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PubMedDate not supplied

Age, sex, and mortality from cardiovascular disease (factor model).

The factor analysis of mortality from cardiovascular diseases in the populations of 17 European countries is presented. The results obtained can be summed up as follows: (1) in different age groups mortality from heart and vessel diseases is determined by various factors which are independent in the statistical sense; (2) the factor structures of mortality from ischemic heart disease, brain vessel damage, and hypertension are only partially coincident; each of these diseases seems to have its own specific pathophysiological mechanisms; and (3) the factor structure of male and female mortality has considerable differences in the young and few differences in the older age group. Some problems of the pathogenesis and prophylactics of cardiovascular diseases are discussed.

Adult↗
PubMed2006

The effect of including C-reactive protein in cardiovascular risk prediction models for women.

BACKGROUND: While high-sensitivity C-reactive protein (hsCRP) is an independent predictor of cardiovascular risk, global risk prediction models incorporating hsCRP have not been developed for clinical use. OBJECTIVE: To develop and compare global cardiovascular risk prediction models with and without hsCRP. DESIGN: Observational cohort study. SETTING: U.S. female health professionals. PARTICIPANTS: Initially healthy nondiabetic women age 45 years and older participating in the Women's Health Study and followed an average of 10 years. MEASUREMENTS: Incident cardiovascular events (myocardial infarction, stroke, coronary revascularization, and cardiovascular death). RESULTS: High-sensitivity CRP made a relative contribution to global risk at least as large as that provided by total, high-density lipoprotein (HDL), and low-density lipoprotein (LDL) cholesterol individually, but less than that provided by age, smoking, and blood pressure. All global measures of fit improved when hsCRP was included, with likelihood-based measures demonstrating strong preference for models that include hsCRP. With use of 10-year risk categories of 0% to less than 5%, 5% to less than 10%, 10% to less than 20%, and 20% or greater, risk prediction was more accurate in models that included hsCRP, particularly for risk between 5% and 20%. Among women initially classified with risks of 5% to less than 10% and 10% to less than 20% according to the Adult Treatment Panel III covariables, 21% and 19%, respectively, were reclassified into more accurate risk categories. Although addition of hsCRP had minimal effect on the c-statistic (a measure of model discrimination) once age, smoking, and blood pressure were accounted for, the effect was nonetheless greater than that of total, LDL, or HDL cholesterol, suggesting that the c-statistic may be insensitive in evaluating risk prediction models. LIMITATIONS: Data were available only for women. CONCLUSIONS: A global risk prediction model that includes hsCRP improves cardiovascular risk classification in women, particularly among those with a 10-year risk of 5% to 20%. In models that include age, blood pressure, and smoking status, hsCRP improves prediction at least as much as do lipid measures.

Age Factors↗
PubMed2000

A reproducible nonlethal animal model for studying cyanide poisoning.

Previous studies using bolus intravenous injections of sodium cyanide have been used to model the sudden exposure to high concentrations of cyanide that could occur on the battlefield. This study was designed to develop a model that would simulate the type of exposure to cyanide gas that could happen during actual low-level continuous types of exposure and then compare it with the bolus model. Cardiovascular and respiratory recordings taken from anesthetized dogs have been used previously to characterize the lethal effects of cyanide. The intravenous, bolus injection of 2.5 mg/kg sodium cyanide provides a model in which a greater than lethal concentration is attained. In contrast, our model uses a slow, intravenous infusion of cyanide to titrate each animal to its own inherent end point, which coincides with the amount of cyanide needed to induce death through respiratory arrest. In this model, therapeutic intervention can be used to restore respiration and allow for the complete recovery of the animals. After recovery, the same animal can be given a second infusion of cyanide, followed again by treatment and recovery, providing a reproducible end point. This end point can then be expressed as the total amount of cyanide per body weight (mg/kg) required to kill. In this study, the average dose of sodium cyanide among 12 animals was 1.21 mg/kg, which is approximately half the cyanide used in the bolus model. Thus, titration to respiratory arrest followed by resuscitation provides a repetitive-use animal model that can be used to test the efficacy of various forms of pretreatment and/or therapy without the loss of a single animal.

