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Reentry wave formation in excitable media with stochastically generated inhomogeneities.

Clinical research shows that the frequency of arrhythmia events depends on the number and area of the border zones of infarct scars. We investigate the possibility that arrhythmia is initiated by reentry waves generated by the inhomogeneity of conduction velocity at the border zone. The interaction of a plane wave with a spatially extended inhomogeneity is simulated in the FitzHugh- Nagumo model. The inhomogeneity is introduced into the model by modifying the spatial dependence of the diffusion coefficient in a stochastic manner. This results in a rich variety of spatial distributions of conductivity. A plane wave propagating through such a system may break up on the regions with low conductivity and produce numerous spiral waves. The frequency of reentry wave formation is studied as a function of the parameters of the inhomogeneity generation algorithm. Three main scenarios of reentry wave formation were found: unidirectional block, main wave-wavelet collision, and wave break up during collision, on a region in which a conduction velocity gradient occurs. These scenarios are likely candidates for the mechanisms of arrhythmia initiation in a damaged tissue, e.g., the border zone of an infarct scar.

Action Potentials↗

Initiation of re-entry in an excitable medium: structural investigation of cardiac tissue using a genetic algorithm.

The detailed mechanisms by which re-entry and ventricular fibrillation are initiated in the heart remain poorly understood because they are difficult to investigate experimentally. We have used a simplified excitable media computational model of action potential propagation to systematically study how re-entry can be produced by diffuse regions of inexcitable tissue. Patterns of excitable and inexcitable tissue were generated using a genetic algorithm. The inexcitable tissue was modeled in two ways: (i) diffusive, electrically connected but inexcitable tissue, or (ii) zero-flux, areas of tissue electrically disconnected in the same way as zero-flux boundary conditions. We were able to evolve patterns of diffuse inexcitable tissue that favored re-entry, but no single structure or pattern emerged. Diffusive inexcitable regions were inherently less arrhythmogenic than zero-flux inexcitable ones.

Algorithms↗

Propagation failures, breathing pulses, and backfiring in an excitable reaction-diffusion system.

We report results from experiments with a pseudo-one-dimensional Belousov-Zhabotinsky reaction that employs 1,4-cyclohexanedione as its organic substrate. This excitable system shows traveling oxidation pulses and pulse trains that can undergo complex sequences of propagation failures. Moreover, we present examples for (i) breathing pulses that undergo periodic changes in speed and size and (ii) backfiring pulses that near their back repeatedly generate new pulses propagating in opposite direction.

Animals↗

Calculation of mitral regurgitant orifice area with use of a simplified proximal convergence method: initial clinical application.

To validate a previously proposed simplified proximal flow convergence method for calculating mitral regurgitant orifice area (ROA), a prospective study was conducted in ambulatory patients and in patients undergoing open heart surgery. Assuming a pressure difference between the left ventricle and left atrium of approximately 100 mm Hg (jet velocity [v(p)] 500 cm/s) and setting the color aliasing velocity (v(a)) to 40 cm/s, we simplified the conventional proximal convergence method formula (ROA = 2pi(r2)v(a)/v(p)) to r2/2, where r is the radius of the proximal convergence isovelocity hemisphere. For 57 ambulatory patients with a wide range of mitral regurgitant severity (1 to 4+), ROA was calculated by the conventional (x) and simplified (y) methods, demonstrating excellent accuracy (r = 0.92; P <.001; DeltaROA [y - x] = 0.004 +/- 0.08 cm2). For 24 intraoperative patients, ROA calculated by the simplified formula (y) correlated well with the pulsed Doppler-thermodilution method (x) (r = 0.84; P <.01; DeltaROA [y - x] = -0.002 +/- 0.08cm2). This simplified proximal convergence formula yields an accurate assessment of ROA for a wide range of regurgitant severity, while the time required for this measurement is shortened by half (1.5 +/- 0.5 minutes versus 3.2 +/- 0.7 minutes). This may increase the frequency of calculating ROA in the clinical laboratory.

