Biomedical subjects

W M Smith

Publications and source records attributed to W M Smith.

At least 55 records · Page 3Linked to original sources

PubMed1999

Can early timed internal atrial defibrillation shocks reduce the atrial defibrillation threshold?

The defibrillation threshold is markedly reduced very early following the initiation of ventricular fibrillation. The purpose of this study was to determine if the same finding holds true for atrial defibrillation. Sustained, reproducible AF was induced with programmed atrial pacing using acetyl-beta-methylcholine chloride (40-640 microL/min) in six adult sheep (heart weight 245-300 g). Seven timing intervals (125 ms, 200 ms, 1 s, 3 s, 10 s, 30 s, and 5 min after AF induction) and two lead configurations: (1) RA as cathode and CS as anode; and (2) RA as cathode and RV apex as anode were tested. Single capacitor biphasic waveforms (3/1 ms) were delivered and atrial defibrillation thresholds (ADFTs) were determined in random order. No significant differences in leading edge voltage and total energy were detected for the RA-CS configuration for the seven timing intervals. For the RA-RV configuration, a significant difference was detected comparing the voltage for 125 ms to the 5-minute timing interval. For all times except 125 ms, the RA-RV threshold was significantly higher than the RA-CS level. In contrast to ventricular defibrillation, the ADFT does not change significantly within the first 5 minutes after the initiation of AF for the RA-CS configuration. However, if the shock is given very early (125 ms after AF induction) with the RA-RV configuration, the ADFT is lowered almost to the RA-CS level.

Animals↗

PubMed1999

Automatic implantable cardioverter-defibrillators.

Ventricular fibrillation, a loss of synchronous electrical activity in the heart which leads to hemodynamic collapse, is a leading cause of death. Because of the devastating personal and societal effects of this phenomenon, the automatic cardioverter-defibrillator has been developed for automatic detection and termination of the arrhythmia and is in widespread clinical use. Advances in circuits, leads, waveforms, and signal processing along with increased knowledge of the mechanisms of fibrillation have led to continuing improvements in this device, extending its use to many patients. A device has also been developed for the automatic or semiautomatic treatment of atrial fibrillation, an arrhythmia less life-threatening than ventricular fibrillation, but still a serious health problem. Continued improvement of these devices and the development of qualitatively new approaches hold great promise for exciting therapeutic advances in this area.

Atrial Fibrillation↗

PubMed1999

Effect of pacing site on ventricular fibrillation initiation by shocks during the vulnerable period.

The critical point hypothesis for the upper limit of vulnerability (ULV) states that the site of S1 pacing should not affect the ULV S2 shock strength for a single S2 shock electrode configuration but may affect the S1-S2 interval at which sub-ULV shocks induce ventricular fibrillation (VF). Furthermore, early post-S2 activations leading to VF should arise in areas with low potential gradients of similar magnitude, regardless of the S1 site. This hypothesis was tested in 10 pigs by determining ULVs for three S1 sites [left ventricular apex (LVA), LV base (LVB), and right ventricular outflow tract (RVOT)] with one S2 configuration (LVA patch to superior vena cava catheter). T-wave scanning was performed with biphasic S2 shocks incremented from 60 V in 40-V steps and stepped up or down in 20- and 10-V steps. Activations and S2 potential gradients were recorded at 528 epicardial sites. Although shocks just below the ULV induced VF significantly earlier in the T wave when the S1 site was the RVOT than when it was the LVA or LVB, ULVs were not significantly different for the three S1 pacing sites. Early post-S2 activations arose closer to the S2 electrode for weak S2s but moved to distant low potential gradient areas as the S2 strengthened. Just below the ULV, early post-S2 activations arose in the RVOT when the S1 site was the LVA or LVB but arose along the RV base when the S1 site was the RVOT. Early site potential gradients were not significantly different just below the ULV (LVA: 8.2 +/- 4.1 V/cm; LVB: 8.6 +/- 4. 9 V/cm; RVOT: 8.7 +/- 4.4 V/cm). At the ULV, early post-S2 activations arose from the same areas but did not induce VF. The results support the critical point hypothesis for the ULV. For this S2 configuration, no single point in the T wave could be used to determine the ULV for all S1 sites.

Animals↗

PubMed1999

Direct mapping of bioelectric activity.

