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PubMedDate not supplied

[Comparison of the SCORE and REGICOR models for calculating cardiovascular risk in cardiovascular disease-free individuals at a healthcare center in Barcelona, Spain].

BACKGROUND: No studies have been published to date comparing SCORE, REGICOR and Framingham models. This study is aimed at analyzing how the REGICOR and SCORE functions classify cardiovascular risk, their correlation and concordance with Framingham (1998) and whether any differences exist among them with regard to the cardiovascular risk factors in high-risk groups. METHODS: Descriptive cross-sectional study conducted in primary care. A total of 851 individuals within the 35-74 age range, free of cardiovascular diseases and selected by simple random sampling were included. A study was made of the percentage of high-risk patients with Framingham (> or = 20% ten-year risk), SCORE (> or = 5% ten-year risk) and REGICOR with cutoff points > or = 20%, > or = 15%, > or = 10% and > or = 5% at 10 years, given that with REGICOR > or = 20% there are hardly any high-risk cases. A comparison was drawn between the correlation (Pearson's r) and concordance (Kappa index) of the REGICOR and SCORE high-risk individuals as compared to Framingham. RESULTS: The high-risk percentages respectively found were: 23.3% with Framingham; 15.2%; with SCORE; and 1.4%, 5.8%, 17.6% and 57.0% with REGICOR with the cutoff points described. REGICOR has a 0.99 correlation, SCORE a 0.78 correlation. REGICOR > or = 10% showed a better concordance (Kappa 0.83) than SCORE (Kappa 0.61). On comparing the cardiovascular risk factors of the high-risk cases (> or = 20% Framingham, > or = 5% SCORE and > or = 10% REGICOR), SCORE showed higher prevalence of diabetes and a lower prevalence of hypercholesterolemia (p<0.05). CONCLUSIONS: REGICOR showed a good correlation with Framingham. With the > or = 10% cutoff point, it classifies a number of individuals as high-risk similar to SCORE and fewer than Framingham. The SCORE model would treat a number of patients similar to the REGICOR > or =10% model with hypolipemiant drugs, however showing lesser evidence of effectiveness of the treatment.

Adult↗
PubMed1997

Multivariate closed-loop model for analysis of cardiovascular dynamics.

This paper introduces a closed-loop model for the analysis of interactions between heart rate and blood pressure variability, and respiration. The respiratory influence is modeled with an anti-causal structure to control the possible phase lead of heart rate to instantaneous lung volume. The closed-loop structure between heart rate and blood pressure allows the analysis of inter-relationships between the signals. Simulations and results on experimental data show the identifiability of the model and the robustness of the noise source contribution analysis over a wide range of model orders.

Blood Pressure↗
PubMed2005

Finite element modelling and simulations in cardiovascular mechanics and cardiology: a bibliography 1993-2004.

The paper gives a bibliographical review of the finite element modelling and simulations in cardiovascular mechanics and cardiology from the theoretical as well as practical points of views. The bibliography lists references to papers, conference proceedings and theses/dissertations that were published between 1993 and 2004. At the end of this paper, more than 890 references are given dealing with subjects as: Cardiovascular soft tissue modelling; material properties; mechanisms of cardiovascular components; blood flow; artificial components; cardiac diseases examination; surgery; and other topics.

Animals↗
PubMed1993

Neural crest ablation versus sham surgical effects in a chick embryo model of defective cardiovascular development.

