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Biomedical subjects

W M Smith

Publications and source records attributed to W M Smith.

At least 19 recordsLinked to original sources
PubMed2001

Cost-effectiveness of spinal cord stimulation in patients with intractable angina.

AIM: To review the cost of healthcare utilisation by patients suffering from intractable angina, unsuitable for coronary revascularisation, before and after treatment with spinal cord stimulation. METHODS: Data were collected for eight patients treated for intractable angina with spinal cord stimulation at Green Lane Hospital before April 1999. Information on consumption of specified medica resources for the twelve months preceding implantation, the implantation period, and the twelve months following implantation was collected. Where available, data were also collected for the eighteen months preceding and following treatment. RESULTS: In six patients successful permanent stimulation was established; in two it proved technically impossible to implant a stimulator. The six patients with successful stimulation spent fewer days in hospital (p=0.028) and consumed fewer resources (p=0.046) following implantation than in the period before implantation. The two patients for whom spinal cord stimulation was unsuccessful spent more days in hospital and consumed more resources in the twelve months following, than in the twelve months preceding attempted implantation. Extrapolation of data for all eight patients suggests that, on average, the cost of implanting a spinal cord stimulator will be recovered in approximately fifteen months. CONCLUSION: Spinal cord stimulation is a cost-effective treatment for intractable angina pectoris.

Aged↗
PubMed2001

PTEN inhibits insulin-stimulated MEK/MAPK activation and cell growth by blocking IRS-1 phosphorylation and IRS-1/Grb-2/Sos complex formation in a breast cancer model.

The tumour suppressor gene PTEN encodes a dual-specificity phosphatase that recognizes protein substrates and phosphatidylinositol-3,4,5-triphosphate. PTEN seems to play multiple roles in tumour suppression and the blockade of phosphoinositide-3-kinase signalling is important for its growth suppressive effects, although precise mechanisms are not fully understood. In this study, we show that PTEN plays a unique role in the insulin-signalling pathway in a breast cancer model. Ectopic expression of wild-type PTEN in MCF-7 epithelial breast cancer cells resulted in universal inhibition of Akt phosphorylation in response to stimulation by diverse growth factors and selective inhibition of MEK/extracellular signal-regulated kinase (ERK) phosphorylation stimulated by insulin or insulin-like growth factor 1 (IGF-1). The latter was accompanied by a decrease in the phosphorylation of insulin receptor substrate 1 (IRS-1) and the association of IRS-1 with Grb2/Sos, without affecting the phosphorylation status of the insulin receptor and Shc, nor Shc/Grb2 complex formation. The MEK inhibitor, PD980059, but not the PI3K inhibitor, wortmannin, abolished the effect of PTEN on insulin-stimulated cell growth. Without addition of insulin, wortmannin reduced PTEN-mediated growth suppression, whereas PD980059 had little effect, suggesting that PTEN suppresses insulin-stimulated cell growth by blocking the mitogen-activated protein kinase (MAPK) pathway. Furthermore, PD980059 treatment led to the downregulation of cyclin D1 and the suppression of cell cycle progression. Our data suggest that PTEN blocks MAPK phosphorylation in response to insulin stimulation by inhibiting the phosphorylation of IRS-1 and IRS-1/Grb2/Sos complex formation, which leads to downregulation of cyclin D1, inhibition of cell cycle progression and suppression of cell growth.

Adaptor Proteins, Signal Transducing↗
PubMed2001

Improvement of defibrillation efficacy and quantification of activation patterns during ventricular fibrillation in a canine heart failure model.

BACKGROUND: Little is known about the effects of heart failure (HF) on the defibrillation threshold (DFT) and the characteristics of activation during ventricular fibrillation (VF). METHODS AND RESULTS: HF was induced by rapid right ventricular (RV) pacing for at least 3 weeks in 6 dogs. Another 6 dogs served as controls. Catheter defibrillation electrodes were placed in the RV apex, the superior vena cava, and the great cardiac vein (CV). An active can coupled to the superior vena cava electrode served as the return for the RV and CV electrodes. DFTs were determined before and during HF for a shock through the RV electrode with and without a smaller auxiliary shock through the CV electrode. VF activation patterns were recorded in HF and control animals from 21x24 unipolar electrodes spaced 2 mm apart on the ventricular epicardium. Using these recordings, we computed a number of quantitative VF descriptors. DFT was unchanged in the control dogs. DFT energy was increased 79% and 180% (with and without auxiliary shock, respectively) in HF compared with control dogs. During but not before HF, DFT energy was significantly lowered (21%) by addition of the auxiliary shock. The VF descriptors revealed marked VF differences between HF and control dogs. The differences suggest decreased excitability and an increased refractory period during HF. Most, but not all, descriptors indicate that VF was less complex during HF, suggesting that VF complexity is multifactorial and cannot be expressed by a scalar quantity. CONCLUSIONS: HF increases the DFT. This is partially reversed by an auxiliary shock. HF markedly changes VF activation patterns.