Aged↗

Steady and pulsatile flow fields in an end-to-side arterial anastomosis model.

We investigated the flow field within a rigid-walled in vitro model of an end-to-side 45 degree anastomosis in an attempt to identify possible hemodynamic factors that may contribute to the pathogenesis of distal anastomotic intimal hyperplasia. A high-resolution photochromic tracer technique was used to visualize the flow in orthogonal planes and to determine the axial wall shear stress profiles for both steady and pulsatile flows over a range of physiologically relevant conditions. The flow field showed qualitative similarities to those seen in curved vessel: rapidly moving fluid from the graft section affects the bed of the host vessel, that is, the wall opposite the anastomosis, eventually advancing down the host vessel in a spiraling motion. A small mobile separation zone was noted at the toe of the anastomosis. Comparison of wall shear stress profiles with previously reported preferential sites for the development of intimal hyperplasia supported a low wall shear stress and/or flow separation pathogenesis hypothesis. One notable exception was the bed of the host artery that appeared to be subjected to a complex hemodynamic environment.

Arteriovenous Shunt, Surgical↗

Net pressure gradients in aortic prosthetic valves can be estimated by Doppler.

BACKGROUND: In aortic prosthetic valves, both the Doppler-estimated gradients and orifice areas are misleading in the assessment of hemodynamic performance. The parameter of major interest is the net pressure gradient after pressure recovery (PR). We, therefore, investigated, in vitro, our ability to predict the net pressure gradient and applied the formulas in a representative patient population with 2 different valve designs. METHODS: We studied the St Jude Medical (SJM) standard valve (size 19-27) and SJM Biocor (size 21-27) in an in vitro steady-flow model with simultaneous Doppler-estimated pressure and catheter pressure measurements. Using echocardiography, we also studied patients who received the SJM (n = 66) and SJM Biocor (n = 45). RESULTS: In the SJM, we observed PR both within the prosthesis and aorta, whereas in the SJM Biocor, PR was only present in the aorta. We estimated the PR within the valve and within the aorta separately from echocardiographic in vitro data, combining a regression equation (valve) with an equation on the basis of fluid mechanics theory (aorta). The difference between estimated and catheter-obtained net gradients (mean +/- SD) was 0.6 +/- 1.6 mm Hg in the SJM and -0.2 +/- 1.9 mm Hg in the SJM Biocor. When these equations were applied in vivo, we found that PR had an overall value of 57 +/- 7% of the peak Doppler gradient in the SJM and 33 +/- 9% in the SJM Biocor. CONCLUSIONS: The in vitro results indicate that it is possible to predict the net pressure gradient by Doppler in bileaflet and stented biologic valves. Our data indicate that important PR is also present in stented biologic valves.

Adult↗

Determination of the mechanical properties of the different layers of blood vessels in vivo.

The structure and materials of the blood vessel wall are layered. This article presents the principle of a method to determine the mechanical properties of the different layers in vivo. In vivo measurement begets in vivo data and avoids pitfalls of in vitro tests of dissected specimens. With the proposed method, we can measure vessels of diameters 100 microns and up and obtain data on vascular smooth muscles and adventitia. To derive the full constitutive equations, one must first determine the zero-stress state, obtain the morphometric data on the thicknesses of the layers, and make mechanical measurements in the neighborhood of the zero-stress state. Then eight small perturbation experiments are done on earth blood vessel in vivo to determine eight incremental elastic moduli of the two layers of the blood vessel wall. The calculation requires the morphometric data and the location of the neutral axis. The experiments are simple, the interpretation is definitive, but the analysis is somewhat sophisticated. The method will yield results that are needed to assess the stress and strain in the tissues of the blood vessel. The subject is important because blood vessels remodel themselves significantly and rapidly when their stress and strain deviate from their homeostatic values, and because cell proliferation, differentiation, adhesion, contraction, and locomotion depend on stress and strain in the tissue.

