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At least 991 records · Page 55Linked to original sources
PubMed1992

Global left ventricular perfusion: noninvasive measurement with cine MR imaging and phase velocity mapping of coronary venous outflow.

Velocity and volumetric flow of left ventricular venous outflow in the distal coronary sinus were measured with magnetic resonance (MR) velocity mapping techniques in 24 healthy men. A total of 16-21 velocity maps were acquired throughout the cardiac cycle. To determine the accuracy of the MR velocity-mapping pulse sequence, measurements were obtained with a flow phantom. Mean blood flow was 144 mL/min +/- 62 (standard deviation); mean velocity, 2.1 cm/sec +/- 1.0; and mean cross-sectional area, 1.2 cm2. Phasic measurements revealed a biphasic flow pattern in the coronary sinus, with a first peak in systole (257 mL/min +/- 174) and a second peak in early diastole (1,090 mL/min +/- 487). The cross-sectional area varied between 0.5 cm2 +/- 0.2 at end diastole and 1.9 cm2 +/- 0.6 in systole, a finding that suggests a capacitance function for venous outflow. Mean blood flow measurements were in agreement with measurements obtained invasively in previous studies. It is concluded that MR velocity mapping can enable noninvasive measurement of coronary venous outflow and global left ventricular perfusion and may become clinically useful in assessment of coronary blood flow reserve.

Adult↗
PubMed1992

Blood flow imaging through detection of temporal variations in magnetization.

Two hypotheses were tested: (a) that view-to-view variations in bulk phase and modulus of magnetization in vascular volume elements can indicate the presence of disordered blood flow, and (b) that a substantial loss of signal intensity on magnetic resonance (MR) angiograms of poststenotic regions is due to view-to-view changes in magnetization. To test these hypotheses, a technique was developed in which view-to-view variations in transverse magnetization were used to create angiographic projection images, which showed only disordered flow (disordered flow maps) in vitro and in vivo. In phantom studies, this technique recovered signal intensity downstream from stenoses. A combination of disordered flow maps with morphologic images improved visualization of stenotic regions and provided information on characteristics of local flow. These results show that view-to-view variations in transverse magnetization occur in regions of disordered flow and are an important cause of loss of signal intensity. This technique can provide information about dynamic blood flow and improve depiction of anatomic structures on MR angiograms.

Blood Circulation↗
PubMed1993

Effect of RR interval variation on image quality in gated, two-dimensional, Fourier MR imaging.

The effect of uneven repetition time (TR) intervals on artifact production during gated two-dimensional Fourier magnetic resonance image acquisition was investigated and a means of compensation presented. In standard spin-echo imaging, incomplete longitudinal recovery combines with normal respiratory heart rate variations to modulate signal intensity and create image copies and smearing along the phase direction. Modulation amplitude, frequency, and pattern, as well as machine parameters including echo time, TR, field of view, and image matrix size, have been found to have a substantial impact on artifact position and intensity. In a group of 10 healthy volunteers, respiratory-induced heart rate modulation produced an average of 17.2% +/- 4.9 variation in the raw data signal, with a mean frequency of 0.36 Hz +/- 0.06. The results of this study indicate that image artifacts caused by heart rate variations within the imaging period are predictable and may be reduced by correcting signal intensity for each phase view before two-dimensional Fourier transformation.

Adult↗
PubMed1993

Comparative evaluation of clinically available inferior vena cava filters with an in vitro physiologic simulation of the vena cava.

PURPOSE: A physiologic in vitro model of the human inferior vena cava (IVC) was developed to evaluate the clot-trapping efficiency of various IVC filters. MATERIALS AND METHODS: The flow model closely simulates the physical parameters of the human IVC in fluid viscosity, specific gravity, temperature, and pulsatility; blood flow velocity, volume, and inherent turbulence; and vein orientation, wall compliance, and clot composition. Five filters--Greenfield (G), Bird's Nest (BN), Vena Tech (VT), Simon nitinol (SN), and titanium Greenfield (TG)--were compared by using two vena cava and blood clot sizes and horizontal and vertical orientation of the model. RESULTS: Each filter varied significantly in its clot-capturing efficiency, depending on vena cava size and orientation and emboli size. Overall, decreasing rank order in filter clot-trapping efficiency was SN, BN, VT, TG, and G. CONCLUSION: The in vitro model of the human IVC is an alternative to multicenter clinical trials in evaluating the relative clot-trapping efficiency of various IVC filters.