Much can be learned about physiological function in heart, brain, and other tissues from measuring the electrical activity that mediates mechanical or neural phenomena. The study of electrophysiology has progressed from acquisition of a single or a few channels to hundreds of signals acquired simultaneously. Data acquisition, signal processing, and visualization in electrophysiology have benefitted from the parallel advances in electronics and computing hardware and software. The two primary technologies for mapping electrical activity at many sites are electrical, using electrodes directly placed on tissue, and optical, using voltage sensitive dyes to estimate membrane parameters. Each is valuable and provides information that is complementary to the other. This article is a description of the current state of electrical and optical mapping.

Animals↗

PubMed1998

Relative efficacy of monophasic and biphasic waveforms for transthoracic defibrillation after short and long durations of ventricular fibrillation.

BACKGROUND: Recently, interest has arisen in using biphasic waveforms for external defibrillation. Little work has been done, however, in measuring transthoracic defibrillation efficacy after long periods of ventricular fibrillation. In protocol 1, we compared the efficacy of a quasi-sinusoidal biphasic waveform (QSBW), a truncated exponential biphasic waveform (TEBW), and a critically damped sinusoidal monophasic waveform (CDSMW) after 15 seconds of fibrillation. In protocol 2, we compared the efficacy of the more efficacious biphasic waveform from protocol 1, QSBW, with CDSMW after 15 seconds and 5 minutes of fibrillation. METHODS AND RESULTS: In protocol 1, 50% success levels, ED50, were measured after 15 seconds of fibrillation for the 3 waveforms in 6 dogs. In protocol 2, defibrillation thresholds were measured for QSBW and CDSMW after 15 seconds of fibrillation and after 3 minutes of unsupported fibrillation followed by 2 minutes of fibrillation with femoral-femoral cross-circulation. In protocol 1, QSBW had a lower ED50, 16.0+/-4.9 J, than TEBW, 20.3+/-4.4 J, or CDSMW, 27.4+/-6.0 J. In protocol 2, QSBW had a lower defibrillation threshold after 15 seconds, 38+/-10 J, and after 5 minutes, 41.5+/-5 J, than CDSMW after 15 seconds, 54+/-19 J, and 5 minutes, 80+/-30 J, of fibrillation. The defibrillation threshold remained statistically the same for QSBW for the 2 fibrillation durations but rose significantly for CDSMW. CONCLUSIONS: In this animal model of sudden death and resuscitation, these 2 biphasic waveforms are more efficacious than the CDSMW at short durations of fibrillation. Furthermore, the QSBW is even more efficacious than the CDSMW at longer durations of fibrillation.

Animals↗

PubMed1998

Spatial changes in the transmembrane potential during extracellular electric stimulation.

The purpose of this study was to determine the spatial changes in the transmembrane potential caused by extracellular electric field stimulation. The transmembrane potential was recorded in 10 guinea pig papillary muscles in a tissue bath using a double-barrel microelectrode. After 20 S1 stimuli, a 10-ms square wave S2 shock field with a 30-ms S1-S2 coupling interval was given via patch shock electrodes 1 cm on either side of the tissue during the action potential plateau. Two shock strengths (2.1+/-0.2 and 6.5+/-0.6 V/cm) were tested with both shock polarities. The recording site was moved across the tissue along fibers with either 200 micrometer (macroscopic group [n=5], 12 consecutive recording sites over a 2. 2-mm tissue length in each muscle) or 20 micrometer (microscopic group [n=5], 21 consecutive recording sites over a 0.4-mm tissue length in each muscle) between adjacent recording sites. In the macroscopic group, the portion of the tissue toward the anode was hyperpolarized, whereas the portion toward the cathode was depolarized, with 1 zero-potential crossing from hyperpolarization to depolarization present near the center of the tissue. In the microscopic group, only 1 zero-potential crossing was observed in the center region of the tissue, whereas, away from the center, only hyperpolarization was observed toward the anode and depolarization toward the cathode. Although these results are consistent with predictions from field stimulation of continuous representations of myocardial structure, ie, the bidomain and cable equation models, they are not consistent with the prediction of depolarization-hyperpolarization oscillation from representations based on cellular-level resistive discontinuities associated with gap junctions, ie, the sawtooth model.

Animals↗

PubMed1998

Rapid design of denaturing gradient-based two-dimensional electrophoretic gene mutational scanning tests.

