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Biomedical subjects

T Arts

Publications and source records attributed to T Arts.

At least 55 records · Page 3Linked to original sources

Dynamic pumping characteristics of the Hemopump.

While pumping blood with the Hemopump in sheep, the ability of predicting the instantaneous pump flow from the pressure difference over the pump system and pump parameters was investigated. For rotational speed n between 300 and 475 revolutions per second (rps), maximum pump flow QO(n) at zero pressure difference, internal pump resistance R(n), and inertia parameter Lc were found to be suitable parameters for Hemopump characterization. The instantaneous pump flow could be estimated with an accuracy of approximately 1.0 [ml/s]. The values of the pump source parameters (+/- sd) were: (the figures in parentheses represent earlier reported values found while pumping water) Lc was a constant of 21.4 +/- 6.4 [Pa.s2/ml] (in water: 10.8). QO(n) is linearly related to rotational speed n according to: QO(n) = QO(ncen) + CQ(n-ncen), with QO(ncen) = 49.4 +/- 4.5 [ml/s] (in water: 60.3), CQ = 142 +/- 22.4 [10(-3) ml] (in water: 146), and ncen = 387.5 [rps]. R(n) is linearly related to rotational speed n according to: R(n) = R(ncen) + CR(n-ncen), with R(ncen) = 556 +/- 124 [Pa.s/ml] (in water: 502) and CR = 1.47 +/- 0.83 [Pa.s2/ml] (in water: 1.67).

Animals↗

Characterization of left ventricle function by analysis of pressure responses to steps in rotational speed of the Hemopump.

Optimizing the procedure of weaning the left ventricle from a left ventricular assist device requires the determination of the momentaneous condition of the left ventricle. In sheep, a method was developed to momentaneously quantify the left ventricular condition. The left ventricular pump condition was quantified by the time-varying parameters elastance and resistance. They were determined from perturbations in the left ventricular pressure of two subsequent beats induced by changes in flow of the assist device. The end-diastolic volume of the ventricle was estimated without directly measuring ventricular volume. Maximum elastance and resistance were 201.3 +/- 32.7 [Pa/ml] and 12.3 +/- 1.6 [Pa.s/ml], respectively (mean +/- SE). The ventricular time constant, defined by the ratio of resistance of elastance, was 84.6 +/- 17.1 [ms] (mean +/- SE).

Animals↗

Asymmetrical changes in ventricular wall mass by asynchronous electrical activation of the heart.

Ventricular pacing causes asynchronous electrical activation of the ventricular wall, because impulse conduction occurs via muscle fibers rather than via the Purkinje system. Chronic (up to 3 months) ventricular pacing caused about 30% decrease of wall mass in early activated regions but did not change wall mass in late activated regions. These are the first data indicating that chronic asynchronous activation induces asymmetrical structural adaptations. This asymmetry is likely to be evoked by regional differences in contractile work, as demonstrated in previous experiments from our laboratory. The nature of the structural adaptation as well as its clinical implications deserve more detailed investigation.

Adaptation, Physiological↗

Macroscopic three-dimensional motion patterns of the left ventricle.

The pattern of displacements in the left ventricle (LV) can be described by 13 modes of motion and deformation. Three functional modes of deformation are essential for ejection: a decrease in cavity volume, torsion, and ellipticalization. Four additional modes are used to describe asymmetric deformation. Six modes of rigid body motion describe rotation and translation. In the LV 14-20 radiopaque markers were inserted in the wall of the LV. They were distributed more or less evenly from base to apex and around the circumference. Torsion and volume changes require the definition of a cardiac coordinate system. The point at which ejection focuses is used as the origin, and the torsion axis is used as the z-axis. In the present study the coordinate system was positioned objectively by a least squares fit of the kinematic model to the measured motion of markers. In five dogs in the control state the kinematic parameters were determined as a function of time for all 13 modes. The torsion axis was displaced 4 +/- 2 mm (mean +/- sd) from the center of the cross-section of the LV towards the lateral free wall. The direction of the torsion axis closely coincided with anatomical landmarks at the apex and base. During systole, a unique relation was found between the ratio of cavity volume to wall volume and torsion. This relation was universal to all LVs, the cylinder-symmetric mathematical model of cardiac mechanics inclusive. In diastole the patterns of deformation seem less universal and reproducible.

Animals↗

Relation between regional electrical activation time and subepicardial fiber strain in the canine left ventricle.