In chick embryos, ablation of premigratory neural crest destined for the third, fourth, and sixth pharyngeal arches results in persistent truncus arteriosus and interrupted aortic arch. Studies of cardiogenesis in these embryos have shown decreased ejection fraction and ventricular dilation with normal cardiac output. The experimental embryos that survive to d 11 of incubation have a higher cardiac output than nonsurvivors at the same earlier stage of development. We hypothesize that this survival is due to a surgically induced decrease in vascular resistance of the embryonic and vitelline vessels. Embryos from 15 opened eggs, eight sham-operated embryos, and 13 neural crest-ablated embryos were examined at stage 18. The sham-operated embryos were treated identically with the experimental embryos except that neural crest was not ablated. Ejection fraction and cardiac output were determined by cinephotography. Mean dorsal aortic and diastolic ventricular (approximates mean atrial) pressures were determined by a servo-null pressure technique and used to calculate vascular resistance. The experimental embryos had a significantly decreased ejection fraction in comparison with either sham-operated embryos or embryos from eggs that remained unopened until just before cinephotography. The experimental and sham-operated embryos had a higher cardiac output than embryos from unopened eggs. The calculated vascular resistance was also significantly lower in both the experimental and sham-operated embryos than in the embryos from unopened eggs. Neural crest ablation appears to cause a decreased ejection fraction. Sham surgery is associated with a higher cardiac output and lower vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

A control system approach to cardiovascular reactivity: behavioral models that behave.

The control system mode of analysis of organism-environment interactions is described and used to derive an explanation of cardiovascular reactivity. This description reveals that a negative feedback control system continuously realizes a goal or purpose over time by producing output that negates the effects of unpredictable and uncontrollable disturbances on a physical variable corresponding to that purpose. Data from tracking experiments fit the control system analysis, but cannot be described by S-O-R analyses or by cognitive analyses that, unlike the control system analysis, do not correctly introduce physical time. Simple computer simulations of negative feedback control systems produce data that are almost perfectly correlated with each subject's behavior over time--these models behave. The existence of consistent behavioral results despite uncontrollable and unpredictable influences, the simple requirements for a negative feedback system, and the identification of continuously varying purposes as representing the unfolding of behavioral events over time argue for the testable hypothesis that most behavior is produced by negative feedback control. It is suggested that error in the operation of negative feedback control systems modulates cardiac performance. The ability of control systems to behave gives this explanation advantages over other theories of reactivity. A program for testing this explanation is described.

Arousal↗
PubMed1992

The coronary bed and its role in the cardiovascular system: a review and an introductory single-branch model.

To investigate cardiovascular haemodynamics under normal and pathological conditions, a closed-loop model of the cardiovascular system already presented in the literature, has been complemented by a model of the coronary bed. Oxygen available to the myocardium is strictly related to the coronary blood flow; we have developed threshold criteria which correlate cardiac output with the coronary flow. The system utilizes control systems related to the cardiac contractility and frequency, and imitates feedback mechanisms peculiar to the heart. The work exemplifies the autoregulation of events that occur when the equilibrium of the system is disturbed. It is suggested that the heart plays an active role in trying to restore the haemodynamic parameters to their physiological values.

Blood Flow Velocity↗
PubMedDate not supplied

[The characteristics of the cardiovascular reactions in modelling a state of orthostatic hypotension in waking hypertensive animals].

This study demonstrates the suppression of chronotropic component and activation of vascular component of baroreceptor reflex evoked by v.cava inferior occlusion in the conscious chronically instrumented cats with renal hypertension. Infusion of nitroprusside caused the depression of both components in the normotensive and hypertensive animals. The values of system hemodynamics indices permit considering that new model of orthostatic hypotension is worked out.

Animals↗
PubMed2000

Effects of the K+ channel opener KRN4884 on the cardiovascular metabolic syndrome model in rats.