Acute Disease↗
PubMed1993

A mathematical model of the cardiovascular response to +Gz acceleration.

The cardiovascular system is the limiting factor for human tolerance to positive Gz (head-to-foot) acceleration induced during maneuvers of fighter aircrafts. Safe handling of modern fighter aircrafts with higher acceleration capabilities require the use of countermeasures such as a G-suit or breathing at a positive pressure. A better understanding of the mechanisms involved in the cardiovascular response to +Gz acceleration would help improve the design and application of protective measures. This paper presents a simple mathematical model of the cardiovascular system which incorporates arterial and cardiopulmonary baroreflexes, left ventricular-peripheral circulation interaction and decreased venous return. This model is capable of reproducing observed overall cardiovascular response to +Gz acceleration.

Acceleration↗
PubMed2004

Cardiovascular risk assessment and triptans.

Identifying the patient for whom triptans are contraindicated because of recognized, diagnosed cardiovascular disease is relatively straightforward. Determining whether a patient with potential unrecognized cardiovascular disease is an appropriate candidate for triptan therapy, however, constitutes a difficult challenge, especially in the absence of a framework for workup of patients. This article discusses the pathophysiology of coronary heart disease and issues involved in assessing cardiovascular risk, and it attempts to provide a framework for cardiovascular risk assessment that can be applied to decisions for prescribing triptans. Current guidelines for cardiovascular risk assessment allow stratification of patients to low, intermediate, or high risk of coronary heart disease events. This framework for risk assessment can be applied to decisions for prescribing triptans. Cardiovascular risk-assessment algorithms discussed elsewhere in this supplement suggest that patients at low risk (1 or no risk factors) of coronary heart disease can be prescribed triptans without the need for a more intensive cardiovascular evaluation. Conversely, patients with established coronary heart disease or coronary heart disease risk equivalents should not be prescribed triptans according to the current prescribing recommendations. Patients at intermediate risk (2 or more risk factors) of coronary heart disease require cardiovascular evaluation before triptans can be prescribed. Current understanding suggests that the risk of future acute coronary events is a function of the absolute number of vulnerable plaques present, a variable that cannot be accurately determined using available technology or risk-prediction models. Cardiovascular risk-assessment guidelines should be evaluated in the context of this limitation.

Contraindications↗
PubMed2004

A cardiovascular-respiratory control system model including state delay with application to congestive heart failure in humans.

This paper considers a model of the human cardiovascular-respiratory control system with one and two transport delays in the state equations describing the respiratory system. The effectiveness of the control of the ventilation rate is influenced by such transport delays because blood gases must be transported a physical distance from the lungs to the sensory sites where these gases are measured. The short term cardiovascular control system does not involve such transport delays although delays do arise in other contexts such as the baroreflex loop (see [46]) for example. This baroreflex delay is not considered here. The interaction between heart rate, blood pressure, cardiac output, and blood vessel resistance is quite complex and given the limited knowledge available of this interaction, we will model the cardiovascular control mechanism via an optimal control derived from control theory. This control will be stabilizing and is a reasonable approach based on mathematical considerations as well as being further motivated by the observation that many physiologists cite optimization as a potential influence in the evolution of biological systems (see, e.g., Kenner [29] or Swan [62]). In this paper we adapt a model, previously considered (Timischl [63] and Timischl et al. [64]), to include the effects of one and two transport delays. We will first implement an optimal control for the combined cardiovascular-respiratory model with one state space delay. We will then consider the effects of a second delay in the state space by modeling the respiratory control via an empirical formula with delay while the the complex relationships in the cardiovascular control will still be modeled by optimal control. This second transport delay associated with the sensory system of the respiratory control plays an important role in respiratory stability. As an application of this model we will consider congestive heart failure where this transport delay is larger than normal and the transition from the quiet awake state to stage 4 (NREM) sleep. The model can be used to study the interaction between cardiovascular and respiratory function in various situations as well as to consider the influence of optimal function in physiological control system performance.