To determine the relation between regional electrical activation time and fiber strain, epicardial electrical activation and deformation were measured in six open-chest dogs at the left ventricular anterior free wall after 15 min of right atrial, left ventricular free wall, left ventricular apex, or right ventricular outflow tract pacing, when end-diastolic pressure was normal or elevated (volume-loading). Regional electrical activation was measured using a 192-electrode brush. Regional subepicardial fiber strain (ef) was measured simultaneously in 16 regions, using optical markers which were attached to the epicardial surface and recorded on video. When relating regional ef during the ejection phase to regional activation time, the best correlation was found when a hemodynamic time reference rather than an electrophysiological one is used. Using the moment of the maximum rate of change of left ventricular pressure as the time reference for electrical activation, regional electrical activation time (t(ea)) and the degree of ef during the ejection phase could be fitted by a linear regression equation ef = a t(ea) + b, in which a = -3.46 +/- 0.73 s-1 an b = -0.28 +/- 0.05. For electrical activation times ranging from -40 to -80 ms, fiber strain was estimated with an accuracy of +/- 0.026 (+/- SE) with this relation. During right atrial pacing, t(ea) and ef were on the average -48 ms and -0.10 respectively. On further investigation, the relation between ef and t(ea) appeared to be influenced by end-diastolic pressure. For normal (1.1 kPa) and elevated end-diastolic pressure (1.8 kPa), the slope of the linear regression line was -3.96 and -2.86 s-1, respectively. Three conclusions may be drawn. Firstly, the time interval between the moment of regional electrical activation and the moment of the maximum rate of change of left ventricular pressure is an index of regional fiber strain. Secondly, it can be concluded from the above equations that electrical asynchrony of more than 30 ms causes non-uniformities in the degree of ef of the order of mean ef during pacing from the right atrium. Finally, differences in fiber strain during asynchronous electrical activation are less pronounced at larger filling pressures.

Animals↗

Extrapolation of incomplete marker tracks by lower rank approximation.

Motion and deformation of an object such as the heart may be measured by tracking optical or radiopaque markers. In the experimental situation markers may fail to be detected due to occlusion or lack of contrast. As a result a continuous marker track is observed in separated parts, which often cannot be directly identified as corresponding to one marker. This paper presents a method of extrapolating a partly known track by using information provided by the known track part and the available complete tracks of other markers. The extrapolations are obtained by iteratively fitting a lower rank matrix to the set of noisy, incomplete marker tracks. The performance is evaluated with computer-simulated data and data obtained in an animal experiment. In both cases 43% of the available complete tracks were made incomplete by removal of track parts varying in length from 3% up to 44%. For the simulated data comparison of the extrapolations with true signal values results in a root mean square (RMS) error about equal to the noise level. For the animal experiment, when comparing the extrapolations with the measured values, in images of 256 x 256 pixels, the RMS error was found to be +/- 0.5 pixel, which is quite small relative to the total excursion of a marker (20 pixels). Estimation of the missing data by applying BMDPAM (BMDP Statistical Software Inc.) to the same data results in RMS errors which are about twice as high.

Algorithms↗

Subepicardial fiber strain and stress as related to left ventricular pressure and volume.

In a mathematical model of the mechanics of the left ventricle (LV) by Arts et al. (1), assuming uniformity of fiber stress (sigma f) and fiber strain (delta epsilon f) in the wall during the ejection phase, fiber stress and fiber strain were related to LV cavity pressure (Plv), LV cavity volume (Vlv) and wall volume (Vw) by the following pair of equations: sigma f = Plv (1 + 3 Vlv/Vw) and delta epsilon f = 1/3 delta ln (1 + 3 Vlv/Vw). The ratio of Vlv to Vw appeared to be the most important geometric parameter, whereas the actual LV shape was of minor importance. The relationships on fiber strain and stress were evaluated experimentally in six anesthetized open-chest dogs during normal and elevated (volume loading) end-diastolic LV pressure. Subepicardial fiber strain was measured simultaneously in 16 adjacent regions of the LV anterior wall, using optical markers that were attached to the epicardial surface and recorded on video. Changes in Vlv were measured by use of four inductive coils sutured to the LV in a tetrahedric configuration. Vw was measured postmortem. During control as well as hypervolemia the following results were found. At the anterior free wall of the LV, the slope of the estimated linear relationship between measured and calculated fiber strain was 1.017 +/- 0.168 (means +/- SD), which is not significantly different from unity. Calculated fiber stress corresponded qualitatively and quantitatively with experimental results reported on isolated cardiac muscle. Calculated subepicardial contractile work per unit of tissue volume was not significantly different from global pump work as normalized to Vw. These findings support the assumption of homogeneity of muscle fiber strain and stress in the left ventricular wall during the ejection phase. Furthermore, average values of fiber stress and strain can be estimated on the basis of measured left ventricular pressure and volume.