Analysis of Variance↗
PubMed2001

Transient ectopic expression of PTEN in thyroid cancer cell lines induces cell cycle arrest and cell type-dependent cell death.

The tumour suppressor gene PTEN/MMAC1/TEP1 has been implicated in a variety of human cancers and several inherited hamartoma tumour syndromes, including Cowden syndrome, which has a high risk of breast and thyroid cancer. We have previously reported that overexpression of PTEN in MCF-7 breast cancer cells induces cell cycle arrest and apoptosis. In this study, we analysed PTEN status at both the structural and expression levels and explored PTEN's growth-suppressive effects on thyroid. We found that 1 of 10 thyroid cancer lines [follicular thyroid carcinoma FTC-133] had hemizygous deletion and a splice variant IVS4--19G-->A in the remaining allele. Four lines, including FTC-133, express PTEN mRNA at low levels. In general, PTEN protein levels correlated with mRNA levels, except for NPA87, which has low levels of transcript and relatively high levels of PTEN protein. Transient expression of PTEN in seven thyroid cancer cell lines resulted in G(1) arrest in two well differentiated papillary thyroid cancer lines (PTCs) and both G(1) arrest and cell death in the remaining five lines, including three FTCs, one poorly differentiated PTC and one undifferentiated thyroid cancer. The level of phosphorylated Akt was inversely correlated with the endogenous level of PTEN protein and overexpression of PTEN-blocked Akt phosphorylation in all cells analysed. Our results suggest that downregulation of PTEN expression at the mRNA level plays a role in PTEN inactivation in thyroid cancer and PTEN exerts its tumour-suppressive effect on thyroid cancer through the inhibition of cell cycle progression alone or both cell cycle progression and cell death.

Adenocarcinoma, Follicular↗
PubMed2001

Reentry site during fibrillation induction in relation to defibrillation efficacy for different shock waveforms.

INTRODUCTION: Unsuccessful defibrillation shocks may reinitiate fibrillation by causing postshock reentry. METHODS AND RESULTS: To better understand why some waveforms are more efficacious for defibrillation, reentry was induced in six dogs with 1-, 2-, 4-, 8-, and 16-msec monophasic and 1/1- (both phases 1 msec) 2/2-, 4/4-, and 8/8-msec biphasic shocks. Reentry was initiated by 141+/-15 V shocks delivered from a defibrillator with a 150-microF capacitance during the vulnerable period of paced rhythm (183+/-12 msec after the last pacing stimulus). The shock potential gradient field was orthogonal to the dispersion of refractoriness. Activation was mapped with 121 electrodes covering 4 x 4 cm of the right ventricular epicardium, and potential gradient and degree of recovery of excitability were estimated at the sites of reentry. Defibrillation thresholds (DFTs) were estimated by an up-down protocol for the same nine waveforms in eight dogs internally and in nine other dogs externally. DFT voltages for the different waveforms were positively correlated with the magnitude of shock potential gradient and negatively correlated with the recovery interval at the site at which reentry was induced by the waveform during paced rhythm for both internal (DFT = 1719 + 64.5VV - 11.1RI; R2 = 0.93) and external defibrillation (DFT = 3445 + 150VV - 22RI; R2 = 0.93). CONCLUSION: The defibrillation waveforms with the lowest DFTs were those that induced reentry at sites of low shock potential gradient, indicating efficacious stimulation of myocardium. Additionally, the site of reentry induced by waveforms with the lowest DFTs was in myocardium that was more highly recovered just before the shock, perhaps because this high degree of recovery seldom occurs during defibrillation due to the rapid activation rate during fibrillation.

Animals↗
PubMed2001

Purkinje and ventricular contributions to endocardial activation sequence in perfused rabbit right ventricle.