Animals↗

Use of intrinsic modes in biology: examples of indicial response of pulmonary blood pressure to +/- step hypoxia.

Recently, a new method to analyze biological nonstationary stochastic variables has been presented. The method is especially suitable to analyze the variation of one biological variable with respect to changes of another variable. Here, it is illustrated by the change of the pulmonary blood pressure in response to a step change of oxygen concentration in the gas that an animal breathes. The pressure signal is resolved into the sum of a set of oscillatory intrinsic mode functions, which have zero "local mean," and a final nonoscillatory mode. With this device, we obtain a set of "mean trends," each of which represents a "mean" in a definitive sense, and together they represent the mean trend systematically with different degrees of oscillatory content. Correspondingly, the oscillatory content of the signal about any mean trend can be represented by a set of partial sums of intrinsic mode functions. When the concept of "indicial response function" is used to describe the change of one variable in response to a step change of another variable, we now have a set of indicial response functions of the mean trends and another set of indicial response functions to describe the energy or intensity of oscillations about each mean trend. Each of these can be represented by an analytic function whose coefficients can be determined by a least-squares curve-fitting procedure. In this way, experimental results are stated sharply by analytic functions.

Animals↗

Haemodynamic modelling for the arterial pulsatile component of the intracranial pulse wave.

Vasospasm of cerebral arteries narrows the amplitude of the intracranial pressure wave, indicating that the arterial segment of the cerebral circulation is partially responsible for its formation. We investigated the fundamental mechanism of pressure pulse transmission from an artery to the surrounding environment. A mathematical model was derived expressing the amplitude of container pulsation (delta Po) as a function of mean intraluminal pressure (MPi), mean container pressure (MPo) and arterial pulse amplitude (delta Pi): delta Po = (-2(MPi - MPo) + b) (MPo + 1) delta Pi. This mathematical model was experimentally validated using an in vivo system of a single artery sealed inside a fluid-filled elastic container.

Animals↗

A non-linear haemodynamic model for the arterial pulsatile component of the intracranial pulse wave.

An indication that pressure pulses in cerebral arteries may play a role in the configuration of intracranial pressure pulsations is given by the observation that vasospasm of cerebral arteries narrows the amplitude of the intracranial pressure wave. The present work develops a mathematical model for the transmission of arterial pressure pulses across the compliant arterial wall to the surrounding intracranial space. Compliance of both the arterial segment and the intracranial space are considered. So as to retain accuracy at higher values of the mean intracranial pressure, a physiological range in which pulse transmission is enhanced due to lower pressure gradients but intracranial compliance is not necessarily decreased, a logistic fit is used to model the intracranial pressure-volume relationship. A sequence of approximations (with error bounds) is obtained for the induced intracranial pressure pulse amplitude as a function of arterial pulse amplitude, mean transmural pressure, and mean intracranial pressure. It is found that at higher mean intracranial pressures, where the usual exponential assumption for the intracranial pressure-volume curve loses validity, the amplitude of the transmitted arterial pressure pulse depends non-linearly on the mean intracranial pressure.

Animals↗

Cerebral venous system mechanics during a constant infusion in subarachanoid space: a model study.

A model has been developed to explain the development of stress under a constant infusion of fluid into the subarachanoid space. When the regulatory mechanism operates, the infused fluid is accommodated by the venous system and hence the tissue 'give' mechanism is under minimal stress. The necessity of maintaining a constant blood flow causes the blood vessel to dilate at higher CSF pressures. This puts the tissue 'give' mechanism under dual pressures, since it has to make room for the expanding ventricle as well as the dilating venous system. The theoretical model developed has been validated by experimental observations.

Animals↗

A computer simulation of the haemodynamic effects of intracranial arteriovenous malformation occlusion.