Animals↗

Description of the deformation of the left ventricle by a kinematic model.

A model of left ventricular (LV) kinematics is essential to identify the fundamental physiological modes of LV deformation during a complete cardiac cycle as observed from the motion of a finite number of markers embedded in the LV wall. Kinematics can be described by a number of modes of motion and deformation in succession. An obvious mode of LV deformation is the ejection of cavity volume while the wall thickens. In the more sophisticated model of LV kinematics developed here, seven time-dependent parameters were used to describe not only volume change but also torsion and shape changes throughout the cardiac cycle. Rigid-body motion required another six parameters. The kinematic model employed a deformation field that had no singularities within the myocardium, and all parameters describing the modes of deformation were dimensionless. Note that torsion, volume and symmetric shape changes all require the definition of a cardiac coordinate system, which has generally been related to the measured cardiac geometry by reference to approximate anatomical landmarks. However, in the present study the coordinate system was positioned objectively by a least-squares fit of the kinematic model to the measured motion of markers. Theoretically, at least five markers are needed to find a unique set of parameters.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Dependence of local left ventricular wall mechanics on myocardial fiber orientation: a model study.

The dependence of local left ventricular (LV) mechanics on myocardial muscle fiber orientation was investigated using a finite element model. In the model we have considered anisotropy of the active and passive components of myocardial tissue, dependence of active stress on time, strain and strain rate, activation sequence of the LV wall and aortic afterload. Muscle fiber orientation in the LV wall is quantified by the helix fiber angle, defined as the angle between the muscle fiber direction and the local circumferential direction. In a first simulation, a transmural variation of the helix fiber angle from +60 degrees at the endocardium through 0 degrees in the midwall layers to -60 degrees at the epicardium was assumed. In this simulation, at the equatorial level maximum active muscle fiber stress was found to vary from about 110 kPa in the subendocardial layers through about 30 kPa in the midwall layers to about 40 kPa in the subepicardial layers. Next, in a series of simulations, muscle fiber orientation was iteratively adapted until the spatial distribution of active muscle fiber stress was fairly homogeneous. Using a transmural course of the helix fiber angle of +60 degrees at the endocardium, +15 degrees in the midwall layers and -60 degrees at the epicardium, at the equatorial level maximum active muscle fiber stress varied from 52 kPa to 55 kPa, indicating a remarkable reduction of the stress range. Moreover, the change of muscle fiber strain with time was more similar in different parts of the LV wall than in the first simulation. It is concluded that (1) the distribution of active muscle fiber stress and muscle fiber strain across the LV wall is very sensitive to the transmural distribution of the helix fiber angle and (2) a physiological transmural distribution of the helix fiber angle can be found, at which active muscle fiber stress and muscle fiber strain are distributed approximately homogeneously across the LV wall.

Computer Simulation↗

The time sequence of electrical and mechanical activation during spontaneous beating and ectopic stimulation.

The relation between the sequence of electrical (E) and mechanical (M) activation was studied at the LV anterior wall of open-chest dogs (n = 11). M activation was defined as the onset of epicardial fibre shortening, as measured with a recently developed video technique. E activation was determined with a brush of extracellular electrodes. The delay between activation of basal and apical regions was consistently larger for M activation than for E activation: during spontaneous beating: 20.5 +/- 7.30 ms vs 8.8 +/- 3.31 ms, during right ventricular outflow tract pacing: 50.3 +/- 7.69 ms vs 39.0 +/- 5.31 ms and during left ventricular apex pacing 40.1 +/- 10.03 ms vs 25.4 +/- 9.30 ms, respectively (P less than 0.05 in all cases). The E-M time interval was consistently shorter in early than in late activated regions: 32 +/- 10 vs 41 +/- 8 ms during RV outflow tract pacing (P = 0.09) and 24 +/- 30 vs 40 +/- 24 ms during LV apex pacing (P less than 0.05). Electrical asynchronies larger than 40 ms resulted in decreases of systolic blood pressure and stroke volume. This study shows that the asynchrony of cardiac motion exceeds that of electrical activation because the time interval between electrical activation and onset of fibre shortening is larger the later a particular region is activated. Possible explanations for this phenomenon are discussed.

Animals↗

Porous medium finite element model of the beating left ventricle.