Interactions between peripheral conduction system and myocardial wave fronts control the ventricular endocardial activation sequence. To assess those interactions during sinus and paced ventricular beats, we recorded unipolar electrograms from 528 electrodes spaced 0.5 mm apart and placed over most of the perfused rabbit right ventricular free wall endocardium. Left ventricular contributions to electrograms were eliminated by cryoablating that tissue. Electrograms were systematically processed to identify fast (P) deflections separated by >2 ms from slow (V) deflections to measure P-V latencies. By using this criterion during sinus mapping (n = 5), we found P deflections in 22% of electrograms. They preceded V deflections at 91% of sites. Peripheral conduction system wave fronts preceded myocardial wave fronts by an overall P-V latency magnitude that measured 6.7 +/- 3.9 ms. During endocardial pacing (n = 8) at 500 ms cycle length, P deflections were identified on 15% of electrodes and preceded V deflections at only 38% of sites, and wave fronts were separated by a P-V latency magnitude of 5.6 +/- 2.3 ms. The findings were independent of apical, basal, or septal drive site. Modest changes in P-V latency accompanied cycle length accommodation to 125-ms pacing (6.8 +/- 2.6 ms), although more pronounced separation between wave fronts followed premature stimulation (11.7 +/- 10.4 ms). These results suggested peripheral conduction system and myocardial wave fronts became functionally more dissociated after premature stimulation. Furthermore, our analysis of the first ectopic beats that followed 12 of 24 premature stimuli revealed comparable separation between wave fronts (10.7 +/- 5.5 ms), suggesting the dissociation observed during the premature cycles persisted during the initiating cycles of the resulting arrhythmias.

Animals↗
PubMed2000

Reduction of atrial defibrillation threshold with an interatrial septal electrode.

BACKGROUND: The standard lead configuration for internal atrial defibrillation consists of a shock between electrodes in the right atrial appendage (RAA) and coronary sinus (CS). We tested the hypothesis that the atrial defibrillation threshold (ADFT) of this RAA-->CS configuration would be lowered with use of an additional electrode at the atrial septum (SP). METHODS AND RESULTS: Sustained atrial fibrillation was induced in 8 closed-chest sheep with burst pacing and continuous pericardial infusion of acetyl-ss-methylcholine. Defibrillation electrodes were situated in the RAA, CS, pulmonary artery (PA), low right atrium (LRA), and across the SP. ADFTs of RAA-->CS and 4 other lead configurations were determined in random order by use of a multiple-reversal protocol. Biphasic waveforms of 3/1-ms duration were used for all single and sequential shocks. The ADFT delivered energies for the single-shock configurations were 1.27+/-0.67 J for RAA-->CS and 0. 86+/-0.59 J for RAA+CS-->SP; the ADFTs for the sequential-shock configurations were 0.39+/-0.18 J for RAA-->SP/CS-->SP, 1.16+/-0.72 J for CS-->SP/RAA-->SP, and 0.68+/-0.46 J for RAA-->CS/LRA-->PA. Except for CS-->SP/RAA-->SP versus RAA-->CS and RAA-->CS/LRA-->PA versus RAA+CS-->SP, the ADFT delivered energies of all of the configurations were significantly different from each other (P:<0. 05). CONCLUSIONS: The ADFT of the standard RAA-->CS configuration is markedly reduced with an additional electrode at the atrial SP.

Animals↗
PubMed2000

Ventricular defibrillation with triphasic waveforms.

BACKGROUND: It has been reported that triphasic defibrillation waveforms cause less myocardial injury than biphasic waveforms. This study compared the defibrillation thresholds (DFTs) of triphasic and biphasic waveforms. METHODS AND RESULTS: ++DFTs were determined for a transvenous lead system and a 300-microF-capacitor defibrillator. In 8 pigs (group 1), DFTs were determined for 5 triphasic waveforms with tilts of 80%, 83%, and 86% and for 1 biphasic waveform. DFTs were determined in another 8 pigs (group 2) for 2 triphasic and 4 biphasic waveforms with tilts of 43%, 49%, and 56%. In both groups, a biphasic waveform from a 140-microF-capacitor defibrillator was also evaluated, and both shock polarities were tested for each waveform. In group 1, with the 300-microF-capacitor defibrillator, the leading-edge voltage and energy stored at DFT were significantly lower for triphasic waveforms with phase-duration ratios of 50/33/17 and an anode at the right ventricular electrode for phase 1 than for biphasic waveforms (P<0.001). In group 2, the stored energy of triphasic waveforms with 56% and 49% tilt was significantly lower than that of biphasic waveforms with the same tilts for anodal but not cathodal phase 1 at the right ventricular electrode. Electrode polarity significantly affected the DFT of triphasic waveforms for both studies. CONCLUSIONS: Some 80% tilt triphasic waveforms defibrillate more efficiently than biphasic waveforms with a 300-microF-capacitor defibrillator. The triphasic waveforms for both groups were not superior to 140-microF-capacitor biphasic waveforms. The efficacy of triphasic waveforms depends on phase durations and electrode polarity.

