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ABSTRACT: Analysis of T waves in the ECG is an essential clinical tool for diagnosis, monitoring, and follow-up of patients with heart dysfunction. During atrial flutter, this analysis has been so far limited by the perturbation of flutter waves superimposed over the T wave. This paper presents a method based on missing data interpolation for eliminating flutter waves from the ECG during atrial flutter. To cope with the correlation between atrial and ventricular electrical activations, the CLEAN deconvolution algorithm was applied to reconstruct the spectrum of the atrial component of the ECG from signal segments corresponding to TQ intervals. The locations of these TQ intervals, where the atrial contribution is presumably dominant, were identified iteratively. The algorithm yields the extracted atrial and ventricular contributions to the ECG. Standard T-wave morphology parameters (T-wave amplitude, T peak-T end duration, QT interval) were measured. This technique was validated using synthetic signals, compared to average beat subtraction in a patient with a pacemaker, and tested on pseudo-orthogonal ECGs from patients in atrial flutter. Results demonstrated improvements in accuracy and robustness of T-wave analysis as compared to current clinical practice.
IEEE Transactions on Biomedical Engineering 05/2011; · 2.28 Impact Factor
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ABSTRACT: Analysis of T waves in the ECG is an essential clinical tool for diagnosis, monitoring, and follow-up of patients with heart dysfunction. During atrial flutter, this analysis has been so far limited by the perturbation of flutter waves superimposed over the T wave. This paper presents a method based on missing data interpolation for eliminating flutter waves from the ECG during atrial flutter. To cope with the correlation between atrial and ventricular electrical activations, the CLEAN deconvolution algorithm was applied to reconstruct the spectrum of the atrial component of the ECG from signal segments corresponding to TQ intervals. The locations of these TQ intervals, where the atrial contribution is presumably dominant, were identified iteratively. The algorithm yields the extracted atrial and ventricular contributions to the ECG. Standard T-wave morphology parameters (T-wave amplitude, T peak-T end duration, QT interval) were measured. This technique was validated using synthetic signals, compared to average beat subtraction in a patient with a pacemaker, and tested on pseudo-orthogonal ECGs from patients in atrial flutter. Results demonstrated improvements in accuracy and robustness of T-wave analysis as compared to current clinical practice.
IEEE transactions on bio-medical engineering 12/2010; 58(4):1104-12. · 2.15 Impact Factor
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ABSTRACT: This paper describes an unsupervised signal processing method applied to three-channel unipolar electrograms recorded from human atria. These were obtained by epicardial wires sutured on the right and left atria after coronary artery bypass surgery. Atrial (A) and ventricular (V) activations had to be detected and identified on each channel, and gathered across the channels when belonging to the same global event. The algorithm was developed and optimized on a training set of 19 recordings of 5 min. It was assessed on twenty-seven 2 h recordings taken just before the onset of a prolonged atrial fibrillation for a total of 1593697 activations that were validated and classified as normal atrial or ventricular activations (A, V) and premature atrial or ventricular activations (PAA, PVA). 99.93% of the activations were detected, and amongst these, 99.89% of the A and 99.75% of the V activations were correctly labelled. In the subset of the 39705 PAA, 99.83% were detected and 99.3% were correctly classified as A. The false positive rate was 0.37%. In conclusion, a reliable fully automatic detection and classification algorithm was developed that can detect and discriminate A and V activations from atrial recordings. It can provide the time series needed to develop a monitoring system aiming to identify dynamic predictors of forthcoming cardiac events such as postoperative atrial fibrillation.
Physiological Measurement 10/2009; 30(12):1303-25. · 1.68 Impact Factor
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ABSTRACT: Electrogram analysis is important in clinical and experimental settings. Activation recovery interval (ARI) has been used to measure ventricular action potential duration (APD) but its suitability for the atria has not been addressed. Mapping of atrial repolarization may be especially important during nerve stimulation since large heterogenous APD changes may manifest. This study assessed the utility of estimating APD in the atria using electrograms. A computer model of the atria was used to compute electrograms. Two different atrial waveforms were used, as well as two ventricular. APD was modulated with an acetylcholine- (ACh) dependent potassium channel and varying the spatial ACh distribution. ARI was computed, as well as the area under the repolarization wave (ATa). APD was measured by four methods. Atrial electrograms were also compared to monophasic action potentials recorded from a dog. ARI computed from atrial action potentials was not very precise, with errors ranging over 30 ms. Determining changes in APD induced by changing [ACh] yielded larger errors. Conversely, ventricular action potentials produced ARIs that very closely correlated with APD, and changes in APD . Positive ATa indicated regions of shortened APD, and islands of ACh release were clearly demarcated by ATa polarity. Experimentally, ARI was able to detect changes in APD, but did not measure APD well. The faster rate of ventricular repolarization produces larger currents that are less susceptible to electrotonic coupling effects, improving correlation with APD. ARI most closely correlated with APD measured as a fixed threshold above rest. Atrial APs produce electrograms that can be used to detect changes in APD. This may be improved by decreasing coupling. The ATa is a robust measure for precisely identifying spatial APD heterogeneities.