Equipment Design↗
PubMed1994

Pulsus tardus: its cause and potential limitations in detection of arterial stenosis.

PURPOSE: To determine, with hydrodynamic experiments, the true cause of pulsus tardus, a Doppler waveform alteration that often occurs distal to an arterial stenosis. MATERIALS AND METHODS: A flow phantom was constructed with a pulsatile pump, interchangeable stenoses of varying degree, and interchangeable poststenotic segments of tubing with various degrees of compliance. With the transstenotic pressure drop held constant for each stenosis, Doppler waveforms were obtained before and after stenosis, while the degree of poststenotic vessel compliance was varied. RESULTS: The degree of pulsus tardus increased as the compliance of the poststenotic segment of vessel increased, independent of the transstenotic pressure drop. CONCLUSION: Poststenotic pulsus tardus is caused by the compliance of the poststenotic vessel wall in conjunction with the stenosis, which produces the tardus effect by damping the high-frequency components of the arterial waveform. This information will allow prediction of conditions that may produce false-positive or false-negative results when the tardus phenomenon is used to predict substantial upstream stenosis.

Blood Flow Velocity↗
PubMed1994

Vascular occlusion with a balloon-expandable stent occluder.

PURPOSE: To evaluate the effectiveness of a new vascular occlusion device. MATERIALS AND METHODS: The device was created by coating a balloon-expandable stent with a silicone sleeve that tapers to a blind-ended nozzle at its leading end. Once crimp-mounted on an angioplasty balloon catheter, the device is introduced over a guide wire through a small end hole in the nozzle. RESULTS: The device was tested for stability and occlusive ability. No migration was measured over a pulsatile pulse range of 50-300 mm Hg, and mean flow rate in the occluded vessel was reduced from 443 mL/min +/- 99 (standard deviation) to 1.9 mL/min +/- 2.7. Subsequently, 12 arteries were occluded in three dogs, and immediate vascular occlusion was achieved in all vessels. An arteriovenous fistula was created in another six dogs and was successfully occluded with the device. Follow-up arteriography at 3 months demonstrated persistent occlusion with no migration of the device. CONCLUSION: This new occlusive device offers immediate vascular occlusion with excellent stability.

Angioplasty, Balloon↗
PubMed1995

Improved ejection fraction and flow velocity estimates with use of view sharing and uniform repetition time excitation with fast cardiac techniques.

PURPOSE: To improve the accuracy of ventricular volume estimates and effective temporal resolution in fast cardiac acquisitions. MATERIALS AND METHODS: Data sets at intermediate temporal phases were generated by means of sharing of views from two temporally adjacent data sets. A simulated model was used, and studies with patients and volunteers were conducted. View sharing was implemented in both fast gradient-echo and fast phase-contrast cine acquisitions; breath holding was used when possible. RESULTS: Uniform repetition time (TR) radio-frequency (RF) excitation allowed a better assessment of the end-diastolic ventricular volume. In addition, view sharing provided a better estimate of end-systolic ventricular volume in cases in which rapid changes in volume occurred at or about the temporal boundary of the source images. View sharing also provided a much smoother representation of dynamic cardiac motion when viewed in a cine loop. CONCLUSION: View sharing and uniform TR RF excitation improve the accuracy of end-systolic and end-diastolic ventricular volume measurements by improving the effective temporal resolution.

Adult↗
PubMed2001

Rapid aortic wave velocity measurement with MR imaging.

The utility of a one-dimensional magnetic resonance (MR) sequence to rapidly and accurately measure wave velocity in vivo was evaluated. Studies were conducted in the thoracic aortas of 20 healthy subjects of varying age, and the MR method was validated in a compliant tube model. Aortic wave velocity ranged from 3.8 to 9.7 m/sec and demonstrated a positive correlation with subjects' age. Peak blood velocity ranged from 47 to 125 cm/sec and exhibited a strong negative correlation with subjects' age.

Adult↗
PubMed2005

An experimental approach to the fundamental principles of hemodynamics.