Animals↗
PubMed2000

Using an artificial neural network to detect activations during ventricular fibrillation.

Ventricular fibrillation is a cardiac arrhythmia that can result in sudden death. Understanding and treatment of this disorder would be improved if patterns of electrical activation could be accurately identified and studied during fibrillation. A feedforward artificial neural network using backpropagation was trained with the Rule-Based Method and the Current Source Density Method to identify cardiac tissue activation during fibrillation. Another feedforward artificial neural network that used backpropagation was trained with data preprocessed by those methods and the Transmembrane Current Method. Staged training, a new method that uses different sets of training examples in different stages, was used to improve the ability of the artificial neural networks to detect activation. Both artificial neural networks were able to correctly classify more than 92% of new test examples. The performance of both artificial neural networks improved when staged training was used. Thus, artificial neural networks may beuseful for identifying activation during ventricular fibrillation.

Diagnosis, Computer-Assisted↗
PubMed2000

Ten-year follow-up for male twins divided into high- or low-risk groups for ischemic heart disease based on risk factors measured 25 years previously.

PURPOSE: To undertake medical follow-up in white males in the National Heart, Lung, and Blood Institute (NHLBI) twin study, previously divided on the basis of cardiovascular disease risk factors. METHODS: Tree structured survival analysis (TSSA) used at a mean age of 63 years to classify twins into high and low risk subgroups for ischemic heart disease (IHD) found that subjects at a mean age of 48 years were at highest risk with high systolic blood pressures and low high density lipoprotein cholesterol levels. Low risk subjects had lower blood pressures, better pulmonary function tests, and a negative family history for IHD or low post load plasma glucose levels. Medical record review was performed ten years later at the 4th Examination of the NHLBI twin cohort conducted in 1995-1997. RESULTS: The percentage of men in the NHLBI twin study who died nearly tripled (from 9.3% to 25.8%) in the ten-year period between the ages of 63 and 73 years. Deaths have tended to remain higher in DZ than MZ twins (27.8% versus 23.7%). At Exam 4, the relative risk of IHD (fatal or non-fatal) was 5.24 times higher for those in the high risk group than those in the low risk class (95% confidence limit 2.72-10.07, p < 0.0001 and 5.86 for any cardiovascular disease (95% confidence limit 3.03-11.33). The proportion of deaths from IHD in subjects with a high risk profile at entry was 51.7%, and 70.0% had died from all cardiovascular related disease. CONCLUSION: The present results indicate TSSA remained effective in classifying subjects into subgroups with greater risk of morbidity and mortality related to cardiovascular disease after ten additional years.

Aged↗
PubMed2000

A comparison of three approaches for attributing hospitalizations to specific diseases in cost analyses.

OBJECTIVES: Calculations of healthcare costs rarely disclose the specific approach used to allocate the cost of hospitalizations by diagnosis. However, the type of approach used can have a major impact on the findings in the case of significant comorbidities. The present analyses compared three approaches for attributing Medicare DRG reimbursements (which were used as surrogates for average costs) for hospitalization by diagnosis. METHODS: Medical resource utilization data from the National Hospital Discharge Survey were analyzed using each of three allocation approaches: a) attributing 100% of the cost of hospitalization to the disease when it was the first-listed diagnosis; b) attributing a portion of the cost of hospitalization to the disease, depending on its position in the list of diagnoses and the relevance of any comorbidities; and c) an incremental analysis of cost based upon the hospitalization experiences of an age and gender matched cohort. These three approaches were applied to the cost of hospitalization for chronic obstructive pulmonary disease (COPD). RESULTS: The first approach projected 206,098 hospitalizations at $3,449 per hospitalization for a projected U.S. annual total of $711 million. The second approach projected 681,547 hospitalizations at $3,205 per hospitalization for a projected U.S. annual total of $2.2 billion. The third approach also projected 681,547 hospitalizations, but at $2,361 per hospitalization, for a projected U.S. annual total of $1.6 billion. CONCLUSIONS: Expanding from the example on COPD, the limitations of each approach are described and their applications to other conditions are presented.