With the current rapid pace at which human disease genes are identified there is a need for practical, cost-efficient genetic screening tests. Two-dimensional electrophoretic separation of PCR-amplified gene fragments on the basis of size and base pair sequence, in non-denaturing and denaturing gradient polyacrylamide gels respectively, provides a rapid parallel approach to gene mutational scanning. Accuracy of the denaturing gradient gel electrophoresis (DGGE) component of this system strongly depends on the design of the PCR primers and the melting characteristics of the fragments they encompass. We have developed a fully automated generally applicable procedure to generate optimal two-dimensional test designs at a minimum amount of time and effort. Designs were generated for the RB1 , TP53 , MLH1 and BRCA1 genes that can be readily implemented in research and clinical laboratories as low cost genetic screening tests.

Adaptor Proteins, Signal Transducing↗

PubMed1998

Locally propagated activation immediately after internal defibrillation.

BACKGROUND: Electrical mapping studies indicate an interval of 40 to 100 ms between a defibrillation shock and the earliest activation that propagates globally over the ventricles (globally propagated activation, GPA). This study determined whether activation occurs during this interval but propagates only locally before being blocked (locally propagated activation, LPA). METHODS AND RESULTS: In five anesthetized pigs, the heart was exposed and a 504-electrode sock with 4-mm interelectrode spacing was pulled over the ventricles. Ten biphasic shocks of a strength near the defibrillation threshold (DFT) were delivered via intracardiac catheter electrodes, and epicardial activation sequences were mapped before and after attempted defibrillation. Local activation was defined as dV/dt < or =-0.5 V/s. Postshock activation times and wave-front interaction patterns were determined with an animated display of dV/dt at each electrode in a computer representation of the ventricular epicardium. LPAs were observed after 40 of the 50 shocks. A total of 173 LPA regions were observed, each of which involved 2+/-2 (mean+/-SD) electrodes. LPAs were observed after both successful and failed shocks but occurred earlier (P<.0001) after failed (35+/-8 ms) than successful (41+/-16 ms) shocks, although the times at which the GPA appeared were not significantly different. On reaching the LPA region, the GPA front either propagated through it (n=135) or was blocked (n=38). The time from the onset of the LPA until the GPA front propagated to reach the LPA region was shorter (P<.01) when the GPA front was blocked (32+/-12 ms) than when it propagated through the LPA region (63+/-20 ms). CONCLUSIONS: LPAs exist after successful and failed shocks near the DFT. Thus, the time from the shock to the GPA is not totally electrically silent.

Animals↗

PubMed1998

The effects of ventricular fibrillation duration and site of initiation on the defibrillation threshold during early ventricular fibrillation.

OBJECTIVES: The purpose of this study was to determine if the defibrillation threshold (DFT) is lower during the first few cycles of ventricular fibrillation (VF) than after 10 s of VF and, if so, if the effect is caused by local or global factors. BACKGROUND: The DFT may be low very early during VF because: (1) for the first few cycles VF arises from a localized region close to a defibrillation electrode where the shock field is strong (local factors), or (2) during early VF the effects of ischemia and sympathetic discharge have not yet fully developed and the heart has not yet completely dilated (global factors). METHODS: Protocol 1 included seven pigs in which a defibrillation electrode and a pacing catheter were both placed in the right ventricular apex. VF was induced by delivering a high current premature stimulus from the pacing catheter that should have caused reentry confined to the right ventricular apex for the first few cycles of VF. A bipolar electrogram was recorded from the tip of the defibrillation catheter. Using a three reversal up-down protocol, the DFT was determined for biphasic shocks delivered after 1, 2, 3, 4, 5, 7, 10, 15, 20 and 25 activations in this electrogram and after 10 s (control). Protocol 2 included seven pigs undergoing the same procedure as in protocol 1 except that an additional pacing catheter was placed in the left ventricle. Defibrillation thresholds were determined after 1, 2, 3, 4 and 5 VF activations following VF induction from the right ventricle (RV) or the left ventricle (LV) and after 10 s (control). RESULTS: In protocol 1, the mean +/- SD DFrs were lower during the first three cycles than after 10 s of VF (3.0 +/- 4.1 J for the first VF cycle vs 15.8 +/- 6.6 J after 10 s of VF, p < 0.05). In protocol 2, the DFF for the first few cycles of VF induced away from the defibrillation electrode in the LV (6.9 +/- 1.4 J for the first VF cycle) was significantly lower than that after 10 s of VF (16.0 +/- 2.2 J), whereas the DFF for the first few cycles induced near the defibrillation electrode in the right ventricular apex was significantly lower (2.3 +/- 2.7 J for the first VF cycle) than that induced from the LV. CONCLUSIONS: This study demonstrates that the DFT is significantly lower during the first few VF cycles of VF than after 10 s of VF and that this decrease may be caused by both local factors and global factors. These results provide an impetus for exploring earlier shock delivery in implantable devices.