IEEE Transactions on Biomedical Engineering 06/2009; · 2.28 Impact Factor
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ABSTRACT: Electrogram analysis is important in clinical and experimental settings. Activation recovery interval (ARI) has been used to measure ventricular action potential duration (APD) but its suitability for the atria has not been addressed. Mapping of atrial repolarization may be especially important during nerve stimulation since large heterogenous APD changes may manifest. This study assessed the utility of estimating APD in the atria using electrograms. A computer model of the atria was used to compute electrograms. Two different atrial waveforms were used, as well as two ventricular. APD was modulated with an acetylcholine- (ACh) dependent potassium channel and varying the spatial ACh distribution. ARI was computed, as well as the area under the repolarization wave (ATa). APD was measured by four methods. Atrial electrograms were also compared to monophasic action potentials recorded from a dog. ARI computed from atrial action potentials was not very precise, with errors ranging over 30 ms. Determining changes in APD induced by changing [ACh] yielded larger errors. Conversely, ventricular action potentials produced ARIs that very closely correlated with APD, and changes in APD . Positive ATa indicated regions of shortened APD, and islands of ACh release were clearly demarcated by ATa polarity. Experimentally, ARI was able to detect changes in APD, but did not measure APD well. The faster rate of ventricular repolarization produces larger currents that are less susceptible to electrotonic coupling effects, improving correlation with APD. ARI most closely correlated with APD measured as a fixed threshold above rest. Atrial APs produce electrograms that can be used to detect changes in APD. This may be improved by decreasing coupling. The ATa is a robust measure for precisely identifying spatial APD heterogeneities.
IEEE transactions on bio-medical engineering 03/2009; 56(5):1546-55. · 2.15 Impact Factor
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ABSTRACT: Summary form only given. The contraction of the heart is triggered by an electrical impulse that propagates from one muscle cell to another. This organized activity generates a potential field that can be measured as an electrocardiogram (ECG) on the body surface, or with a catheter inside the heart. The measured signals provide a wealth of diagnostic information. This information has traditionally been decoded by clinicians in a strictly empirical way. As more and more becomes known about the underlying processes in the cell membrane, it becomes more common to hypothesize links between malfunctions on the cellular level and ECG abnormalities. Due to the startling complexity of the basic processes and the heart's anatomy, large-scale mathematical modeling can be necessary to verify such hypotheses. The dynamics of the heart are described by a coupled system of elliptic and parabolic differential equations. Spatial step sizes have to be as small as 0.1 mm in some cases. This leads to systems of hundreds of millions of linear equations when a whole human heart is modeled. The difficulty of solving such large systems has for some time limited the size of heart models to those of mice and rabbits, requiring only about a million equations. A breakthrough was obtained two years ago when we found a combination of algorithms that could solve a system of 60 million equations. Deployed on a newly arrived SGI Altix system, these methods allowed us to model an entire human heart. This heart model has since then provided important new insights in a wide range of cardiological subjects from myocardial ischemia to repolarisation measurement in the heart. The more recent arrival of a 768-processor Altix 4700 system has allowed us to test our methods on an even larger scale. With its 1.5 TB memory, this machine could handle a model with 2 billion equations. A short test showed convergence with an iteration count that was not much larger than for much smaller systems. Currently, we - cannot obtain such resouces for routine work. However, our test shows that it is only a matter of time before heart models with over a billion nodes can be used. We expect that this will have a great impact on the understanding of sudden cardiac death syndromes related to congenital cardiomyopathies degenerative diseases that cause fragmentation of the heart muscle on a sub-millimeter scale.