Aged↗
PubMed2000

Electrode impedance: an indicator of electrode-tissue contact and lesion dimensions during linear ablation.

Pre-ablation impedance was evaluated for its ability to detect electrode-tissue contact and allow creation of long uniform linear lesions with a multi-electrode ablation catheter. The study consisted of 2 parts, both of which used the in vivopig thigh muscle model. In part 1, a 7 Fr. multi-electrode catheter was held in 3 electrode-tissue contact conditions: (1) non-contact; (2) light contact with a 30g downward force; and (3) tight contact with a 90g downward force. Impedances were measured in unipolar, modified unipolar and bipolar configurations using a source with frequencies from 100Hz to 500kHz. Compared with non-contact, the impedance increased 35 +/- 22 % with 30g contact pressure and 68 +/- 40% when the contact pressure was increased to 90g across the range of frequencies studied. In part 2, the same catheter was held against the tissue with different forces. Pre-ablation impedance was measured using a 10kHz current. Phased radiofrequency energy was applied to the 5 electrodes simultaneously using 10W power at each electrode for 120s. A total of 32 linear lesions were created. The lesion dimensions correlated with pre-ablation impedance. A unipolar impedance > or = 190 Omega indicates 95% possibility to create a uniform linear lesion of at least 3mm depth with our ablation system. We conclude that pre-ablation impedance may be a useful indicator for predicting electrode-tissue contact and the ability to create a continuous and transmural linear lesion with a multi-electrode catheter.

Analysis of Variance↗
PubMed2000

Continuous telemetry from a chronic canine model of sudden cardiac death.

INTRODUCTION: We sought to develop a continuously telemetered animal model of sudden cardiac death (SCD) to study the role of existing infarcts and acute ischemia in fatal arrhythmias. METHODS AND RESULTS: A telemetry system capable of recording eight channels of electrophysiologic data continuously and chronically has been developed. To demonstrate the use of this technology in an animal model of sudden death, 12 anesthetized dogs were instrumented with eight electrodes located in endocardium of the right side of the heart, epicardium of the left ventricle (LV), or in the subcutaneous tissues. The left anterior descending (LAD) coronary artery was occluded for 90 minutes and reperfused to produce LV infarction. A copper wire was placed in the left circumflex (LCX) coronary artery to cause intimal injury in a second arterial bed. The telemetry unit recorded deaths in seven animals between 19 to 64 hours after surgery. Five animals that did not experience SCD by the fifth postoperative day served as controls. There were three modes of SCD: complex ventricular ectopy that degenerated into ventricular fibrillation (VF, n = 4); normal sinus rhythm that suddenly degenerated into VF (n = 1); and bradycardia (RR intervals >1,000 msec) that lasted >3 minutes and preceded VF (n = 2). ST segment changes were significantly greater in the LCX-bed electrograms for tachyarrhythmic compared to bradyarrhythmic deaths (mean +/- SD; 4.0 +/- 3.4 mV and 0.2 +/- 0.8 mV, respectively). Fast Fourier transform showed the peak frequency of VF 10 seconds after onset was significantly higher in the five dogs with initial tachyarrhythmias compared with the VF that followed profound bradycardia (6.5 +/- 3.1 Hz and 3.7 +/- 0.6 Hz, respectively). Computer-assisted planimetry of postmortem heart slices revealed that infarcts in the two dogs with bradycardic events were larger (19.7% +/- 2.2% of the LV and septal mass) than in the five dogs with tachyarrhythmias (7.7% +/- 2.4%) or in the five control dogs (11.9% +/- 8.1%). CONCLUSION: It is possible to record via telemetry the events leading to SCD in an animal model. Continuous telemetry monitoring demonstrated that both tachyarrhythmias and bradyarrhythmias ultimately resulted in VF in an animal model of SCD. Animals with tachyarrhythmic deaths had greate ischemia in the LCX bed, smaller preexisting infarcts, and higher VF peak frequency than animals with bradyarrhythmic deaths.

Animals↗
PubMed2000

Fibrillation is more complex in the left ventricle than in the right ventricle.