The axisymmetric model described represents myocardial tissue as a spongy anisotropic viscoelastic material. It includes torsion around the axis of symmetry of the ventricle, transmural variation of fiber angle, and redistribution of intracoronary blood in the myocardial wall. In simulations, end-systolic principal strains were equal to 0.45, -0.01, and -0.24 at two-thirds of the wall thickness from the epicardium and 0.26, 0.00, and -0.19 at one-third of the wall thickness from the epicardium. The direction of maximal shortening varied by less than 30 degrees from epicardium to endocardium, whereas fiber direction varied by greater than 100 degrees from epicardium to endocardium. During a normal cardiac cycle peak, equatorial intramyocardial pressure differed by less than 5% from peak intraventricular pressure. When redistribution of intracoronary blood in the ventricular wall was suppressed, peak equatorial intramyocardial pressure was found to exceed peak intraventricular pressure by greater than 30%. Simulated contraction of an unloaded left ventricle (left ventricular pressure = 0 kPa) produced similar magnitude for systolic intramyocardial pressures as the normal cardiac cycle. Transmural systolic fiber stress distribution was very sensitive to the chosen transmural fiber angle distribution.

Animals↗

Mapping the sequence of contraction of the canine left ventricle.

A method has been developed to map the sequence of contraction as measured at the epicardial surface of the anterior free wall of the canine left ventricle during sinus rhythm and electrical stimulation of the ventricle. In an area of 35 x 45 mm, 40-60 white markers were attached to the epicardial surface. The motion of the markers was recorded on video and analysed off-line by computer. In an array of 35 regions, regional surface deformation and epicardial fibre strain were calculated from the motion of the markers. Between all adjacent regions, the differences in timing of contraction were determined by cross-correlation of the related fibre strain signals. A map of the time sequence of contraction has been calculated so that the sum of the squares of the deviations between time intervals of the map and the measurements was minimised. If individual correlation coefficients were found to be less than 0.85, the related time difference was discarded from the analysis. If more than 25% of the time differences were discarded because of this reason, the whole map was obtained by determining time of the negative peak of the second time derivative in the early phase of contraction. The accuracy in time marking was sufficient (+/- 7 ms), as compared to the time differences over the epicardial surface, which were found to be on the average between 10 and 80 ms in case of sinus rhythm and electrical stimulation of the right ventricular outflow tract, respectively.

Animals↗

Performance of the isolated, ejecting heart: effects of aortic impedance and exogenous substrates.

The workload of the isolated, left-ventricular ejecting heart (i.e. working heart) is determined by the left atrial filling pressure and the afterload imposed on the left ventricular outflow tract. In addition to the level of end-diastolic aortic pressure, afterload is highly determined by the aortic impedance. For the isolated, ejecting heart optimum matching of the left ventricle to its afterload requires the highest possible similarity between the impedance of the artificial aortic conduit and the natural aortic impedance. The present study shows that the haemodynamic performance of the ejecting rat heart preparation can be affected by the impedance of the aortic conduit. A proper choice of substrates in the perfusion fluid further improves the performance of the heart in the artificial set-up. The present paper also provides guidelines with respect to the design of the aortic cannula and compliance chamber. The occurrence of turbulence, which is related to the Bernoulli pressure drop, is a major determinant of the impedance of the aortic conduit. This effect is used to simulate the natural resistance component of the aortic impedance. Further, the applicability of the perfusion model can be extended by the so-called assisted-mode perfusion, which allows automatic adjustment from antegrade to retrograde perfusion if the heart is not able to generate sufficient pumping power to provide its own coronary perfusion.

Animals↗

A two-phase finite element model of the diastolic left ventricle.

A porous medium finite element model of the passive left ventricle is presented. The model is axisymmetric and allows for finite deformation, including torsion about the axis of symmetry. An anisotropic quasi-linear viscoelastic constitutive relation is implemented in the model. The model accounts for changing fibre orientation across the myocardial wall. During passive filling, the apex rotates in a clockwise direction relative to the base for an observer looking from apex to base. Within an intraventricular pressure range of 0-3 kPa the rotation angle of all nodes remained below 0.1 rad. Diastolic viscoelasticity of myocardial tissue is shown to reduce transmural differences of preload-induced sarcomere stretch and to generate residual stresses in an unloaded ventricular wall, consistent with the observation of opening angles seen when the heart is slit open. It is shown that the ventricular model stiffens following an increase of the intracoronary blood volume. At a given left ventricular volume, left ventricular pressure increases from 1.5 to 2.0 kPa when raising the intracoronary blood volume from 9 to 14 ml (100 g)-1 left ventricle.

Animals↗

The constitutive behaviour of passive heart muscle tissue: a quasi-linear viscoelastic formulation.