We examined the effects of the potassium channel opener KRN4884 (5-amino-N-[2-(2-chlorophenyl)ethyl]-N'-cyano-3-pyridinecarboxamidine ) on cardiovascular metabolic syndrome (i.e., syndrome X), in rats. High-fructose diet rats developed hypertension, hypertriglyceridemia, increased total cholesterol/HDL (high-density lipoprotein)-cholesterol ratio, and hyperinsulinemia, KRN4884 (0.3-3.0 mg/kg, twice a day for 14 days, p.o.) alleviated the risk factors in fructose-fed rats. Furthermore, fructose-fed rats exhibited impairment of glucose tolerance and excess insulin secretion when loaded with glucose orally. Treatment with KRN4884 (1.0 mg/kg, twice a day for 14 days, p.o.) improved the glucose intolerance and inhibited hypersecretion of insulin in the glucose-loaded, fructose-fed rats. In contrast, KRN4884 (0.3-1.0 mg/kg, twice a day for 10 days, p.o.) did not affect serum triglyceride, cholesterol, glucose, or insulin concentrations in normal rats. LPL (lipoprotein lipase) activities in skeletal muscle and adipose tissue, and HTGL (hepatic triglyceride lipase) activity in liver were measured after administration of KRN4884 or vehicle twice a day for 14 days in fructose-fed rats. KRN4884 caused a significant increase in LPL activity in muscle and tended to increase LPL activity in adipose tissue in fructose-fed rats. HTGL was decreased in fructose-fed rats as compared with normal controls and was unaffected by KRN4884. These findings suggested that KRN4884 enhances insulin sensitivity and LPL activity, which are related to glucose and lipid metabolism and may be useful for the treatment of syndrome X.

Animals↗
PubMed1978

Mathematical model of the cardiovascular system under acceleration stress.

The pooling of blood in the lower part of the human body when it is subjected to longitudinal +Gz acceleration is one of the major reasons for cardiac insufficiency and the consequent impairment of certain important physiological functions. Headache, abdominal pain, change in heart rate, chest pain, impairment of vision, and hemorrhage are some of the manifestations of acceleration trauma. To predict the effects of time-dependent accelerations on the circulation, a mathematical model independent of assumptions extrapolated from normal G conditions must be considered. The model in the present study consists of a closed-loop hydrodynamic system comprising a heart pump, elastic tubes to represent the large arteries and veins, and a baroreceptor feedback mechanism to help to overcome cardiac insufficiency. The governing equations consist of the Navier-Stokes equations for fluid motion in the blood vessels, and equations of motion for time-dependent blood vessel deformation and ventricular contraction derived from nonlinear elasticity theory. In a numerical example, an experimentally measured deceleration profile is used and the calculated aortic flow is compared with the experimental values.

Acceleration↗
PubMed2005

A concentrated parameter model for the human cardiovascular system including heart valve dynamics and atrioventricular interaction.

Numerical modeling of the human cardiovascular system has always been an active research direction since the 19th century. In the past, various simulation models of different complexities were proposed for different research purposes. In this paper, an improved numerical model to study the dynamic function of the human circulation system is proposed. In the development of the mathematical model, the heart chambers are described with a variable elastance model. The systemic and pulmonary loops are described based on the resistance-compliance-inertia concept by considering local effects of flow friction, elasticity of blood vessels and inertia of blood in different segments of the blood vessels. As an advancement from previous models, heart valve dynamics and atrioventricular interaction, including atrial contraction and motion of the annulus fibrosus, are specifically modeled. With these improvements the developed model can predict several important features that were missing in previous numerical models, including regurgitant flow on heart valve closure, the value of E/A velocity ratio in mitral flow, the motion of the annulus fibrosus (called the KG diaphragm pumping action), etc. These features have important clinical meaning and their changes are often related to cardiovascular diseases. Successful simulation of these features enhances the accuracy of simulations of cardiovascular dynamics, and helps in clinical studies of cardiac function.

Atrial Function↗
PubMed2001

Modelling couplings among the oscillators of the cardiovascular system.

A mathematical model of the cardiovascular system is simulated numerically. The basic unit in the model is an oscillator that possesses a structural stability and robustness motivated by physiological understanding and by the analysis of measured time series. Oscillators with linear couplings are found to reproduce the main characteristic features of the experimentally obtained spectra. To explain the variability of cardiac and respiratory frequencies, however, it is essential to take into account the rest of the system, i.e. to consider the effect of noise. It is found that the addition of noise also results in epochs of synchronization, as observed experimentally. Preliminary analysis suggests that there is a mixture of linear and parametric couplings, but that the linear coupling seems to dominate.

