L. The results show that during the shortened AP in H, the AP in L is shortened, which is consistent with intracellular current from L to H during repolarization. During the prolonged AP in H, the AP in L is prolonged compared with the paced AP preceding it, consistent with intracellular current from H to L during repolarization. Thus, nonuniform shocks can induce a dispersion of repolarization and may induce cell-to-cell interactions during repolarization.

Action Potentials↗