High Performance Computing Systems and Applications, 2008. HPCS 2008. 22nd International Symposium on; 07/2008
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ABSTRACT: As a measure of local repolarization time (T<sub>R</sub>), the instant of maximum slope (T<sub>up</sub>) of the T wave in the local unipolar electrogram is commonly used. Measurement of T<sub>up</sub> can be difficult, especially in positive T waves. These difficulties have led some researchers to propose the instant of maximum downslope (<sub>Tdown</sub>) as a marker of T<sub>R</sub> when the T wave is positive. To improve understanding of T-wave parameters, we simulated electrograms with a bidomain model of the human heart. To test T-wave parameters, we compared them to T<sub>R</sub> determined from the local membrane potential. We propose a simple model of the electrogram, which we validated by comparison to the bidomain model. With the simple model, it is straightforward to show that the sign of the T wave is almost uniquely determined by T<sub>R</sub>. We then used the bidomain model to simulate the effects of a variety of pathologies and technical difficulties, which the simple model could not account for. Generally, T<sub>up</sub> was a much better estimate for T<sub>R</sub> than T<sub>down</sub>. Regional fibrosis could attenuate local electrogram components and reduce accuracy of T<sub>up</sub> as a marker for T<sub>R</sub>. In fibrotic tissue, T<sub>down</sub> was not related to T<sub>R</sub> at all. This investigation of electrogram slopes required the simulation of extracellular potentials with about 100 times more precision than needed for simulation of visually acceptable waveforms alone. This requirement is more difficult to meet in larger models, but it was actually possible for a human-heart model with 60 million nodes. By sacrificing some spatial resolution, we kept the computational requirements within acceptable limits for multiple simulations.
Engineering in Medicine and Biology Society, 2007. EMBS 2007. 29th Annual International Conference of the IEEE; 09/2007
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ABSTRACT: Myocardial ischemia leads to an efflux of potassium ions from affected cells. The resulting depolarization of the resting membrane is one of the main features of ischemic myocardium. It has been shown experimentally that a part of the surplus interstitial potassium is transported out of the ischemic zone, even if no coronary blood flow is present in the affected area. We propose to model this transport mechanism mathematically with a diffusion equation. This model explains the measured spatial profiles of extracellular potential and potassium concentration. In addition, it allows a quantitative prediction of the transmembrane current that flows as a result of ischemia-induced depolarization. This current is thought to play a role in arrhythmogenicity, which is an important cause of mortality in acute myocardial infarction. Our model predicts that this current reaches its maximum exactly on the border of the hypoxic area. An important depolarizing current would be present just within the border, where hypoxia is accompanied by a resting membrane potential that is only slightly elevated, due to coupling with the adjacent normal tissue. Still, in the presence of potassium transport the predicted current density is not large enough to explain ectopic activation on the lateral border of the ischemia. This suggests that activation is more likely to occur at the endocardium, where the potassium gradient is steeper.
Engineering in Medicine and Biology Society, 2007. EMBS 2007. 29th Annual International Conference of the IEEE; 09/2007
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ABSTRACT: A bidomain reaction-diffusion model of the human heart was developed and potentials resulting from normal depolarization and repolarization were compared with results from a compatible monodomain model. Comparisons were made for an empty isolated heart and for a heart with fluid-filled ventricles. Both sinus rhythm and ectopic activation were simulated. The model took 2 days on 32 processors to simulate a complete cardiac cycle. Differences between monodomain and bidomain results were very small, even for the extracellular potentials which, for the monodomain model, were computed with a high-resolution forward model. Electrograms computed with monodomain and bidomain models were visually indistinguishable. We conclude that, in the absence of applied currents, propagating action potentials on the scale of a human heart can be studied with a monodomain model
Engineering in Medicine and Biology Society, 2006. EMBS '06. 28th Annual International Conference of the IEEE; 10/2006