A quasi-linear viscoelastic law with a continuous relaxation spectrum describing triaxial constitutive behaviour of heart muscle tissue is presented. The elastic response of the viscoelastic law is anisotropic, while the relaxation behaviour is assumed isotropic. The law is designed for a biphasic description (fluid-solid) of the myocardial tissue. Biaxial and uniaxial stress-strain curves from the literature are used to evaluate the parameters of the model. The non-linear elastic response, the difference between fibre and cross-fibre stiffness, the phenomenon of stress relaxation, the stiffening of the stress-strain relationship with increasing strain rate and the weak frequency dependency of the dissipated energy during cyclic loading are fairly well described by the proposed law. However, it is found that the model produces realistic values for the dissipated energy during cyclic loading only when relaxation parameter values are chosen which result in an overestimation of the stress relaxation data by more than 100%. This finding may indicate non-quasi-linearity of viscoelasticity of passive heart muscle tissue.

Biomechanical Phenomena↗

Relation between left ventricular cavity pressure and volume and systolic fiber stress and strain in the wall.

Pumping power as delivered by the heart is generated by the cells in the myocardial wall. In the present model study global left-ventricular pump function as expressed in terms of cavity pressure and volume is related to local wall tissue function as expressed in terms of myocardial fiber stress and strain. On the basis of earlier studies in our laboratory, it may be concluded that in the normal left ventricle muscle fiber stress and strain are homogeneously distributed. So, fiber stress and strain may be approximated by single values, being valid for the whole wall. When assuming rotational symmetry and homogeneity of mechanical load in the wall, the dimensionless ratio of muscle fiber stress (sigma f) to left-ventricular pressure (Plv) appears to depend mainly on the dimensionless ratio of cavity volume (Vlv) to wall volume (Vw) and is quite independent of other geometric parameters. A good (+/- 10%) and simple approximation of this relation is sigma f/Plv = 1 + 3 Vlv/Vw. Natural fiber strain is defined by ef = In (lf/lf,ref), where lf,ref indicates fiber length (lf) in a reference situation. Using the principle of conservation of energy for a change in ef, it holds delta ef = (1/3)delta In (1 + 3Vlv/Vw).

Animals↗

Experimental evaluation of the correlation interpolation technique to measure regional tissue velocity.

A newly developed correlation interpolation method to measure the regional velocity of moving tissue is evaluated in an experimental setup. Pulsed ultrasound echo signals (center frequency 3.5 MHz) are received from a rotating Agar disk containing scattering particles. When averaging over a depth range of 2.2 mm at a pulse repetition frequency (PRF) of 930 Hz, the standard deviation of the measured displacement between 2 successive pulses was found to be +/- 6 microns. In a second series of experiments, the angular velocity of the disk is estimated from the displacement, as measured simultaneously in two different regions located on separate echo lines (PRF = 465 Hz per line). The exact position of both regions in respect to the center of rotation was found to be irrelevant. The accuracy of the calculated angular velocity was found to be better for large angles between the two lines of observation than for small angles.

Agar↗

Transmural differences in energy metabolism of the left ventricular myocardium: fact or fiction.

It is a matter of continuous debate whether mechanical and metabolic activities are differently distributed across the left ventricular wall. It has been suggested that under normal circumstances the subendocardial layers have a higher workload and, hence, higher energy requirements than the subepicardial layers. Direct assessment of the transmural distribution of workload in the left ventricular wall is hampered by technical difficulties. Recent attempts to estimate the transmural heterogeneity in workload by mathematical models indicate that major differences between subendocardial and subepicardial layers are not very likely. Flow determinations with adequately sized microspheres or molecular flow markers indicate that transmural flow distribution is close to unity. The observation in some studies that oxygen pressure and venous hemoglobin oxygen saturation is lower in subendocardial than in subepicardial layers suggests a higher metabolic activity in the former layers. However, other biochemical parameters, such as metabolic fluxes, enzyme activities, or concentrations of substrates, cofactors and high-energy phosphates and related compounds, fail to reveal a consistent and substantial transmural difference in energy metabolism. It cannot be excluded that under certain circumstances energy requirements are unevenly distributed across the left ventricular wall. For example, the size of the heart, the awake or anesthetized state of the animal, the level of overall cardiac workload and the efficiency of metabolic-mechanical conversion might influence to some extent the distribution of energy metabolism across the left ventricular wall. Although at present no definite conclusions can be drawn, it is likely that the transmural differences in energy requirements of normally functioning, intermediate-size hearts are limited. Small differences in the order of 10-20% between the subendocardial and subepicardial layers cannot be excluded.

Adenosine Triphosphate↗