Animals↗

PubMed1998

Accurate, high-throughput "snapshot" detection of hMLH1 mutations by two-dimensional DNA electrophoresis.

The human genome and related projects have resulted in the isolation of a rapidly growing number of genes that cause susceptibility to human cancer. With rare exception, these genes are large and have disease-associated mutations scattered along the length of the genes. Therefore, the development of accurate and cost-efficient mutation detection tests that can scan entire genes singly or in combination is warranted. hMLH1, encoding a mismatch repair enzyme, is a susceptibility gene for hereditary nonpolyposis colon cancer syndrome. This gene comprises 19 exons; mutations are scattered, typical of many susceptibility genes. Here, we present a strategy that combines extensive PCR multiplexing and two-dimensional DNA electrophoresis (Two-Dimensional Gene Scanning, TDGS) to scan accurately for mutations that lie within the exons and splice junctions of hMLH1. All target fragments, designed to have optimal melting characteristics, were prepared in a two-stage PCR--a four-plex long-distance PCR followed by short PCR in two multiplex groups of 10 and 11 amplicons. The mixture of amplicons was subjected to two-dimensional electrophoresis: separation by size in the first dimension and by melting characteristics in the second. Using this design, 41 samples containing known hMLH1 sequence variants or no alterations were blindly subjected to TDGS. All mutations were detected; there were no genuine false-positive or false-negative results. These results confirm that TDGS is a generally applicable, rapid, accurate, and reproducible mutation detection technology that would serve large-scale molecular epidemiologic studies as well as clinical molecular diagnostic purposes.

Adaptor Proteins, Signal Transducing↗

PubMed1998

A simple system for automated two-dimensional electrophoresis: applications to genetic testing.

Two-dimensional gene scanning (TDGS) is a method for mutation detection based on two-dimensional electrophoretic separation of PCR-amplified DNA fragments according to size and base pair sequence. To facilitate two-dimensional electrophoresis without manual interference, a simple three-chamber unit was designed on top of an existing vertical electrophoresis instrument. Application of this system to genetic testing is demonstrated by the performance of a complete two-dimensional mutational scanning assay of one of the hereditary nonpolyposis colon cancer syndrome susceptibility genes, hMLH1.

Adaptor Proteins, Signal Transducing↗

PubMed1998

Acute deleterious effects of cocaine on cardiac conduction, hemodynamics, and ventricular fibrillation threshold: effects of interaction with a selective dopamine D1 antagonist SCH 39166.

Cocaine has demonstrated cardiotoxicity that has led to sudden death by unknown mechanisms. SCH 39166, a selective dopaminergic D1-receptor antagonist, suppresses the compulsive drug-intake actions of cocaine in primates. This study examined the cumulative toxic effects of cocaine after the long-term administration of SCH 39166. After pretreatment with oral placebo/SCH 39166 for 5 days, an i.v. infusion of 0.25 mg/kg/min of cocaine HCl was delivered to 14 anesthetized dogs, and cardiac conduction, arterial blood pressure, ventricular refractoriness, and arrhythmogenesis were examined. The cocaine infusion was stopped when QRS width increased by 20% from baseline (QRS20). In Coc + Placebo regimen, the QRS and His-Ventricular (HV) intervals showed a dose-dependent lengthening. Initially, the mean blood pressure (MBP) increased followed by a precipitate decrease at a mean dose of 2.03 +/- 0.5 mg/kg of cocaine. At QRS20, the ventricular effective refractory period (ERP) increased significantly, whereas the ventricular fibrillation threshold (VFT) showed a significant reduction from the baseline. In Coc + SCH, the QRS, HV intervals, and ERP increased similarly, but the decrease in MBP was attenuated, and the VFT was increased. A relatively small infusion of cocaine causes a hemodynamic compromise. The His-ventricular conduction delay and lengthened ERP suggest a predominant direct local anesthetic effect. Cocaine additionally decreased the VFT, suggesting an increased susceptibility to VF. SCH 39166 did not potentiate the cardiotoxic effects of cocaine. It displayed a protective trend by suppressing the arrhythmogenic effects and the hemodynamic compromise caused by cocaine.

Animals↗

PubMed1998

Estimation of conduction velocity vector fields from epicardial mapping data.