INTRODUCTION: The mechanisms that maintain ventricular fibrillation (VF) are not completely understood. It has been proposed that increased ventricular wall thickness destabilizes VF wavefronts and therefore is an important determinant of VF activation patterns. We hypothesized that if this is the case, then VF patterns on the thin-walled right ventricle (RV) should be simpler than those on the thick-walled left ventricle (LV). METHODS AND RESULTS: In seven open chest pigs, we mapped VF simultaneously from two epicardial recording arrays, one on the RV and one on the LV. Each array contained 504 unipolar electrodes (in a 21 x 24 grid) spaced by 2 mm. We used specialized pattern analysis methods to compute quantitative descriptors of RV and LV activation patterns. Our data show that VF is more organized in the RV than the LV, containing fewer, larger wavefronts that follow fewer distinct pathways and are less likely to fragment or collide with other wavefronts. The incidence, size, and cycle length of reentrant circuits were similar in the two ventricles, but RV reentry persisted for more cycles. These results are not predicted by the differences in electrophysiologic properties between LV and RV that have been reported in mammalian hearts. CONCLUSION: The geometry of the ventricular wall, particularly wall thickness, is an important determinant of VF activation patterns.

Action Potentials↗
PubMed2000

Direct medical cost of chronic obstructive pulmonary disease in the U.S.A.

The aim of this study was to estimate the direct medical costs of chronic obstructive pulmonary disease (COPD) in the United States using a public-payor perspective. Cost estimates were derived separately for 10 components of care using national survey databases and valued using Medicare and Medicaid reimbursement rates. COPD affects 15 million people in the U.S.A. and the total annual U.S. payment for care is $6.6 billion. Approximately one-third ($2.3 billion) is due to the cost of long-term oxygen therapy, one-quarter is attributed to hospitalizations and inpatient physician services ($1.9 billion), and one-seventh ($942 million) is due to nursing home stays. Other annual costs are outpatient physician visits ($480 million), prescription medications ($462 million), home healthcare ($309 million), emergency department visits ($148 million), outpatient diagnostic procedures ($55 million) and hospice care ($28 million). The cost of COPD is therefore considerable. The significant expenditure for long-term oxygen therapy indicates that disease severity is a major driver of costs. However, the cost of hospitalizations, nursing home stays, emergency department and physician visits are not insignificant.

Aged↗
PubMed2000

A telemetry system for the study of spontaneous cardiac arrhythmias.

The characteristics of spontaneous cardiac arrhythmias leading to sudden cardiac death are largely unknown. To study arrhythmias in animal models, an eight-channel implantable radio telemetry system has been developed to record continuously cardiac electrograms over a period of weeks to months, with maintenance restricted to changing batteries. The inputs are connected in a unipolar manner. Each channel has a gain of fifty and is AC coupled, band limited to 0.07-260 Hz. The signals are digitized with 12 bits resolution at 1000 samples/s. The amplifiers, analog-to-digital converter, and control logic are packaged in an implantable unit. An umbilical cable is passed through the skin to an external backpack unit for power and data transmission. A custom serial interface card, a PC/104 form factor 25-MHz 80386-based single-board computer with a PCMCIA wireless local area network (WLAN) card, and battery power supply make up the backpack. Data are read into the parallel port of the computer, buffered, then transmitted over the WLAN to the laboratory network where it can be analyzed and archived. Approximately 12 h of 14,000 bytes/s data can be collected with each set of batteries. The system is suitable for continuous monitoring of animal models of spontaneous arrhythmias and sudden cardiac death.

Animals↗
PubMed2000

Estimation of 3-D conduction velocity vector fields from cardiac mapping data.

A method to estimate three-dimensional (3-D) conduction velocity vector fields in cardiac tissue is presented. The speed and direction of propagation are found from polynomial "surfaces" fitted to space-time (x, y, z, t) coordinates of cardiac activity. The technique is applied to sinus rhythm and paced rhythm mapped with plunge needles at 396-466 sites in the canine myocardium. The method was validated on simulated 3-D plane and spherical waves. For simulated data, conduction velocities were estimated with an accuracy of 1%-2%. In experimental data, estimates of conduction speeds during paced rhythm were slower than those found during normal sinus rhythm. Vector directions were also found to differ between different types of beats. The technique was able to distinguish between premature ventricular contractions and sinus beats and between sinus and paced beats. The proposed approach to computing velocity vector fields provides an automated, physiological, and quantitative description of local electrical activity in 3-D tissue. This method may provide insight into abnormal conduction associated with fatal ventricular arrhythmias.

Animals↗