To study the effect of AVM occlusion on cerebrovascular haemodynamics, a simplified model was simulated consisting of a feeding artery supplying a capillary bed in parallel with a fistula-like malformation, both emptying into a draining vein. An electrical circuit analogue of the physiologic system was developed using lumped proximal and distal pressure dependent resistances, and capacitors representing vascular compliance. Autoregulation was introduced as a pressure varying precapillary arteriolar resistance. Equations derived from the circuit model were simulated using a graphical modeling program. The model successfully simulates phenomena angiographically observed during embolization procedures. Fistula pressure is shown to rapidly fall following proximal AVM occlusion, in contrast to a marked rise seen with distal occlusion, which is associated with biphasic flow into and out of the fistula and the arterial feeder. The model predicts an increase in capillary pressure and capillary flow which, depending on the magnitude of the flow increase and the state of autoregulation, may result either in reversal of ischaemia or hyperperfusion injury. Vascular overload is predicted in the absence of autoregulation. There is, however, little potential for vascular overload when autoregulation is intact. The model represents a first step in the mathematical characterization of the phenomenon of hyperperfusion following AVM occlusion.

Arterial Occlusive Diseases↗

A nonlinear mathematical model for the development and rupture of intracranial saccular aneurysms.

Mathematical models of aneurysms are typically based on Laplace's law which defines a linear relation between the circumferential tension and the radius. However, since the aneurysm wall is viscoelastic, a nonlinear model was developed to characterize the development and rupture of intracranial spherical aneurysms within an arterial bifurcation and describes the aneurysm in terms of biophysical and geometric variables at static equilibrium. A comparison is made between mathematical models of a spherical aneurysm based on linear and nonlinear forms of Laplace's law. The first form is the standard Laplace's law which states that a linear relation exists between the circumferential tension, T, and the radius, R, of the aneurysm given by T = PR/2t where P is the systolic pressure. The second is a 'modified' Laplace's law which describes a nonlinear power relation between the tension and the radius defined by T = ARP/2At where A is the elastic modulus for collagen and t is the wall thickness. Differential expressions of these two relations were used to describe the critical radius or the radius prior to aneurysm rupture. Using the standard Laplace's law, the critical radius was derived to be Rc = 2Et/P where E is the elastic modulus of the aneurysm. The critical radius from the modified Laplace's law was R = [2Et/P]2At/P. Substituting typical values of E = 1.0 MPa, t = 40 microns, P = 150 mmHg, and A = 2.8 MPa, the critical radius is 4.0 mm using the standard Laplace's law and 4.8 mm for the modified Laplace's law.(ABSTRACT TRUNCATED AT 250 WORDS)

Aneurysm, Ruptured↗

Numerical study of unsteady stenosis flow: parametric evaluation of power-law model.

Currently the best indicator for surgical treatment of arterio-sclerosis is the degree of stenosis. Although X-ray angiography is currently the standard, cost and morbidity are distinct disadvantages. By modelling stenosis and studying its biofluid mechanics, one can apply its results in the field of arterial disease research. This formed the motivation for this work. A non-Newtonian (power law) incompressible Navier-Stokes (N-S) solver was developed using the method of operator splitting and artificial compressibility. The vehicle used is the computational fluid dynamics (CFD) numerical library FASTFLO. The power-law model developed is then used to do a parametric study of the effect of 'n' on blood flow mechanics where 'n' is the power index that determines the haematocrit of blood. A pulsatile pressure wave over a cardiac cycle of a second was used to simulate transient flow over a hypothetical two-dimensional stenotic geometry. By comparing the different velocity pressure, wall shear stress and viscosity profiles, it has been found when 'n' increases, the vortex formation and peak wall shear stress decreases (magnitudes of < 1.5 Pa). Since the formation of vortices and low oscillatory wall shear stress on the stenotic wall is detrimental to the well-being of the arterial tract, it can therefore be inferred that there might be a relationship between the diseased state of blood (power law) and early genesis of atherosclerosis. However, the conclusion of this paper marks the advent of new research directions in this field of study.