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ABSTRACT: ST-segment depression in epicardial electrograms can be a "reciprocal" effect of remote myocardial ischemia (MI), and can also be due to local partial-thickness or "subendocardial" MI. Experimental studies have shown either ST elevation or depression in leads overlying a subendocardial ischemic region. Those reporting elevation have shown depression over the lateral borders of the ischemia. Simulation studies with anisotropic models have explained the ST-elevation results. Presently, while experimentalists may have difficulty understanding the ST elevation, most model studies fail to explain ST depression in overlying leads during partial-thickness ischemia. We have simulated partial-thickness ischemia in a 3-dimensional model of the human heart. Our results show that the conductivity of the intracavitary blood, geometry of the ischemic region, and bidomain anisotropy ratios can all have a decisive influence on the sign of the ST deviation. We hypothesize that ST depression in leads overlying an ischemic zone is due to subendocardial ischemia in tissue where a redistribution of gap junctions has taken place
Engineering in Medicine and Biology Society, 2006. EMBS '06. 28th Annual International Conference of the IEEE; 10/2006
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ABSTRACT: To show that cycle-length (CL) prolongation occurring at the onset of reentrant tachycardias may be associated with an increase in conduction time (CT), and to investigate the involvement of Na+ and Ca2+ channel activity, reentrant activity was induced by programmed stimulation in thin ventricular muscle slices with a central cryothermal lesion, as documented with 7 to 12 bipolar recordings. We studied the course of the CL measured in successive tachycardia beats, as well as the course of conduction times after abrupt transition from a pacing CL of 1,000 to 400 ms (pacing paradigm). The majority of the tachycardias displayed a dynamic behavior in which CL increased progressively, with an exponential rate constant of 37 +/- 35 beats (mean +/- SD), stabilizing at 325 +/- 67 ms after a total increase of 17 +/- 17 ms. In the pacing paradigm, CT was prolonged from 68 +/- 21 ms to 79 +/- 24 ms according to a biphasic course consisting of an abrupt increase in the first response to 400 ms, followed up by an exponential increase, stabilizing with a rate constant of 18 +/- 23 beats. Lidocaine 5 x 10(-5) mol/L induced an increase in steady-state CT, which was not further modified by adding verapamil 10(-5) mol/L. However, verapamil prolonged the rate constant of the exponential course by 60 +/- 40 beats. Thus, the onset dynamics of reentrant tachycardias share common features with the dynamic behavior of CT in the pacing paradigm, in which both Na+ channel activity and Ca2+-modulated cellular coupling appear to be involved.
Journal of Electrocardiology 11/2000; 33(4):349-60. · 1.14 Impact Factor
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ABSTRACT: Previous studies on atrial flutter (AF) presumed that resetting was due to the prematurity effect (PE) in which the stimulated antegrade wavefront travels in the tail of the AF preexisting wavefront. We studied the collision effect (CE) between the AF and the stimulated retrograde wavefronts, its contribution to resetting, and its relationship to AF termination and how they are affected by the Class IC agent propafenone (PPF). A canine model of AF was created using a Y-shaped lesion in the right atrium in 14 dogs (33 +/- 3 kg). Five atrial bipolar electrodes were positioned around the tricuspid valve. In a subsequent set of 11 dogs, we used 16 bipolar electrodes for recording. AF was induced by burst pacing. Single and multiple stimuli were applied to measure conduction time and reset-response curves (RRCs). This was repeated after the administration of PPF (1 mg/kg loading dose for 10 minutes, followed by 1.8 mg/kg/per hour infusion). Three distinct mechanisms were found to contribute to the RRC: the PE, the CE, and heterogeneity. PPF stabilized the RRC, increased significantly the cycle length (CL), the duration of the effective refractory period, as well as the duration of the excitable gap. However, PPF did not alter the duration of the fully excitable portion. We studied 36 annihilations without and 48 with PPF. Transient fibrillation was found in 75% of the episodes without, compared to 22% with PPF. Other types of termination such as conduction block, CL oscillations, and reversal of activation were found for 25% of the episodes without and 78% with PPF. In many cases, conduction block and CL oscillations were associated with a failure of propagation of the stimulated antegrade wavefront in the region of collision. Termination by reversal of activation suggests that propagation was two dimensional and could not be represented by a one dimensional movement. The average coupling interval (in percent of CL), that induced fibrillation was not significantly different from that at which conduction block occurred. This suggests that transient fibrillation is associated with a weak CE rather than with rapid pacing. The CE is amplified by multiple stimuli and PPF. The incidence of transient fibrillation in AF annihilation diminishes with PPF as the CE becomes more important. This suggests that the evaluation of PE and CE in AF may be an indication of the risk of atrial fibrillation.
Pacing and Clinical Electrophysiology 09/2000; 23(8):1200-19. · 1.35 Impact Factor
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ABSTRACT: Postinfarction monomorphic ventricular tachycardias induced by programmed stimulation may display initial cycle length (CL) variations before stabilizing.