An experimental model has been developed to give students hands-on experience with the fundamental laws of hemodynamics. The proposed experimental setup is of simple construction but permits the precise measurements of physical variables involved in the experience. The model consists in a series of experiments where different basic phenomena are quantitatively investigated, such as the pressure drop in a long straight vessel and in an obstructed vessel, the transition from laminar to turbulent flow, the association of vessels in vascular networks, or the generation of a critical stenosis. Through these experiments, students acquire a direct appreciation of the importance of the parameters involved in the relationship between pressure and flow rate, thus facilitating the comprehension of more complex problems in hemodynamics.

Hemodynamics↗
PubMed1994

A mathematical model of a rabbit sinoatrial node cell.

A mathematical model for the electrophysiological responses of a rabbit sinoatrial node cell that is based on whole cell recordings from enzymatically isolated single pacemaker cells at 37 degrees C has been developed. The ion channels, Na(+)-K+ and Ca2+ pumps, and Na(+)-Ca2+ exchanger in the surface membrane (sarcolemma) are described using equations for these known currents in mammalian pacemaker cells. The extracellular environment is treated as a diffusion-limited space, and the myoplasm contains Ca(2+)-binding proteins (calmodulin and troponin). Original features of this model include 1) new equations for the hyperpolarization-activated inward current, 2) assessment of the role of the transient-type Ca2+ current during pacemaker depolarization, 3) inclusion of an Na+ current based on recent experimental data, and 4) demonstration of the possible influence of pump and exchanger currents and background currents on the pacemaker rate. This model provides acceptable fits to voltage-clamp and action potential data and can be used to seek biophysically based explanations of the electrophysiological activity in the rabbit sinoatrial node cell.

Animals↗
PubMed1997

Kinetics of creatine kinase in an experimental model of low phosphocreatine and ATP in the normoxic heart.

To study the dependence of the forward flux of creatine kinase (CK) on its substrates and products we designed an acute normoxic model of steady-state depletion of phosphocreatine (PCr) and adenylate in the isovolumic acetate-perfused rat heart. Various concentrations of PCr and ATP were induced by prior perfusion with 2 deoxy-D-glucose in the presence of insulin. The apparent rate constant (k(f)) and the forward CK flux were measured under metabolic and contractile steady state by progressive saturation-transfer 31P nuclear magnetic resonance (NMR). At high adenylate content CK flux was constant for a twofold reduction in PCr concentration ([PCr]); CK flux was 6.3 +/- 0.6 mM/s (vs. 6.5 +/- 0.2 mM/s in control) because of a doubling of k(f). Although, at the lowest ATP concentration and [PCr], CK flux was reduced by 50%, it nevertheless always remained higher than ATP synthesis estimated by parallel oxygen consumption measurement. NMR-measured flux was compared with the flux computed under the hypothesis of CK equilibrium. CK flux could not be fully predicted by the concentrations of CK metabolites. This is discussed in terms of metabolite and CK isozyme compartmentation.

Adenosine Triphosphate↗
PubMed2006

Pulsatile blood flow in the entire coronary arterial tree: theory and experiment.

The pulsatility of coronary circulation can be accurately simulated on the basis of the measured branching pattern, vascular geometry, and material properties of the coronary vasculature. A Womersley-type mathematical model is developed to analyze pulsatile blood flow in diastole in the absence of vessel tone in the entire coronary arterial tree on the basis of previously measured morphometric data. The model incorporates a constitutive equation of pressure and cross-section area relation based on our previous experimental data. The formulation enables the prediction of the impedance, the pressure distribution, and the pulsatile flow distribution throughout the entire coronary arterial tree. The model is validated by experimental measurements in six diastolic arrested, vasodilated porcine hearts. The agreement between theory and experiment is excellent. Furthermore, the present pulse wave results at low frequency agree very well with previously published steady-state model. Finally, the phase angle of flow is seen to decrease along the trunk of the major coronary artery and primary branches toward the capillary vessels. This study represents the first, most extensive validated analysis of Womersley-type pulse wave transmission in the entire coronary arterial tree down to the first segment of capillaries. The present model will serve to quantitatively test various hypotheses in the coronary circulation under pulsatile flow conditions.

Animals↗
PubMed2002

Contribution of laminar myofiber architecture to load-dependent changes in mechanics of LV myocardium.