Adult↗
PubMed2005

A gene-environment interaction model of stress-induced hypertension.

The case for a gene-environment interaction model of stress-induced hypertension is detailed in this paper. We hypothesize that repeated exposure to stress in combination with an environmentally and/or genetically mediated susceptibility may lead to the development of essential hypertension. Previously, we reviewed the evidence for a genetic influence on the two major intermediate phenotypes of our model: cardiovascular reactivity to psychological stress and stress-induced sodium retention, representing the cardiovascular and renal stress response, respectively. Here we first describe how genes underlying the physiological systems mediating the stress response of heart, vasculature, and kidney (i.e., the sympathetic nervous system, renin-angiotensin- aldosterone system and sodium reabsorption, and the endothelial system) may increase vulnerability to stress and confer susceptibility to development of essential hypertension. Next, we extend our model and review genes underlying three additional systems that may mediate the influence of stress on the development of essential hypertension: the parasympathetic nervous system, the serotonergic system, and the hypothamamus-pituitary-adrenal axis. The elucidation of our gene-environment interaction model of stress-induced essential hypertension will improve the understanding of the contribution of stress to the development of essential hypertension. This knowledge may lead to more effective primary and secondary prevention programs involving lifestyle interventions in which the role of stress, both acute and chronic, will be taken into account, particularly for individuals at increased genetic risk of essential hypertension.

Animals↗
PubMed1986

The effects of PAF-acether on the cardiovascular system and their inhibition by a new highly specific PAF-acether receptor antagonist BN 52021.

BN 52021, a new specific PAF-acether receptor antagonist, was evaluated on several cardiovascular models. BN 52021 antagonized PAF-acether-induced extravasation in rats. Inhibition of the hypotensive action of PAF-acether was obtained by administration of the antagonist, given preventively or curatively. In isolated guinea-pig hearts, BN 52021 inhibited the vasoconstriction induced by PAF-acether whereas a small inhibition was observed with papaverine. On the other hand, phosphodiesterase inhibitors were very effective against coronary vasoconstriction induced by vasopressin while BN 52021 was without effect. PAF-acether increased the tonus of rat isolated portal vein; this effect was inhibited by BN 52021, without any reduction in basal myogenic activity. In this model Ca2+ antagonists (D 600, diltiazem) showed a small inhibitory effect but they strongly reduced basal myogenic activity. Neither PAF-acether nor BN 52021 modified phenylephrine-induced contraction of the isolated rabbit aorta with or without endothelium demonstrating that endothelium-dependent relaxing factor is not related to PAF-acether. Our results suggest that BN 52021 specifically block the cardiovascular effects of PAF-acether. This agent may thus be an useful tool for a better understanding of the role of PAF-acether in hemodynamic changes involved in anaphylaxis or shock.

Animals↗
PubMed1988

Parameter extraction from heart rate and arterial blood pressure variability signals in dogs for the validation of a physiological model.

The paper describes an automatic procedure for improving the extraction of parameters in heart rate (HR) and arterial blood pressure (ABP) beat-to-beat variability signals. Auto- and cross-spectral analysis of such signals is carried out through parametric models and the distribution of the power of the spectra and the phase relationships are compared in various physiological situations induced in the dogs via drug infusion or surgical interventions which do influence the control mechanisms of HR and ABP. This "black-box" approach allows the obtention, directly from the processing of the above-mentioned signals, of the estimation of parameters relative to cardiovascular models, as the ones described by simple equations (Windkessel and Starling laws are introduced as examples). These parameters seem to validate significantly the capability of such models to describe the physiological interactions existing between the two considered signals. Applications may be foreseen both for research and clinical purposes.

