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At least 91 records · Page 5Linked to original sources
PubMed2001

Phenotype-driven genetic approaches in mice: high-throughput phenotyping for discovering new models of cardiovascular disease.

Cardiovascular diseases such as hypertension, atherosclerosis, cardiac hypertrophy homocysteinemia and arrhythmias impose great health, social and financial costs. Some of these diseases are single gene traits that segregate in a simple Mendelian manner. Most are genetically complex, however, and result from combinations of large numbers of genes (polygenic and epistatic traits) or from interactions between genetic and environmental factors (multifactorial traits). Insights into the genetic control of these diseases could lead to improved diagnosis and treatment as well as a deeper understanding of basic physiological processes.

Animals↗
PubMed1996

Clinical models of cardiovascular regulation after weightlessness.

After several days in microgravity, return to earth is attended by alterations in cardiovascular function. The mechanisms underlying these effects are inadequately understood. Three clinical disorders of autonomic function represent possible models of this abnormal cardiovascular function after spaceflight. They are pure autonomic failure, baroreflex failure, and orthostatic intolerance. In pure autonomic failure, virtually complete loss of sympathetic and parasympathetic function occurs along with profound and immediate orthostatic hypotension. In baroreflex failure, various degrees of debuffering of blood pressure occur. In acute and complete baroreflex failure, there is usually severe hypertension and tachycardia, while with less complete and more chronic baroreflex impairment, orthostatic abnormalities may be more apparent. In orthostatic intolerance, blood pressure fall is minor, but orthostatic symptoms are prominent and tachycardia frequently occurs. Only careful autonomic studies of human subjects in the microgravity environment will permit us to determine which of these models most closely reflects the pathophysiology brought on by a period of time in the microgravity environment.

Autonomic Nervous System↗
PubMed2007

Incorporation of myofilament activation mechanics into a lumped model of the human heart.

The success and usefulness of lumped cardiovascular models are directly dependent on the physiological fidelity of their formulation. In most existing lumped formulations for the heart, the compliance of the chamber is modeled based on its electrical analog, the capacitor. This has traditionally resulted in the use of a pre-described time-varying stiffness modulus for simulating the cardiac contractions. Unfortunately, such a time-varying stiffness does not include any physiological contractile machinery and thus no dependency on fiber sarcomere length and intracellular calcium concentrations, key mechanisms responsible for proper cardiac function. In this paper a lumped cardiovascular model is presented that is based on the incorporation of detailed myofilament activation for simulating the ventricular calcium binding and cross-bridging mechanism. Upon validation against experimental data, it is shown that the new myofilament activation-based model considerably increases the physiological validity and internal consistency of the cardiovascular simulations in comparison to the traditional variable compliance-based models. It is also shown, through specific case studies, that the present model can serve as a quick response tool for testing various hypotheses concerning the impact of the calcium binding and crossbridge kinetics on the overall performance of the cardiovascular system.

Actin Cytoskeleton↗
PubMed1992

Theoretical analysis of the relationship between the ratio of ventricular systolic elastance to diastolic stiffness and stroke volume.

The maintenance of adequate blood circulation requires a sufficient ventricular contractility; in addition, to eject blood, the ventricles must first receive a sufficient volume, requiring a low diastolic stiffness. A simplified cardiovascular model was used to derive formulae for stroke volume (SV) as a function of atrial pressure and the ratio of ventricular end-systolic elastance to end-diastolic stiffness. A more complex cardiovascular model was used to assess the ability of the expressions to predict stroke volume under various steady-state conditions. The predicted SV correlated linearly with the model SV over a wide range of diastolic stiffnesses and systolic elastance. The formulae predict that with fixed right atrial pressure the SV is proportional to the ratio of end-systolic elastance to end-diastolic stiffness (GR) for the right ventricle, but relatively insensitive to the ratio (GL) for the left ventricle provided that GL is greater than GR. Model simulations confirmed this. When the right atrial pressure was not fixed increases in GR with fixed GL reduced the right atrial pressure with little change in SV. Similarly, varying GL with fixed GR produced little change in SV. The ratios highlight the importance of diastole to cardiac function.

Diastole↗
PubMed1999

Computational models of cardiovascular function for analysis of post-flight orthostatic intolerance.

The work presented in this paper is part of an ongoing effort to use mathematical models to investigate the effects of microgravity on the cardiovascular system. In particular, a thirteen compartment lumped parameter representation of the cardiovascular system is used to simulate some of the current hypotheses concerning the mechanism of post-flight orthostatic intolerance. Simulations are compared to astronaut stand test data pre - and post-flight in an effort to quantitatively evaluate alternative hypotheses.

Aerospace Medicine↗
PubMed2002

Biomedical signal processing and modeling in cardiovascular systems.