Artifacts↗
PubMed1995

Pharmacokinetic-pharmacodynamic modelling of the cardiovascular effects of R- and S-N6-phenylisopropyladenosine in conscious normotensive rats.

Recently, the commercially available adenosine receptor agonist S-N6-phenylisopropyladenosine (S-PIA) has been demonstrated to be contaminated with the more potent R-diastereomer. The potency of S-PIA may therefore have been overestimated in previously published in vivo studies. Our objective was to determine the potency of both diastereomers in conscious normotensive rats by using an integrated pharmacokinetic-pharmacodynamic model. In a cross-over designed study, the animals received i.v. infusions of 177 micrograms/kg (0.51 mumol/kg) R-N6-phenylisopropyladenosine (R-PIA) and 4000 micrograms/kg (11.6 mumol/kg) S-PIA. The infusion of S-PIA corresponded to a simultaneous administration of 3823 micrograms/kg (11.1 mumol/kg) and 177 micrograms/kg (0.51 mumol/kg) of the S- and R-diastereomer, respectively. During the experiment, time courses of heart rate and blood pressure were recorded continuously. Serial arterial blood samples were collected and concentrations were determined by using a stereoselective high-performance liquid chromatography assay. After administration of R-PIA, the individual concentration-effect relationships could be quantified by the sigmoidal Emax model, yielding an EC50 value of 24 +/- 3 ng/ml for the reduction in heart rate (mean +/- S.E., n = 12). After administration of S-PIA, a similar EC50 value was obtained when heart rate was correlated to concentrations of R-PIA. Modelling of the concentration-effect data according to a competitive interaction model did not yield pharmacodynamic parameter estimates for S-PIA. In conclusion, the cardiovascular effects observed after infusion of S-PIA may be attributed entirely to the presence of R-PIA.

Animals↗
PubMed1993

Criteria for anatomical compatibility of the total artificial heart: computerized three-dimensional modeling of the cardiovascular anatomy.

A quantitative study of cardiovascular anatomy was performed by obtaining three-dimensional reconstructions from regular computed tomography scan images in 15 patients, all candidates for heart transplantation. Volumetric estimates of the cardiovascular structures were obtained from these three-dimensional reconstructions using data directly related to total artificial heart (TAH) implantations. By using computerized three-dimensional modeling of these structures, reproducible measurements of the parameters defining the shape and the anatomical connections of the intrathoracic space available for TAH implantation could be derived. The results are intended to be used for both technical and clinical applications such as computer-assisted drawing of the pericardial cavity and the anatomical connections (useful for improving the design of TAH) and combined statistical calculations (multiple regressions, cluster algorithm) of the measurement results, which will then enable the best selection to be made among two or three TAH models for each patient.

Aortography↗
PubMed2002

Animal models of the cardiovascular effects of exogenous hormones.

As early as the 1950s, animal studies showed that exogenous estrogen could inhibit coronary atherosclerosis. Since then, additional animal studies have helped to further elucidate the cardiovascular effects of hormone replacement therapy and the importance of the timing of therapy initiation. Although estrogen's cardioprotective effects in women are believed to be related, in part, to its effects on lipoprotein levels, studies in monkeys show that estrogen acutely modulates the vasomotor response of atherosclerotic coronary arteries without significantly changing lipoprotein levels, indicating a direct vascular effect. Studies in both rats and primates indicate that some of the antiatherogenic effects of estrogens may be counteracted by specific progestins. Models using a nonselective estrogen receptor (ER) antagonist (ICI 182,780) indicate that the antiatherogenic effects of 17 beta-estradiol are mediated via ERs. Recent studies with ER knockout mice indicate that ER-alpha and ER-beta mediate the protective effects of estrogen on the vasculature. Additional studies are ongoing to define the mechanisms through which specific estrogens and progestins affect cardiovascular function and to clarify the impact of the timing of initiation of therapy on the atherosclerotic process.