The ventricular myocardium consists of a syncytium of myocytes organized into branching, transmurally oriented laminar sheets approximately four cells thick. When systolic deformation is expressed in an axis system determined by the anatomy of the laminar architecture, laminar sheets of myocytes shear and laterally extend in an approximately radial direction. These deformations account for ~90% of normal systolic wall thickening in the left ventricular free wall. In the present study, we investigated whether the changes in systolic and diastolic function of the sheets were sensitive to alterations in systolic and diastolic load. Our results indicate that there is substantial reorientation of the laminar architecture during systole and diastole. Moreover, this reorientation is both site and load dependent. Thus as end-diastolic pressure is increased and the left ventricular wall thins, sheets shorten and rotate away from the radial direction due to transverse shearing, opposite of what occurs in systole. Both mechanisms of thickening contribute substantially to normal left ventricular wall function. Whereas the relative contributions of shear and extension are comparable at the base, sheet shear is the predominant factor at the apex. The magnitude of shortening/extension and shear increases with preload and decreases with afterload. These findings underscore the essential contribution of the laminar myocardial architecture for normal ventricular function throughout the cardiac cycle.

Animals↗
PubMed2006

Modeling of IK1 mutations in human left ventricular myocytes and tissue.

Elucidation of the cellular basis of arrhythmias in ion channelopathy disorders is complicated by the inherent difficulties in studying human cardiac tissue. Thus we used a computer modeling approach to study the mechanisms of cellular dysfunction induced by mutations in inward rectifier potassium channel (K(ir))2.1 that cause Andersen-Tawil syndrome (ATS). ATS is an autosomal dominant disorder associated with ventricular arrhythmias that uncommonly degenerate into the lethal arrhythmia torsade de pointes. We simulated the cellular and tissue effects of a potent disease-causing mutation D71V K(ir)2.1 with mathematical models of human ventricular myocytes and a bidomain model of transmural conduction. The D71V K(ir)2.1 mutation caused significant action potential duration prolongation in subendocardial, midmyocardial, and subepicardial myocytes but did not significantly increase transmural dispersion of repolarization. Simulations of the D71V mutation at shorter cycle lengths induced stable action potential alternans in midmyocardial, but not subendocardial or subepicardial cells. The action potential alternans was manifested as an abbreviated QRS complex in the transmural ECG, the result of action potential propagation failure in the midmyocardial tissue. In addition, our simulations of D71V mutation recapitulate several key ECG features of ATS, including QT prolongation, T-wave flattening, and QRS widening. Thus our modeling approach faithfully recapitulates several features of ATS and provides a mechanistic explanation for the low frequency of torsade de pointes arrhythmia in ATS.

Action Potentials↗
PubMed2006

Relationship of pulmonary vein flow to left ventricular short-axis epicardial displacement in diastole: model-based prediction with in vivo validation.

Previous studies in healthy humans have established that the (approximately 850 ml) volume enclosed by the pericardial sac is nearly constant over the cardiac cycle, exhibiting a transient approximately 5% decrease (approximately 40 ml) from end diastole to end systole. This volume decrease manifests as a "crescent" at the ventricular free wall level when short-axis MRI images of the epicardial surface acquired at end systole and end diastole are superimposed. On the basis of the (near) constant-volume property of the four-chambered heart, the volume decrease ("crescent effect") must be restored during subsequent early diastolic filling via the left atrial conduit volume. Therefore, volume conservation-based modeling predicts that pulmonary venous (PV) Doppler D-wave volume must be causally related to the radial displacement of the epicardium (Delta) (i.e., magnitude of "crescent effect" in the radial direction). We measured Delta from M-mode echocardiographic images and measured D-wave velocity-time integral (VTI) from Doppler PV flow of the right superior PV in 11 subjects with catheterization-determined normal physiology. In accordance with model prediction, high correlation was observed between Delta and D-wave VTI (r=0.86) and early D-wave VTI measured to peak D-wave velocity (r=0.84). Furthermore, selected subjects with various pathological conditions had values of Delta that differed significantly. These observations demonstrate the volume conservation-based causal relationship between radial pericardial displacement of the left ventricle and the PV D-wave-generated filling volume in healthy subjects as well as the potential role of the M-mode echo-derived radial epicardial displacement index Delta as a regional (radial) parameter of diastolic function.