Arteriosclerosis↗

Computational haemodynamics analysis and comparison study of arterio-venous grafts.

Haemodialysis arterio-venous graft failure is related to the development of stenotic lesions most commonly located near the venous anastomosis, especially in the toe region. 'Disturbed flow' interaction with the vessel wall surface, characterized by haemodynamic parameters based on the local wall shear stress or the radial pressure gradient, have been widely recognized as the trigger mechanism of a cascade of abnormal biological events leading to occlusive developments. Assuming incompressible laminar flow and rigid, in-plane vessel walls, validated haemodynamics are numerically simulated for a constant-diameter end-to-side base case, the Venaflo graft, and an improved graft-end configuration. The geometric design of the new graft-end was based on the reduction of three time- and area-averaged haemodynamic parameters, i.e. the wall shear stress gradient, wall shear stress angle gradient, and radial pressure gradient. Considering the critical toe region, the Venaflo graft has demonstrated measurable improvements over the base case configuration in predictive computer simulations as well as in clinical trials. The performance improvement should be further enhanced with the modifications illustrated by the new design.

Arteriovenous Shunt, Surgical↗

Automatic adjustment of biphasic pulse duration in transthoracic defibrillation.

Many studies have proven that biphasic defibrillation pulses are more efficient than the damped sinusoid monopolar waveform. Transthoracic resistance was shown to change during the two phases. On the other hand, it was proven that transthoracic resistance plays an important role in the defibrillation process, yielding the current for selected energy or voltage. Pre-shock measurement of the resistance may lead to improved selection. Stabilized current defibrillators are of low stored-to-delivered energy ratio. Therefore, automatic dynamic adjustment of some defibrillator parameters with respect to transthoracic resistance changes seems rational. An approach is known for modifying the pulse duration, in order to deliver a selected energy. A method is proposed here and an experimental defibrillator is developed for dynamic pulse duration adjustment with the purpose of obtaining a desired optimal time-course of the cardiac cell transmembrane potential.

Animals↗

The time relationships of the constituent components of the human electrocardiogram.

This paper reports the results of an examination of the timing relationships of the principal constituent components of the human electrocardiogram (ECG). ECG recordings were obtained from 21 healthy subjects, 10 male and 11 female aged between 13 and 65 years, over a wide range of heart rates extending from 46 to 184 beats per minute (bpm). A wavelet transform method based on the Mexican Hat wavelet was then used to precisely locate the positions of the onset, peak, termination and the duration of individual components in the ECG. Component times were then classified according to the heart rate associated with the cardiac cycle to which the component belonged. Second-order equations in the square root of the cardiac cycle time, TR-R of theform AT(1/2)R-R+BT R-R+C were fitted to the data obtained for each component to characterize its timing variation. These equations may be used to synthesize an ECG signal having a profile that varies with heart rate in a manner which reflects the in vivo variation.

Adolescent↗

QRS detection using new wavelets.

This paper deals with a new wavelet (WVT) which has been developed and very effectively and efficiently used for the detection of QRS segments from the ECG signal. After carrying out the detection using five existing wavelets (two symmetric--WT1 and WT2--and three asymmetric--WT3, WT4 and WT5), two new wavelets (WT6 and WT7) were constructed and used for QRS detection. WT6 is a symmetric wavelet and has been constructed by a trial-and-error method. WT7 is an adaptive symmetric wavelet and adjusts its threshold as per the amplitude of the ECG signal. The accuracy of QRS detection obtained from WT6 is 99.8 % and from WT7 100%. The CSE DS-3 database has been used for tests. Both WT6 and WT7 have been proved to be superior in performance to the existing wavelets. Out of WT6 and WT7, WT7 holds high promise for error-free reliable QRS detection in computer-aided feature extraction and disease diagnostics.

Algorithms↗