Animals↗
PubMed2000

The spontaneously hypertensive rat as a model of human cardiovascular disease: evidence of exacerbated cardiopulmonary injury and oxidative stress from inhaled emission particulate matter.

Cardiovascular disease is considered a probable risk factor of particulate matter (PM)-related mortality and morbidity. It was hypothesized that rats with hereditary systemic hypertension and underlying cardiac disease would be more susceptible than healthy normotensive rats to pulmonary injury from inhaled residual oil fly ash (ROFA) PM. Eight spontaneously hypertensive (SH) and eight normotensive Wistar-Kyoto (WKY) rats (12-13 weeks old) were implanted with radiotelemetry transmitters on Day -10 for measurement of electrocardiographic (ECG) waveforms. These and other nonimplanted rats were exposed to filtered air or ROFA (containing leachable toxic levels of metals) on Day 0 by nose-only inhalation (ROFA, 15 mg/m(3) x 6 h/day x 3 days). ECGs were monitored during both exposure and nonexposure periods. At 0 or 18 h post-ROFA exposure, rats were assessed for airway hyperreactivity, pulmonary and cardiac histological lesions, bronchoalveolar lavage fluid (BALF) markers of lung injury, oxidative stress, and cytokine gene expression. Comparisons were made in two areas: (1) underlying cardiopulmonary complications of control SH rats in comparison to control WKY rats; and (2) ROFA-induced cardiopulmonary injury/inflammation and oxidative burden. With respect to the first area, control air-exposed SH rats had higher lung and left ventricular weights when compared to age-matched WKY rats. SH rats had hyporeactive airways to acetylcholine challenge. Lung histology revealed the presence of activated macrophages, neutrophils, and hemorrhage in control SHrats. Consistently, levels of BALF protein, macrophages, neutrophils, and red blood cells were also higher in SH rats. Thiobarbituric acid-reactive material in the BALF of air-exposed SH rats was significantly higher than that of WKY rats. Lung inflammation and lesions were mirrored in the higher basal levels of pulmonary cytokine mRNA expression. Cardiomyopathy and monocytic cell infiltration were apparent in the left ventricle of SH rats, along with increased cytokine expression. ECG demonstrated a depressed ST segment area in SH rats. With regard to the second area of comparison (ROFA-exposed rats), pulmonary histology indicated a slightly exacerbated pulmonary lesions including inflammatory response to ROFA in SH rats compared to WKY rats and ROFA-induced increases in BALF protein and albumin were significantly higher in SH rats than in WKY rats. In addition, ROFA caused an increase in BALF red blood cells in SH rats, indicating increased hemorrhage in the alveolar parenchyma. The number of alveolar macrophages increased more dramatically in SH rats following ROFA exposure, whereas neutrophils increased similarly in both strains. Despite greater pulmonary injury in SH rats, ROFA-induced increases in BALF GSH, ascorbate, and uric acid were attenuated when compared to WKY rats. ROFA inhalation exposure was associated with similar increases in pulmonary mRNA expression of IL-6, cellular fibronectin, and glucose-6-phosphate dehydrogenase (relative to that of beta-actin) in both rat strains. The expression of MIP-2 was increased in WKY but attenuated in SH rats. Thus, SH rats have underlying cardiac and pulmonary complications. When exposed to ROFA, SH rats exhibited exacerbated pulmonary injury, an attenuated antioxidant response, and acute depression in ST segment area of ECG, which is consistent with a greater susceptibility to adverse health effects of fugitive combustion PM. This study shows that the SH rat is a potentially useful model of genetically determined susceptibility with pulmonary and cardiovascular complications.

Air Pollutants↗