Modeling volatility in heat rate variability

Modeling Heart Rate Variability (HRV) data has become important for clinical applications and as a research tool. These data exhibit long memory and time-varying conditional variance (volatility). In HRV, volatility is traditionally estimated by recursive least squares combined with short memory AutoRegressive (AR) models. This work considers a parametric approach based on long memory Fractionally Integrated AutoRegressive Moving Average (ARFIMA) models with heteroscedastic errors. To model the heteroscedasticity nonlinear Generalized Autoregressive Conditionally Heteroscedastic (GARCH) and Exponential Generalized Autoregressive Conditionally Heteroscedastic (EGARCH) models are considered. The latter are necessary to model empirical characteristics of conditional volatility such as clustering and asymmetry in the response, usually called leverage in time series literature. The ARFIMA-EGARCH models are used to capture and remove long memory and characterize conditional volatility in 24 hour HRV recordings from the Noltisalis database. © 2016 IEEE

Volatility leveraging in heart rate: Health vs disease

Heart Rate Variability (HRV) data exhibit long memory and time-varying conditional variance (volatility). These characteristics are well captured using Fractionally Integrated AutoRegressive Moving Average (ARFIMA) models with Generalised AutoRegressive Conditional Heteroscedastic (GARCH) errors, which are an extension of the AR models usual in the analysis of HRV. GARCHmod-els assume that volatility depends only on the magnitude of the shocks and not on their sign, meaning that positive and negative shocks have a symmetric effect on volatility. However, HRV recordings indicate further dependence of volatility on the lagged shocks. This work considers Exponential GARCH (EGARCH) models which assume that positive and negative shocks have an asymmetric effect (leverage effect) on the volatility, thus better copping with complex characteristics of HRV. ARFIMA-EGARCH models, combined with adaptive segmentation, are applied to 24 h HRV recordings of 30 subjects from the Noltisalis database: 10 healthy, 10 patients suffering from congestive heart failure and 10 heart transplanted patients. Overall, the results for the leverage parameter indicate that volatility responds asymmetrically to values of HRV under and over the mean. Moreover, decreased leverage parameter values for sick subjects, suggest that these models allow to discriminate between the different groups. © 2016 CCAL

PEDAGOGICAL CONCEPTIONS AND PRACTICES OF YOUTH AND ADULT EDUCATION TEACHERS IN THE INCLUSION OF STUDENTS WITH INTELLECTUAL DISABILITY

Background: Youth and Adult Education (YAE) is a teaching modality in Brazil aimed at people who have not had access to mainstream school or not completed their schooling. Objective of the study was to characterise the pedagogical practices of teachers in the mainstream classroom and special education, working with students with intellectual disabilities at YAE. Method: Qualitative descriptive approach. Observations in classrooms and interviews with teachers. Data consolidated by content analysis and arranged in themes. Results: Teachers have difficulty meeting the student’s specific needs and developing pedagogical resources and strategies to promote access to knowledge. Conclusions: Need exists for greater collaboration between regular and special education teachers to organize the pedagogical planning enabling more assertive pedagogical practices. Article visualizations

Current pathophysiological concepts and management of pulmonary hypertension

Pulmonary hypertension (PH), increasingly recognized as a major health burden, remains underdiagnosed due mainly to the unspecific symptoms. Pulmonary arterial hypertension (PAH) has been extensively investigated. Pathophysiological knowledge derives mostly from experimental models. Paradoxically, common non-PAH PH forms remain largely unexplored. Drugs targeting lung vascular tonus became available during the last two decades, notwithstanding the disease progresses in many patients. The aim of this review is to summarize recent advances in epidemiology, pathophysiology and management with particular focus on associated myocardial and systemic compromise and experimental therapeutic possibilities. PAH, currently viewed as a panvasculopathy, is due to a crosstalk between endothelial and smooth muscle cells, inflammatory activation and altered subcellular pathways. Cardiac cachexia and right ventricular compromise are fundamental determinants of PH prognosis. Combined vasodilator therapy is already mainstay for refractory cases, but drugs directed at these new pathophysiological pathways may constitute a significant advance

Urotensin II-Induced Increase in Myocardial Distensibility Is Modulated by Angiotensin II and Endothelin-1

Endogenous regulators, such as angiotensin-II (AngII), endothelin-1 (ET-1) and urotensin-II (U-II) are released from various cell types and their plasma levels are elevated in several cardiovascular diseases. The present study evaluated a potential crosstalk between these systems by investigating if the myocardial effects of U-II are modulated by AngII or ET-1. Effects of U-II (10(-8), 10(-7), 10(-6) M) were tested in rabbit papillary muscles in the absence and in the presence of losartan (selective AT, receptor antagonist), PD-145065 (nonselective ET-1 receptors antagonist), losartan plus PD-145065, AngII or ET-1. U-II promoted concentration-dependent negative inotropic and lusitropic effects that were abolished in all experimental conditions. Also, U-II increased resting muscle length up to 1.008 +/- 0.002 L/L(max). Correcting it to its initial value resulted in a 19.5 +/- 3.5 % decrease of resting tension, indicating increased muscle distensibility. This effect on muscle length was completely abolished in the presence of losartan and significantly attenuated by PD-145065 or losartan plus PD-145065. This effect was increased in the presence of AngII, resulting in a 27.5 +/- 3.9 % decrease of resting tension, but was unaffected by the presence of ET-1. This study demonstrated an interaction of the U-II system with the AngII and ET-1 systems in terms of regulation of systolic and diastolic function