Algorithms↗
PubMed1994

Acute toxicosis in two dogs associated with etomidate-propylene glycol infusion.

Etomidate, formulated in propylene glycol, was used as the primary anesthetic agent in two dogs (No. 1 and 2) and etomidate, formulated in saline, was used as the primary anesthetic agent in an additional 20 dogs, while developing a canine model for baroreceptor sensitivity testing. Dogs 1 and 2 had signs of acute toxicosis after infusion of etomidate in propylene glycol. Dog 1 received less total etomidate than did dog 2, 5.9 mg/kg vs 15.8 mg/kg, respectively. Average infusion rates were 4.7 and 9 mg/kg/h, respectively. Dog 1 developed clinical signs of mild hemoglobinuria, whereas dog 2 recovered from anesthesia slowly, was obtunded, bradycardic, and hypothermic, with marked hemoglobinuria and intravascular hemolysis. After supportive treatment, dog 2 regained consciousness and hemodynamic variables improved within 12 h. None of the additional 20 dogs that received infusion of etomidate in saline had any clinical adverse effects, suggesting a causal relationship between the etomidate-propylene glycol formulation and the adverse effects in dogs 1 and 2. Although etomidate may be useful in designing cardiovascular models under general anesthesia, such complications may warrant use of a different etomidate formulation in the dog when the agent is administered at these infusion rates.

Anesthesia, General↗
PubMed2002

Modeling of dynamic cardiovascular responses during G-transition-induced orthostatic stress in pitch and roll rotations.

Dynamic and fuzzy models for a typical subject's cardiovascular response to the orthostatic stress have been developed based on experimental data. In our original study (Cheung et al., 1999), arterial blood pressure (BP) time-series data were obtained using a man-rated tilt table that applies gigahertz-acceleration transitions from +0.861 Gz [head-up (HU)] to -0.707 G [head-down (HD)] and back to +0.861 Gz (HU) using either pitch or roll rotations (Cheung et al., 1999). G transitions of different duration and onset rates are common in fighter maneuvers. Based on these data, two types of predictive models have been developed in this paper: 1) second-order discrete-time models that predict BP dynamics during pitch and roll rotations and 2) fuzzy logic models that predict important variations in a subject's cardiovascular dynamics induced by HU-to-HD and HD-to-HU transitions. These two types of models assist in providing an operationally important predictive view on the characteristics of BP responses to orthostatic stress induced by pitch and roll rotations of a fighter jet pilot. The new models are being currently utilized in the design of operational recommendations for more G-tolerant operational flight regimes (e.g., split-S tactical maneuver) than the ones currently in use for modern combat aircraft.

Acceleration↗
PubMed1987

Adenosine receptors: development of selective agonists and antagonists.

Adenosine modulates a variety of physiological functions through interaction with A1 and A2 adenosine receptors, where agonists mediate inhibition and stimulation, respectively, of adenylate cyclase. In the cardiovascular system, A2 receptors mediate vasodilation and reduction in blood pressure, while A1 receptors mediate cardiac depression. The involvement of adenylate cyclase in these responses remains unresolved. Adenosine analogs in particular the N6-substituted compounds are more potent at A1 receptors than at A2 receptors. The subregion of the adenosine receptor that interacts with the N6-substituent is different for A1 and A2 receptors, particularly with respect to phenyl interactions, bulk tolerance and stereoselectivity. A series of para-substituted N6-phenyladenosines have been synthesized based on a "functionalized congener" approach in which a chemically reactive group, such as an amine or carboxylic acid, is introduced at the terminus of a chain. From the "functionalized congener" are synthesized a variety of conjugates each containing a common pharmacophore. Certain of the adenosine conjugates are highly selective for A1 receptors. Xanthines are classical antagonists for adenosine receptors for many of their pharmacological actions may be due to blockade of adenosine receptors. Caffeine and theophylline are virtually non-selective for A2 and A2 receptors. Replacement of the methyl groups of theophylline with n-propyl or larger alkyl groups yields xanthines with selectivity for A1 receptors, particularly when combined with an 8-phenyl moiety. Most 1,3-dialkyl-8-phenyl xanthines are very insoluble, but incorporation of polar aryl substituents, such as sulfo or carboxy to increase solubility, results in marked reduction in potency and selectivity. A new series of more hydrophilic 1,3-dipropyl-8-phenylxanthines has been synthesized using the "functionalized congener" approach. Certain conjugates of 8-[4-(carboxymethyloxy)phenyl 1]1,3-dipropylxanthine display A1 selectivity in biochemical and cardiovascular models. Certain analogs of caffeine in which the methyl group at the 1- or 7-position is replaced with a propargyl or propyl group display selectivity for A2 receptors. The profile of a series of adenosine analogs or of xanthine antagonists can be used to define the nature of adenosine receptors.

