Cardiovascular Engineering (dordrecht, Netherlands)最新文献

Short-term regulation of cerebral blood flow (CBF) is controlled by myogenic, metabolic and neurogenic mechanisms, which maintain flow within narrow limits, despite large changes in arterial blood pressure (ABP). Static cerebral autoregulation (CA) represents the steady-state relationship between CBF and ABP, characterized by a plateau of nearly constant CBF for ABP changes in the interval 60-150 mmHg. The transient response of the CBF-ABP relationship is usually referred to as dynamic CA and can be observed during spontaneous fluctuations in ABP or from sudden changes in ABP induced by thigh cuff deflation, changes in posture and other manoeuvres. Modelling the dynamic ABP-CBFV relationship is an essential step to gain better insight into the physiology of CA and to obtain clinically relevant information from model parameters. This paper reviews the literature on the application of CA models to different clinical conditions. Although mathematical models have been proposed and should be pursued, most studies have adopted linear input-output ('black-box') models, despite the inherently non-linear nature of CA. The most common of these have been transfer function analysis (TFA) and a second-order differential equation model, which have been the main focus of the review. An index of CA (ARI), and frequency-domain parameters derived from TFA, have been shown to be sensitive to pathophysiological changes in patients with carotid artery disease, stroke, severe head injury, subarachnoid haemorrhage and other conditions. Non-linear dynamic models have also been proposed, but more work is required to establish their superiority and applicability in the clinical environment. Of particular importance is the development of multivariate models that can cope with time-varying parameters, and protocols to validate the reproducibility and ranges of normality of dynamic CA parameters extracted from these models.

This research is aimed to the determination of the changes in the cardiac energetic output for three different modes of cardiac rhythm pacing. The clinical investigation of thirteen patients with the permanent dual-chamber pacemaker implantation was carried out. The patients were taken to echocardiography examination conducted by way of three pacing modes (AAI, VVI and DDD). The myocardial energetic parameters-the stroke work index (SWI) and the myocardial oxygen consumption (MVO2) are not directly measurable, however, their values can be determined using the numerical model of the human cardiovascular system. The 24-segment hemodynamical model (pulsating type) of the human cardiovascular system was used for the numerical simulation of the changes of myocardial workload for cardiac rhythm pacing. The model was fitted by well-measurable parameters for each patient. The calculated parameters were compared using the two-tailed Student's test. The differences of SWI and MVO2 between the modes AAI and VVI and the modes DDD and VVI are statistically significant (P<0.05). On the other hand, the hemodynamic effects for the stimulation modes DDD and AAI are almost identical, i.e. the differences are statistically insignificant (P>0.05).

Isolated systolic hypertension (ISH) is prevalent in the elderly and the contributing factors are predominantly vascular in origin. We previously showed that the hemodynamic manifestation of ISH is the result of a concurrently mild increase in peripheral resistance with a large reduction in arterial compliance or greatly increased vascular stiffness. Such elastic mismatching can lead to increased wave reflections. Therefore, we hypothesize that significantly increased pulse wave reflections associated with a drastically reduced arterial compliance beyond normal aging is a principle contributing factor to the production of ISH. To investigate this, we developed a new allometric hemodynamic model that can account for the arterial compliance and peripheral resistance changes during the progression of aging. This model also affords the time domain analysis of forward and reflected waves during aging and ISH. Results show that a further and much greater reduction in arterial compliance beyond normal aging is necessary to produce ISH. Comparison of ISH with normal aging at 60-year old showed that in ISH the amount of wave reflections is much more pronounced, with a greater amplitude and earlier arrival in systole. The increased wave reflections in ISH further amplify the cyclic stress on the already stiffened blood vessels. Therefore, therapies to treat ISH patients need to focus on reducing pulse wave reflections as well as on improving large vessel compliance.

Contraction-relaxation coupling is often characterized in terms of its effects on contraction or relaxation parameters, such as the time-constant of isovolumic relaxation (tau). While thermodynamics-based LV function characterization methods exist, landmark relaxation-onset determination studies used surgical methods. One classic, open-chest preparation study found that relaxation-onset occurs during early ejection, i.e. 34% of systolic time, TSYS, defined as the time from end-diastolic pressure to peak negative dP/dt. Because ventricular pumping is a steady state system, the laws of thermodynamics and nonlinear dynamics require that energy generation (during contraction) and energy utilization (during relaxation) must be balanced in a time-averaged (steady-state) sense. We calculated both energy generation and energy utilization, via novel pressure phase-plane (PPP) based parameters, including isovolumic stiffness analogs, in 29 subjects, 20 cardiac cycles per subject (580 beats). Results in control subjects show that relaxation-onset occurs near or prior to 34% of TSYS. In hearts with sever dysfunction including prolonged tau, relaxation-onset commences after 50% of TSYS (p<0.05). We conclude that PPP-based analysis can characterize relaxation-onset in vivo in thermodynamic and nonlinear dynamics terms without requiring an open-chest preparation, and may facilitate characterization of cellular mechanisms of relaxation-onset at the organ system level.