Coronary Circulation↗
PubMed2006

Multiple coherence of cerebral blood flow velocity in humans.

The coherence function has been used in transfer function analysis of dynamic cerebral autoregulation to assess the statistical significance of spectral estimates of gain and phase frequency response. Interpretation of the coherence function and choice of confidence limits has not taken into account the intrinsic nonlinearity represented by changes in cerebrovascular resistance due to vasomotor activity. For small spontaneous changes in arterial blood pressure (ABP), the relationship between ABP and cerebral blood flow velocity (CBFV) can be linearized, showing that corresponding changes in cerebrovascular resistance should be included as a second input variable. In this case, the standard univariate coherence function needs to be replaced by the multiple coherence, which takes into account the contribution of both inputs to explain CBFV variability. With the use of two different indicators of cerebrovascular resistance index [CVRI = ABP/CBFV and the resistance-area product (RAP)], multiple coherences were calculated for 42 healthy control subjects, aged 20 to 40 yr (28 +/- 4.6 yr, mean +/- SD), at rest in the supine position. CBFV was measured in both middle cerebral arteries, and ABP was recorded noninvasively by finger photoplethysmography. Results for the ABP + RAP inputs show that the multiple coherence of CBFV for frequencies <0.05 Hz is significantly higher than the corresponding values obtained for univariate coherence (P < 10(-5)). Corresponding results for the ABP + CVRI inputs confirm the principle of multiple coherence but are less useful due to the interdependence between CVRI, ABP, and CBFV. The main conclusion is that values of univariate coherence between ABP and CBFV should not be used to reject spectral estimates of gain and phase, derived from small fluctuations in ABP, because the true explained power of CBFV in healthy subjects is much higher than what has been usually predicted by the univariate coherence functions.

Adult↗
PubMed1989

Impedance of arterial system simulated by viscoelastic t tubes terminated in windkessels.

An improved asymmetric t-tube model of the arterial system is proposed. The model consists of two viscoelastic tubes of differing lengths, each terminated in a modified windkessel with inductance as well as resistance and compliance. Equations for calculating the input impedance of this model are presented. Using typical data from the literature, the model predicts a more realistic impedance modulus and phase than previous models of the circulation. Parametric analysis shows that when peripheral compliances are altered, sharp peaks in the very low frequency portions of the impedance spectra are produced, whereas alterations of either the characteristic impedances or inductances of the terminations have little effect on input impedance. Alteration of the elasticity or relative lengths of the tubes results in shifts in the positions of the maxima and minima akin to those observed experimentally. Change in the viscosity of the walls or of the blood only affects the fluctuations of the impedance spectra without affecting the positions of the maxima and minima. Thus, with this still simple model, very realistic impedance spectra are obtainable. The model provides more insight than previously proposed models into the individual influence of various parameters of the proximal and peripheral vasculature on central hemodynamics.

Arteries↗
PubMed1994

Mathematical model of acetylcholine kinetics in neuroeffector junctions.

Acetylcholine (ACh) kinetics in neuroeffector junctions (NEJ) of the sinus node plays a key role in vagal control of heart rate. Prior studies have shown that the concentration of ACh ([ACh]) in NEJ appears to follow first-order linear kinetics. To find out the reason why, we examine mathematically diffusion, degradation, and receptor binding of ACh in NEJ. We identify seven conditions that potentially influence ACh kinetics. Because these conditions are satisfied for NEJ in the sinus node, 1) the nonlinearity of ACh binding to muscarinic receptors has little effect on [ACh]; 2) [ACh] does not depend on the distribution of acetylcholinesterase between the interstitial space and the pacemaker cells; 3) the interval from trough to subsequent peak [ACh] at the pacemaker cells is negligible; 4) the mean [ACh] at the pacemaker cells is proportional to the frequency of vagal activity multiplied by the amount of ACh released per vagal stimulus and divided by the rate coefficient of ACh degradation; and 5) [ACh] at pacemaker cells nearly follows first-order linear kinetics but does not at other sites in the NEJ. We conclude that earlier studies showed that [ACh] follows first-order linear kinetics, because they predicted [ACh] only at pacemaker cells. ACh kinetics at other sites in the NEJ, such as at nerve endings, is different.

Acetylcholine↗