To show that tachycardia onset dynamics depend on rate-dependent electrical properties of the reentrant substrate, we extracted activation times and maximum negative slopes of local activation complexes (-dV/dt(max)) from 191 unipolar electrograms recorded in the anterior left ventricular wall of anesthetized, 3-day-old infarct canine preparations. Measurements were made of the responses to programmed stimulation, as well as in early and later beats of tachycardias, which displayed either a constant trend in CL (group A, n = 5 preparations) or one in which CL prolongation occurred according to an exponential course before stabilizing (group B, n = 9). Stimulation protocols inducing the tachycardias were more aggressive and their CL was significantly shorter (CL = 159 +/- 24 msec) in group A than in group B (stabilized CL = 206 +/- 34 msec). Reentrant activity occurred in subepicardial areas in which the absolute value of -dV/dt(max) (absolute value(-dV/dtmax)) was heterogeneously depressed (<2 mV/msec). Absolute value(-dV/dtmax) was reduced and activation delay increased in the successive responses to extrastimuli. Further reductions in absolute value(-dV/dtmax) (10% to 23%) were shown to occur between early and later beats in 5 of the 9 tachycardias in group B (no change in the 4 others), and they were associated with localized prolongation of conduction times in reentrant pathways. In contrast, absolute value(-dV/dtmax) improved in all group A tachycardias (7% to 25%).
This study provides evidence that the onset dynamics of postinfarction ventricular tachycardias are determined by interval-dependent electrical changes occurring in the reentrant substrate.
Journal of Cardiovascular Electrophysiology 05/2000; 11(5):531-44. · 3.06 Impact Factor
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ABSTRACT: Inappropriate shocks can complicate cardioverter defibrillator therapy. Among solutions proposed to avoid oversensing are algorithms to reduce inappropriate detection of atrial fibrillation (AF) or sinus tachycardia. In patients not on antiarrythmic drugs, an interval stability criterion of 40 ms has been validated with the Medtronic PCD to discriminate ventricular tachycardia (VT) from AF. With this algorithm, VT is considered stable if no interval varies from one of the three preceding intervals by more than 40 ms. If an interval does not fulfill this criterion, the VT event counter is reset to zero. The aim of this study was to investigate the incidence of underdetection when this criterion is applied in patients treated with antiarrhythmic drugs. We studied 132 sustained monomorphic VTs induced in 42 patients during 101 electrophysiological studies (EPS). EPS were performed without treatment (group I, 24 patients, 44 VTs); on Class Ia drug (group II, 17 patients, 24 VTs); Class Ic drug (group III, 22 patients, 39 VTs); or sotalol (group IV, 17 patients, 25 VTs). The endocardial electrogram of all VT episodes was digitized and the stability algorithm was applied. The reset arrhythmias were distributed among no delay, small, moderate (< 10 s) and important (> 15 s) delay in VT detection. The relation between drug use and reset was analyzed. Reset was found in 86 (65%) of induced VTs. No difference in heart rate or induction mode was shown between reset and nonreset VTs. There was a significative association between drug use and reset probability (Chi2 significantly different, P < 0.05). In patients treated with Class Ic drugs, the probability of finding an important delay in VT detection was 12.5% versus 0% in nontreated patients or in patients treated with sotalol. We conclude that a stability criterion of 40 ms is probably safe in nontreated patients but should be used with caution in patients treated with antiarrhythmics, especially in the presence of Class Ic drugs.
Pacing and Clinical Electrophysiology 12/1997; 20(12 Pt 1):2882-92. · 1.35 Impact Factor
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ABSTRACT: The aim of this study was to determine whether cycle length (CL) variations at the onset of monomorphic ventricular tachycardias follow distinctive patterns.
We retrospectively analyzed 59 monomorphic ventricular tachycardias induced in 40 patients in whom intraoperative mapping was performed with 63 epicardial and 64 endocardial electrograms recorded simultaneously. Activation times and CL were determined at each electrode site over several beats (36+/-10 beats, mean+/-SD) starting with the first after programmed stimulation. In the majority of the tachycardias, CL variations were accounted for by fitting to an exponential function: CL=CLs+Ae-b/tau, where CLs is the stable CL, b is beat number, tau is the time constant (in beat number), and A is the magnitude of CL relaxation. A decelerating trend (with reference to rate) (negative A) accounted for 21 tachycardias, an accelerating trend in rate (positive A) accounted for 12 tachycardias, and 4 others displayed a double dynamic behavior, with an initial acceleration followed by a decelerating trend in rate. Among the ventricular tachycardias that were not fitted to exponential models, 12 showed a constant trend and 10 others showed irregular CL fluctuations. The monomorphic character of the tachycardias was established by principal-component analysis, which also indicated that CL dynamics associated with the accelerating and decelerating trends may be related to shortening and prolongation of activation times, respectively, occurring in equal proportion at all recording sites. In canine preparations in which reentry circuits could be mapped with high resolution, CL showed an accelerating trend in rate when circus movement of excitation occurred around a transmural scar in muscle generating unipolar electrograms with relatively high -dV/dtmax, and a decelerating trend in rate occurred when functional reentry occurred in muscle generating unipolar electrograms with depressed -dV/dtmax.