Adenosine↗
PubMedDate not supplied

Nomegestrol acetate and vascular reactivity: nonhuman primate experiments.

Prevention of coronary artery disease has been recognized as a major benefit of estrogen replacement therapy (ERT) in postmenopausal women. However, endometrial hyperplasia induced by unopposed ERT has raised important safety concerns. Progesterone or synthetic progestins have been used in combined hormone replacement therapy (HRT) to prevent endometrial cancer risk. Therefore, a major concern has been to ensure that the vascular beneficial effects of estrogens are not opposed when combined with progestins. Nomegestrol acetate (NOMAC) is an orally active progestin widely prescribed for HRT. Its vascular effects were evaluated in two models of coronary vascular reactivity in primates: 1) the paradoxical vasoconstriction to acetylcholine (Ach) coronary infusion after 5 months of mildly atherogenic diet in ovariectomized (OVX) Cynomolgus monkeys and 2) the pharmacologically evoked coronary vasospasm in the OVX Rhesus monkey. In the first model, after 3 months of continuous oral administration in the diet at 0.1 mg/kg/day, E2 prevented the paradoxical response to Ach, alone as well as combined with 0.25 mg/kg/day NOMAC, whereas NOMAC counteracted the endometrial stimulation. In the second model, after one artificial cycle consisting of 28 days of E2 subcutaneous (s.c.) implant and of daily oral gavage with 1 mg/kg/day of NOMAC for the last 14 days, no vasospasm (0 of 11 tested animals) occurred when the complete challenge protocol, including serotonin and the thromboxane agonist U46619, was administered to OVX Rhesus monkeys. In the balanced crossover design, identical artificial cycles with medroxyprogesterone acetate (MPA) at the same dose resulted in 7 vasospasms in 12 animals. In parallel, effective progestative activity was demonstrated by a secretory pattern in endometrial sections obtained at the end of the cycle. In these two nonhuman primate cardiovascular models, NOMAC did not have the negating effects observed with MPA.

Acetylcholine↗
PubMed2026

Proteomic Profiling Captures Residual Cardiovascular Risk Beyond the PREVENT Model in Individuals With Cardiovascular-Kidney-Metabolic Syndrome Stages 2-3.