This article revisits the subject of short-term heart-rate and arterial-pressure variability from the perspective of model structures that can be useful in defining signal processing algorithms. We draw a general scheme of the oscillation sources and interactions that contribute to cardiovascular control mechanisms and highlight the elements that were considered in different modeling works. The origin, superposition, and interaction of respiratory high-frequency (HF) and vasomotor low-frequency (LF) rhythms is presented as the integration of supraspinal and spinal circuits, vasomotor activity, and pressure control loops. We analyze in detail the necessity of considering all relevant interactions for the algorithms designed to estimate the baroreflex sensitivity. We also pinpoint the components of cardiorespiratory coupling in relation to the analysis of data from the acoustic quantification of the left ventricular volume. Finally, we analyze the tendency to produce complex behaviors even in extremely simplified systems involving interactions between oscillatory mechanisms.

Animals↗
PubMed2002

Noninvasive identification of the total peripheral resistance baroreflex.

We propose two identification algorithms for quantitating the total peripheral resistance (TPR) baroreflex, an important contributor to short-term arterial blood pressure (ABP) regulation. Each algorithm analyzes beat-to-beat fluctuations in ABP and cardiac output, which may both be obtained noninvasively in humans. For a theoretical evaluation, we applied both algorithms to a realistic cardiovascular model. The results contrasted with only one of the algorithms proving to be reliable. This algorithm was able to track changes in the static gains of both the arterial and cardiopulmonary TPR baroreflex. We then applied both algorithms to a preliminary set of human data and obtained contrasting results much like those obtained from the cardiovascular model, thereby making the theoretical evaluation results more meaningful. This study suggests that, with experimental testing, the reliable identification algorithm may provide a powerful, noninvasive means for quantitating the TPR baroreflex. This study also provides an example of the role that models can play in the development and initial evaluation of algorithms aimed at quantitating important physiological mechanisms.

Adult↗
PubMedDate not supplied

Development of a flow feedback pulse duplicator system with rhesus monkey arterial input impedance characteristics.

An in vitro pulsatile pump flow system that is capable of producing physiologic pressures and flows in a mock circulatory system tuned to reproduce the first nine harmonics of the input impedance of a rhesus monkey was developed and tested. The system was created as a research tool for evaluating cardiovascular function and for the design, testing, and evaluation of electrical-mechanical cardiovascular models and chronically implanted sensors. The system possesses a computerized user interface for controlling a linear displacement pulsatile pump in a controlled flow loop format to emulate in vivo cardiovascular characteristics. Evaluation of the pump system consisted of comparing its aortic pressure and flow profiles with in vivo rhesus hemodynamic waveforms in the time and frequency domains. Comparison of aortic pressure and flow data between the pump system and in vivo data showed good agreement in the time and frequency domains, however, the pump system produced a larger pulse pressure. The pump system can be used for comparing cardiovascular parameters with predicted cardiovascular model values and for evaluating such items as vascular grafts, heart valves, biomaterials, and sensors. This article describes the development and evaluation of this feedback controlled cardiovascular dynamics simulation modeling system.

Animals↗
PubMed1994

A multidimensional measurement model for cardiovascular reactivity: stability and cross-validation in two adult samples.

The factor structure for measures of stress-related cardiovascular reactivity was examined in 2 samples: a university campus employee sample (N = 72) and a sample of young adult twins (N = 113). In both samples, 5 noninvasive cardiovascular measures were monitored during a series of challenging laboratory tasks. We developed a 2-factor model depicting vascular and cardiac influences on responding. With confirmatory factor analysis, this model was shown to be consistent with the data across both samples, across 2 testing sessions, and across 2 sets of tasks. Latent variables measuring cardiac and vascular reactivity were highly reliable on retest as well. Individual differences in cardiovascular reactivity to mental stress may be characterized by a stable, 2-dimensional pattern of response.

Adolescent↗
PubMed2000

Gene expression profiling of cardiovascular disease models.

Recent development of gene expression profiling technologies has enabled the large-scale analysis of gene expression changes during disease progression. Frequently, cardiovascular diseases involve complex interactions of multiple cell types over prolonged periods of time. A better understanding of the pathology of cardiovascular diseases and the potential identification of underlying genetic defects are currently being explored by using profiling methodologies in a number of animal and tissue-culture models.

Animals↗
PubMed2000

Computational model of cardiovascular function during orthostatic stress.

Orthostatic intolerance following spaceflight remains a critical problem in the current life-science space program. The study presented in this paper is part of an ongoing effort to use mathematical models to investigate the effects of gravitational stresses on the cardiovascular system of normals and microgravity adapted individuals. We employ a twelve compartment lumped parameter representation of the hemodynamic system coupled to set-point models of the arterial baroreflex and the cardiopulmonary reflex to investigate the transient response of heart rate to orthostatic stress. We simulate current hypotheses concerning the mechanisms underlying post-spaceflight orthostatic intolerance over a range of physiologically reasonable values and compare the simulations to astronaut stand-test data pre- and post-flight. Furthermore, we explore the effects of a potential countermeasure.