An automated method to estimate vector fields of propagation velocity from observed epicardial extracellular potentials is introduced. The method relies on fitting polynomial surfaces T(x, y) to the space-time (x, y, t) coordinates of activity. Both speed and direction of propagation are computed from the gradient of the local polynomial surface. The components of velocity, which are total derivatives, are expressed in terms of the partial derivatives which comprise the gradient of T. The method was validated on two-dimensional (2-D) simulations of propagation and then applied to cardiac mapping data. Conduction velocity was estimated at multiple epicardial locations during sinus rhythm, pacing, and ventricular fibrillation (VF) in pigs. Data were obtained via a 528-channel mapping system from 23 x 22 and 24 x 21 arrays of unipolar electrodes sutured to the right ventricular epicardium. Velocity estimates are displayed as vector fields and are used to characterize propagation qualitatively and quantitatively during both simple and complex rhythms.

Animals↗

PubMed1998

Evolution of the organization of epicardial activation patterns during ventricular fibrillation.

INTRODUCTION: This study quantified how the organization of epicardial activation changes during the first 40 seconds of ventricular fibrillation (VF). METHODS AND RESULTS: Unipolar potentials were mapped from a 504 (24 x 21) electrode array (2-mm interelectrode spacing) on the anterior right ventricle (RV) and left ventricle (LV) epicardium. The array covered approximately 20% of the epicardial surface. In each of seven pigs, six episodes of VF were induced by premature stimulation. One-half second epochs of VF were analyzed, starting 0, 10, 20, 30, and 40 seconds post induction and using novel pattern analysis algorithms. Eight parameters were quantified: (1) the number of wavefronts; (2) the epicardial area activated by wavefronts; (3) the fraction of wavefronts arising from epicardial breakthrough or from a focus; (4) the fraction of wavefronts terminated by conduction block; (5) the multiplicity index (number of distinct activation pathways in the rhythm); (6) the repeatability index (number of times activation pathways are traversed); (7) the activation rate; and (8) the wavefront propagation velocity. The results showed that VF patterns were less organized at 10 than at 0 seconds, with more, smaller wavefronts traversing a larger variety of pathways for fewer repetitions. VF activation patterns then gradually reorganized up to 40 seconds, but by a different mechanism: the spatial size of subpatterns grew, but the dynamics otherwise appeared unchanged. During both transitions, both activation rate and propagation velocity slowed monotonically. CONCLUSION: Thus, changes in organization during VF can occur by multiple mechanisms.

Action Potentials↗

PubMed1998

Transmembrane potential changes caused by monophasic and biphasic shocks.

Transmembrane potential change (DeltaVm) during shocks was recorded by a double-barrel microelectrode in 12 isolated guinea pig papillary muscles. After 10 S1 stimuli, square-wave S2 shocks of both polarities were given consisting of 10-ms monophasic and 10/10-ms and 5/5-ms biphasic waveforms that created potential gradients from 1.1 +/- 0.3 to 11.9 +/- 0.4 V/cm. S2 shocks were applied with 30, 60- to 70-, and 90- to 130-ms S1-S2 coupling intervals so that they occurred during the plateau, late portion of the plateau, and phase 3 of the action potential, respectively. Some shocks were given across as well as along the fiber orientation. The shocks caused hyperpolarization with one polarity and depolarization with the opposite polarity. The ratio of the magnitude of hyperpolarization to that of depolarization at the three S1-S2 coupling intervals was 1.5 +/- 0.3, 1.1 +/- 0.2, and 0.5 +/- 0.2, respectively. DeltaVm during the shock was significantly greater for the monophasic than for the two biphasic shocks. The prolongation of total repolarizing time (TRT) was significantly greater for monophasic (119.8 +/- 19.1%) and 10/10-ms biphasic (120.5 +/- 18.2%) than for 5/5-ms biphasic (113.0 +/- 12.9%) waveforms. The dispersion of the normalized TRT between instances of hyperpolarization and depolarization caused by the two shock polarities was 7.4 +/- 7.1% for monophasic, 3.0 +/- 4.1% for 10/10-ms biphasic, and 2.8 +/- 3.1% for 5/5-ms biphasic shocks (P < 0.05 for monophasic vs. biphasic). Shock fields along fibers produced a larger DeltaVm and prolongation of TRT than those across fibers. We conclude that 1) a change in shock polarity causes an asymmetrical change in membrane polarization depending on shock timing; 2) the 5/5-ms biphasic waveform causes the smallest DeltaVm, prolongs repolarization the least, and causes the smallest polarity-dependent dispersion; and 3) the changes in transmembrane potential and repolarization are influenced by fiber orientation.