Beat-to-beat CL variations may occur at the onset of sustained monomorphic ventricular tachycardia as a result of uniform acceleration or deceleration of activation times while the overall activation pattern remains constant. The associated initial trends in the rate of sustained monomorphic ventricular tachycardia follow typical patterns that might provide "signatures" corresponding to reentry substrates with distinctive functional properties.
Circulation 06/1996; 93(10):1845-59. · 14.74 Impact Factor
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Engineering in Medicine and Biology Society, 1992. Vol.14. Proceedings of the Annual International Conference of the IEEE;
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ABSTRACT: Heart Rate Variability (HRV) represents an instantaneous heart rate signal including the beat-to-beat fluctuation in heart rate. In obtaining this signal, nonlinear filtering with thresholding is a common approach by which QRS complex in the ECG signal can be detected. In this paper, two QRS detection algorithms are described and compared. These algorithms involve adaptive thresholding and fixed thresholding methods, respectively. Each algorithm has its advantages and disadvantages in terms of accuracy and speed. Future work can be done to improve the algorithms with a better tradeoff between accuracy and speed. By processing the accurate and real time HRV signals, useful physiological information can be obtained
Engineering in Medicine and Biology Society, 1997. Proceedings of the 19th Annual International Conference of the IEEE;
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ABSTRACT: The authors determined subjective fatigue level among twenty healthy subjects by two questionnaires (CFSI and POMS) and classified them into very fatigued group (B-group) and scarcely fatigued group (G-group). Then the authors gave a simple task to each group and assessed autonomic function indicators of HRV (CV-RR, LF,HF, and LF/HF). Moreover the authors performed the same experiment 8 or 9 times among three subjects that were classified into very fatigued state (B-state) and scarcely fatigued state (G-state). As the result, B-group tended to indicate lower CV-RR and higher LF/HF than G-group, and when the task was given, B-group had an individual difference in LF/HF although G-group indicated lower LF/HF. Similarly, B-state tended to indicate higher LF/HF than G-state. The results showed when one was in a fatigue state, the parasympathetic activity was at a low level, and sympathetic activity was dominant, and the balance of sympathetic and parasympathetic activity became different from a scarcely fatigued state. These tendencies indicated that one enters a tension state during fatigue. As autonomic function indicators of HRV reflected fatigue level, assessment of the cumulative fatigue from physiological reaction could be possible
Engineering in Medicine and Biology Society, 1997. Proceedings of the 19th Annual International Conference of the IEEE;
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ABSTRACT: The purpose of this study was to examine the spontaneous changes
in cycle length during episodes of sustained monomorphic (MVT) and
polymorphic (PVT) ventricular tachycardias and to relate these changes
with the sites of earliest epicardial activation. Isochronal activation
maps were obtained from 127 unipolar electrograms recorded from the
surface of both ventricles with a sock electrode array in open chest
anesthetized dogs. Cycle length (431±80 msec) in MVT (7 dogs) had
beat to beat variations of 15±17 msec corresponding with small
shifts in sites of epicardial breakthrough clustered along the border of
the ischemic myocardium. In PVT (5 dogs), the cycle length
(352±90 msec) had a variability of 61±23 msec,
corresponding to wide changes on the sites of epicardial breakthrough.
Mean cycle length and variability were significantly different
(p<0.01) between MVT and PVT. Linear regression analysis showed a
strong and significant correlation between cycle length variability and
the number of electrodes detecting the earliest activation (r=0.77,
p<0.0001)
Engineering in Medicine and Biology Society, 1997. Proceedings of the 19th Annual International Conference of the IEEE;
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ABSTRACT: This paper reports two attempts at estimating the magni-tude of atrial flutter amplitude modulation caused by atrial motion during heart contraction. The first approach con-sists in analyzing the ECG of a patient in flutter with atrio-ventricular block and an implanted pacemaker. These con-ditions facilitate QRST cancellation, even in the presence of time-varying flutter wave amplitude. The second ap-proach is based on a computer model of atrial flutter em-bedded in a torso model featuring predetermined motion of the atria. The results suggests that this lead-dependent effect is usually not large enough to preclude reasonably accurate QRST cancellation or T-wave extraction.