Aerospace Medicine↗
PubMed1998

Effect of on-line conductivity plasma ultrafiltrate kinetic modeling on cardiovascular stability of hemodialysis patients.

The aim of this multicenter, prospective, randomized cross-over study was to clarify whether on-line conductivity ultrafiltrate kinetic modeling (treatment B), as a substitute for sodium kinetic modeling, is capable of reducing intradialytic cardiovascular instability in comparison with standard treatment (treatment A), by reducing the sodium balance variability. Both treatments were performed by means of a modified hemodiafiltration technique. Treatment A was performed using fixed dialysate conductivity; treatment B made use of the dialysate conductivity derived from a conductivity kinetic model, in order to obtain an end-dialysis ultrafiltrate conductivity at each dialysis session that was equal to the mean value determined in the same patient during the four-week run-in period. Thus, during treatment B, the expected end-dialysis ultrafiltrate conductivity value of each patient should have been constant. The study was carried out according to a multicenter cross-over design of 16 weeks with two treatments (A or B), two sequences (1 = ABB and 2 = BAA), a run-in period of four weeks (period 1, treatment A), and three consecutive experimental periods of four weeks each. Analysis of variance for a cross-over design was used for the statistical analysis. Forty-nine hemodialysis patients prone to intradialytic hypotension (> 25% of sessions) were enrolled from 16 participating centers, and randomly assigned to either sequence 1 (26 patients) or sequence 2 (23 patients). Six patients dropped out and four were protocol violators, which left 39 patients selected for statistical analysis. There was no difference in the average dialysate conductivity, predialysis and end-dialysis plasma water ultrafiltrate conductivity or body weight between treatment A and treatment B. Thus, the observed mean sodium balance was not different and, as expected, only the intra-patient variability of end-dialysis ultrafiltrate conductivity (index of sodium balance variability) was reduced (21%). During treatment A, systolic blood pressure decreased by 23 mm Hg (95% confidence intervals 21 to 24 mm Hg) at the end of dialysis with respect to the pre-dialysis values. Treatment B reduced this intradialytic decrease (P = 0.001) with a maximum effect at the third hour of dialysis (4.4 mm Hg, 95% confidence intervals 1.9 to 6.9 mm Hg, 23% less than during treatment A, P 0.0005) without any period or carry-over effect (P = 0.53 and 0.08, respectively). There was no treatment effect on intradialytic diastolic blood pressure (P = 0.291). In conclusion, intradialytic cardiovascular stability was significantly improved by matching the interdialytic sodium load with intradialytic sodium removal using on-line conductivity ultrafiltrate kinetic modeling as an alternative to sodium kinetic modeling. Although highly significant, this effect was clinically not very large. By applying this conductivity kinetic model to patients with a more variable sodium intake from one session to another, a greater benefit can be expected.

Aged↗
PubMedDate not supplied

Apparent and internal validity of a Monte Carlo-Markov model for cardiovascular disease in a cohort follow-up study.

OBJECTIVE: To determine the apparent and internal validity of the Rotterdam Ischemic heart disease & Stroke Computer (RISC) model, a Monte Carlo-Markov model, designed to evaluate the impact of cardiovascular disease (CVD) risk factors and their modification on life expectancy (LE) and cardiovascular disease-free LE (DFLE) in a general population (hereinafter, these will be referred to together as (DF)LE). METHODS: The model is based on data from the Rotterdam Study, a cohort follow-up study of 6871 subjects aged 55 years and older who visited the research center for risk factor assessment at baseline (1990-1993) and completed a follow-up visit 7 years later (original cohort). The transition probabilities and risk factor trends used in the RISC model were based on data from 3501 subjects (the study cohort). To validate the RISC model, the number of simulated CVD events during 7 years' follow-up were compared with the observed number of events in the study cohort and the original cohort, respectively, and simulated (DF)LEs were compared with the (DF)LEs calculated from multistate life tables. RESULTS: Both in the study cohort and in the original cohort, the simulated distribution of CVD events was consistent with the observed number of events (CVD deaths: 7.1% v. 6.6% and 7.4% v. 7.6%, respectively; non-CVD deaths: 11.2% v. 11.5% and 12.9% v. 13.0%, respectively). The distribution of (DF)LEs estimated with the RISC model consistently encompassed the (DF)LEs calculated with multistate life tables. CONCLUSIONS: The simulated events and (DF)LE estimates from the RISC model are consistent with observed data from a cohort follow-up study.

Aged↗
PubMed1992

Transgenic animal models of cardiovascular disease.

Transgenic experimentation has become a crucial part of hypertension and atherosclerosis research, and is growing more important in several other areas of cardiovascular disease. It has recently made a particular contribution to understanding the role of the renin-angiotensin system in controlling hypertension. The study of blood pressure regulation, cardiac hypertrophy, atherogenesis and thrombosis are also benefiting from the transgenic approach.

Animals↗