Ageing is one of the main contributing factors towards increasing arterial stiffness, leading to changes in peripheral pulses propagation. Therefore the characteristics of the photoplethysmogram (PPG) pulse, especially the rising edge and peak position, are greatly affected. In this study, the PPG pulse rising edge and corresponding peak position have been investigated non-invasively in human subjects as a function of age. Fifteen healthy subjects were selected and grouped in five age intervals, from 20 to 59 years, based on their comparable systolic-diastolic blood pressure and PPG amplitude. As expected, the peripheral pulse shows a steep rise and early peak in younger subjects. With age, the slope becomes blunted and in older subjects, the rise is very gradual and the pulse peak appears much later. Qualitative results were further verified by a modified 10-element Windkessel model to quantify the lumped parameter changes with ageing. This verification highlighted some specific changes in vascular parameters with aging. The rising edge could be considered as one parameter in determining the age-dependent vascular state.

A set of multiscale simulations has been created to examine the dynamic behavior of the human aortic valve (AV) at the cell, tissue, and organ length scales. Each model is fully three-dimensional and includes appropriate nonlinear, anisotropic material models. The organ-scale model is a dynamic fluid-structure interaction that predicts the motion of the blood, cusps, and aortic root throughout the full cycle of opening and closing. The tissue-scale model simulates the behavior of the AV cusp tissue including the sub-millimeter features of multiple layers and undulated geometry. The cell-scale model predicts cellular deformations of individual cells within the cusps. Each simulation is verified against experimental data. The three simulations are linked: deformations from the organ-scale model are applied as boundary conditions to the tissue-scale model, and the same is done between the tissue and cell scales. This set of simulations is a major advance in the study of the AV as it allows analysis of transient, three-dimensional behavior of the AV over the range of length scales from cell to organ.

We have developed a novel method for estimating subject-specific hemodynamics during hemorrhage. First, a mathematical model representing a closed-loop circulation and baroreceptor feedback system was parameterized to match the baseline physiology of individual experimental subjects by fitting model results to 1 min of pre-injury data. This automated parameterization process matched pre-injury measurements within 1.4 +/- 1.3% SD. Tuned parameters were then used in similar open-loop models to simulate dynamics post-injury. Cardiac output (CO) estimates were obtained continuously using post-injury measurements of arterial blood pressure (ABP) and heart rate (HR) as inputs to the first open-loop model. Secondarily, total blood volume (TBV) estimates were obtained by summing the blood volumes in all the circulatory segments of a second open-loop model that used measured CO as an additional input. We validated the estimation method by comparing model CO results to flowprobe measurements in 14 pigs. Overall, CO estimates had a Bland-Altman bias of -0.30 l/min with upper and lower limits of agreement 0.80 and -1.40 l/min. The negative bias is likely due to overestimation of the peripheral resistance response to hemorrhage. There was no reference measurement of TBV; however, the estimates appeared reasonable and clearly predicted survival versus death during the post-hemorrhage period. Both open-loop models ran in real time on a computer with a 2.4 GHz processor, and their clinical applicability in emergency care scenarios is discussed.

The radial artery (RA) pressure waveform is commonly used to reconstruct the central aortic pressure waveform. Because the RA pressure waveform has been used as input to this process, its features that are dependent on the local arterial properties can influence the final reconstructed aortic waveform. In this study, we determined the effects of altered upper limb pulse wave velocity (PWV) and local wave reflection parameters on RA pressure waveform augmentation (RA-AIx). Twenty healthy volunteers (10 men) between the ages of 18 and 35 years of age were recruited. Simultaneous pressure waveforms were acquired using arterial tonometers from the right carotid and the radial arteries, prior to and following tourniquet induced hyperemia. The phase velocities from the pressure wave transfer function were used to estimate the pulse wave velocity (PWV(infinity)), the local reflection coefficient (Gamma) and an estimate of the terminal impedance of the upper limbs, PWV(0+). The RA-AIx was represented as a linear, three-parameter model that included the input (the AIx of the carotid artery pressure waveform, CA-AIx), the Gamma and PWV(infinity) of the arm. Tourniquet induced hyperemia did not alter Gamma but reduced PWV(infinity), and PWV(0+) and increased RA-AIx. Multiple linear regression analysis indicated that RA-AIx was increased by high levels of CA-AIx and PWV(infinity) and decreased by elevated Gamma. The relative weighing of CA-AIx, Gamma and PWV(infinity) on RA-AIx were 3:2:1, respectively. The AIx of RA is determined to an equal extent by the input and local factors. Interpretation of the AIx of the RA and the reconstructed central aortic waveform should be made in the context of this relationship.

Introduction: Pacing site is known to influence the contractile state of the ventricle. Non-physiologic pacing sites such as the right ventricular apex (RVA) or left ventricular freewall (LVFW) have been shown to decrease the contractile state of normal myocardium, due to abnormal electrical propagation. The impact of pacing at these sites may alter mechanical restitution (MR), a fundamental cardiac property involving the electro-mechanical regulation of contraction. This, in turn, may affect cardiac function. The present study was conducted to determine if pacing site alters the time constant of MR: tau.

Methods and results: Anesthetized canines (n = 6) were acutely paced at four sites: right atrium (RA), RVA, right ventricular septum (RVS), and LVFW. MR data was captured by the S1-S2 pacing protocol and used to create MR curves, generating a restitution time constant, tau, at each site. No significant difference in tau was found between pacing sites. A linear regression analysis of MR curves revealed that there was no significant difference in slope between pacing sites.

Conclusion: Although pacing site has been found to influence the contractile state of the ventricle, this is the first known study to demonstrate no change in tau in an in vivo preparation. This suggests that alteration of electro-mechanical coupling described by MR is not sufficiently robust to provide insight into pacing site and cardiac function in healthy hearts.