Animals↗

PubMed1998

Hemispheric and facial asymmetry: faces of academe.

Facial asymmetry (facedness) of selected academic faculty members was studied in relation to brain asymmetry and cognitive specialization. Comparisons of facedness were made among humanities faculty (H), faculty members of mathematics and physics (M-P), psychologists (P), and a group of randomly selected individuals (R). Facedness was defined in terms of the relative sizes (in square centimeters) of the two hemifaces. It was predicted that the four groups would show differences in facedness, namely, H, right face bias; M-P, left face bias; P, no bias; and R, no bias. The predictions were confirmed, and the results interpreted in terms of known differences in hemispheric specialization of cognitive functions as they relate to the dominant cognitive activity of each of the different groups. In view of the contralateral control of the two hemifaces (below the eyes) by the two hemispheres of the brain, the two sides of the face undergo differential muscular development, thus creating facial asymmetry. Other factors, such as gender, also may affect facial asymmetry. Suggestions for further research on facedness are discussed.

Analysis of Variance↗

PubMed1997

Internal cardioversion of atrial fibrillation: marked reduction in defibrillation threshold with dual current pathways.

BACKGROUND: The ultimate acceptance of a fully automatic atrial defibrillator will depend on the reduction of pain to acceptable levels, requiring a marked decrease in defibrillation thresholds. The purpose of this study was to determine whether atrial defibrillation thresholds can be reduced by sequential shocks delivered through two current pathways. METHODS AND RESULTS: Sustained atrial fibrillation was induced with rapid atrial pacing in 12 adult sheep. Defibrillation electrodes were positioned in the right atrial appendage (RAap), distal coronary sinus (DCS), proximal coronary sinus (CSos), main/left pulmonary artery junction (PA), and right ventricular apex (RV). Single-capacitor biphasic waveforms (3/1 ms) were delivered through combinations of these electrodes. Probability-of-success curves were determined for single shocks with a single current pathway and sequential shocks with either single- or dual current pathways. The ED50 for delivered energy for the dual current pathway RAap to DCS then CSos to PA was 0.36+/-0.13 J, which was significantly lower than the ED50 of the standard single current pathway RAap to DCS (1.31+/-0.3 J) and was significantly lower than all other configurations tested. CONCLUSIONS: Internal atrial defibrillation thresholds can be markedly reduced with two sequential biphasic shocks delivered over two current pathways compared with the standard single shock delivered over a single current pathway or with sequential shocks delivered over a single current pathway.

Animals↗

PubMed1997

Effects of transvenous electrode polarity and waveform duration on the relationship between defibrillation threshold and upper limit of vulnerability.

BACKGROUND: The upper limit of vulnerability (ULV) hypothesis for defibrillation predicts that maneuvers that alter the ULV will cause a similar alteration in the defibrillation threshold (DFT). The purpose of this study was to test this prediction by evaluating the effects of electrode polarity and waveform duration on the relationship between the DFT and the ULV. METHODS AND RESULTS: Platinum spring electrodes were placed in the right ventricular (RV) apex and the superior vena cava in 12 pigs. Strength-duration curves were constructed for the DFT and ULV for each electrode polarity with monophasic waveforms (6 pigs) of different durations (2 to 14 ms) and biphasic truncated exponential waveforms (6 pigs) having phase 1 equal to 4 ms and phase 2 of different durations (0 to 10 ms). ULV data were gathered by scanning of the T wave. The ventricular pacing threshold (VPT) and ventricular fibrillation threshold (VFT) were also determined with these same waveforms. For the RV electrode as a cathode for monophasic and the first phase of biphasic stimuli, VPTs for the same waveform duration were significantly lower than for the configuration with the RV electrode as an anode. VFTs were not significantly different for the two electrode polarities with either monophasic or biphasic waveforms. The DFT changed in a fashion similar to the ULV with changes in electrode polarity and phase duration for both monophasic and biphasic waveforms. The ULV and DFT for each waveform duration for each polarity were strongly correlated (r=.83 to .99). CONCLUSIONS: The almost identical changes in ULV and DFT with changes in electrode polarity and waveform duration provide new evidence to support the ULV hypothesis of defibrillation.

Animals↗