BACKGROUND: Cardiovascular-kidney-metabolic (CKM) syndrome reflects complex pathobiological interactions among metabolic disorders, kidney injury, and cardiovascular disease (CVD). Stages 2 and 3 represent critical phases of disease progression characterised by high pathological heterogeneity. This study aimed to develop a CVD protein risk score (PRS) for this population and evaluate its incremental predictive value over the PREVENT model. METHODS: This study included 24 017 participants with CKM Stages 2-3 from the UK Biobank. Using 2923 plasma proteins measured via the Olink platform, a PRS was developed in a training set (n = 19 218) using the LASSO method. In the validation set (n = 4799), the incremental predictive performance of this score over the PREVENT model was assessed using Harrell's C-statistic, net reclassification improvement (NRI) and integrated discrimination improvement (IDI). RESULTS: A risk score comprising 63 proteins was constructed, primarily reflecting inflammation, kidney injury and matrix remodelling. Key proteins included growth differentiation factor 15 (GDF15), hepatitis A virus cellular receptor 1 (HAVCR1), matrix metallopeptidase 12 (MMP12) and NT-proBNP. In the validation set, after adjusting for PREVENT risk factors, individuals in the high PRS group had a 2.56-fold higher risk of CVD compared to those in the low score group (HR: 2.56, 95% CI: 1.96-3.37). Integrating the score into the PREVENT model improved the C-statistic by 0.034 (0.672-0.706) and achieved a 10-year NRI of 15.8% (95% CI: 9.5%-20.9%) and an IDI of 2.2% (95% CI: 1.3%-3.3%). CONCLUSION: Combining the PREVENT model with the PRS developed in this study enhances the prediction of future CVD events in the CKM Stages 2-3 population. This approach facilitates the capture of residual risk and supports precision risk stratification and management for this high-risk group.

Humans↗
PubMed1992

Cardiovascular simulation using a multiple modeling method on a digital computer--simulation of interaction between the cardiovascular system and angiotensin II.

A cardiovascular system model that simulates interactive responses to drugs has been developed on a small digital computer. The overall model basically consists of three models. The first is a momentum transport model that represents relations between blood pressure and flow in the cardiovascular system. In this model, the cardiovascular system is divided into 14 components and modeled by using equivalent electrical circuits. The second is a mass transport model comprising 14 compartments corresponding to the respective components of the cardiovascular system. This model represents the distribution of the administered drug in the various cardiovascular components. The third is an interaction model that represents the relationships between the momentum and mass transport models. This model causes variations in the resistance and capacitance parameters of the momentum transport model as a function of the current drug concentrations in the appropriate compartments of the mass transport model. The capacitances representing the ventricles are varied in a time-dependent fashion to simulate the beat of the heart. Simulation is performed by using the Euler method to solve a system of 28 ordinary differential equations governing the momentum and mass transport models on a 32-bit microcomputer, a Macintosh II. The model was assessed by performing two demonstrations of the cardiovascular response to the vasopressor angiotensin II (AT II). They first examined the interaction between the cardiovascular system and AT II. The effect of AT II on the cardiovascular system was incorporated into the interaction model. Administration of AT II as a constant infusion (200 micrograms/hr) resulted in an elevation of mean arterial pressure from approximately 100 to 150 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed2004

New bioactive angiotensins formation pathways and functional involvements.

After a brief review of the actual knowledge concerning the circulating and tissue Renin-Angiotensin System (RAS) as a unitary hormonal system, the cognitive acquisitions regarding the formation and action mechanisms of the new biologically active angiotensins will be presented. The review of the enzymatic pathways for their synthesis and inactivation, as metabolism products of angiotensin II (1-8), will be followed by the presentation of the main physio-pharmacological actions of angiotensin III (2-8), angiotensin IV (3-8) and angiotensin (1-7). The functional involvements of the cerebral angiotensin IV in what concerns its possible participation in the normal neurochemical processes of memory and in the neurodegenerative processes of Alzheimer disease will be exposed, together with the vasodilating effects of angiotensin (1-7) as counteracting factor for the constricting effects of angiotensin II. The data concerning the bioactive fragments of angiotensin II will be accompanied by those regarding its implication in the cardiovascular modeling and the induction of oxidative stress, inflammation, atherogenesis, etc. In their turn, personal researches bring new experimental evidences in favor of interactions between angiotensin (1-7) and angiotensin II within the rat thoracic aorta. Biphasic, dose-dependent effects were observed for angiotensin (1-7), induced both through nitric oxide, kinins and prostaglandin release for counteracting the vasoconstricting effects of angiotensin II and the modulation of its own vasodilator action.

Angiotensins↗