Modulation of Myocardial Stiffness by beta-Adrenergic Stimulation Its Role in Normal and Failing Heart

The acute effects of ß-adrenergic stimulation on myocardial stiffness were evaluated. New-Zealand white rabbits were treated with saline (control group) or doxorubicin to induce heart failure (HF) (DOXO-HF group). Effects of isoprenaline (10 -10-1 -5 M), a non-selective ß-adrenergic agonist, were tested in papillary muscles from both groups. In the control group, the effects of isoprenaline were also evaluated in the presence of a damaged endocardial endothelium, atenolol (ßi-adrenoceptor antagonist), ICI-118551 (ßz-adrenoceptor antagonist), KT-5720 (PKA inhibitor), L-NNA (NO-synthase inhibitor), or indomethacin (cyclooxygenase inhibitor). Passive length-tension relations were constructed before and after adding isoprenaline (10 -5 M). In the control group, isoprenaline increased resting muscle length up to 1.017±0.006 L/L max. Correction of resting muscle length to its initial value resulted in a 28.5±3.1% decrease of resting tension, indicating decreased muscle stiffness, as confirmed by the isoprenaline-induced right-downward shift of the passive lengthtension relation. These effects were modulated by ßr and ß 2adrenoceptors and PKA. In DOXO-HF group, the effect on myocardial stiffness was significantly decreased. We conclude that ß-adrenergic stimulation is a relevant mechanism of acute neurohumoral modulation of the diastolic function. Furthermore, this study clarifies the mechanisms by which myocardial stiffness is decreased. (c) 2011 Institute of Physiology v.v.i., Academy of Sciences of the Czech Republic, Prague, Czech Republic

Echocardiographic evaluation including tissue Doppler imaging in New Zealand white rabbits sedated with ketamine and midazolam

Limited data are available on the use of more recent echocardiographic parameters in the rabbit. Echocardiographic examination, including conventional echocardiography and tissue Doppler imaging (TDI), was performed on 26 male New Zealand white rabbits under ketamine-midazolam sedation. Particular emphasis was placed on the more recent systolic and diastolic parameters, such as myocardial performance index (Tei index) and mitral annular motion (from septal and lateral sides of the left ventricle) obtained using pulsed TDI. Parameters that assessed systolic and diastolic function (fractional shortening, Tei index, and maximal mitral E- and A-wave velocities) were comparable to those reported in the literature for rabbits in the awake state. The less cardiodepressive anaesthetic protocol could offer a good alternative in performing echocardiographic evaluation whenever such caution is necessary. TDI is feasible in healthy rabbits and potentially suitable for the investigation of left ventricle systolic and diastolic function

Activation profile of pro-inflammatory cytokines in acute cardiac overload

INTRODUCTION:Pro-inflammatory cytokines have been implicated in ventricular remodeling during heart failure progression. In the present study, we investigated the effects of acute volume and RV pressure overload on biventricular hemodynamics and myocardial gene expression of IL-6 and TNF-alpha.METHODS:Male Wistar rats (n = 45) instrumented with RV and LV tip micromanometers were randomly assigned to one of three protocols: i) acute RV pressure overload (PrOv) induced by pulmonary trunk banding in order to double RV peak systolic pressure, for 120 or 360 min; ii) acute volume overload (VolOv) induced by dextran40 infusion (5 ml/h), for 120 or 360 min; iii) Sham. Free wall samples from the RV and LV were collected for mRNA quantification.RESULTS:In the RV, acute overload induced IL-6 and TNF-alpha gene expression, higher in VolOv (IL-6: + 669.7 +/- 263.4%; TNF-alpha: + 5149.9 +/- 1099.0%; 360 min) than in PrOv (IL-6: + 64.9 +/- 44.2%; TNF-alpha: + 628.1 +/- 229.3%; 360 min). In PrOv, TNF-alpha mRNA levels in the LV were increased, in the absence of ventricular overload. IL-6 and TNF-alpha mRNA levels did not correlate in the LV, while in the RV a positive correlation was found (r = 0.574; p < 0.001).CONCLUSIONS:Acute cardiac overload induces overexpression of pro-inflammatory cytokines. This gene activation is not uniform, being higher in volume overload and involving both load-dependent and load-independent mechanisms

Long-term HRV in critically ill pediatric patients: coma versus brain death

Dysfunctions of the autonomic nervous system in critically ill patients with Acute Brain Injury (ABI) lead to changes in Heart Rate Variability (HRV) which appear to be particularly marked in patients subsequently declared in Brain Death (BD). HRV series are non-stationary, exhibit long memory in the mean and time-varying conditional variance (volatility), characteristics that are well modeled by AutoRegressive Fractionally Integrated Moving Average (ARFIMA) models with Generalized AutoRegressive Conditional Heteroscedastic (GARCH) errors. The long memory is estimated by the parameter d of the ARFIMA-GARCH model, whilst the time-varying conditional variance parameters, u and v characterize, respectively, the short-range and the persistence in the conditional variance. In this work, the ARFIMA-GARCH approach is applied to HRV series of 15 pediatric patients with ABI admitted in a pediatric intensive care unit, 5 of which has BD confirmed and 9 patients survived. The long memory and time-varying conditional variance parameters estimated by ARFIMA-GARCH modeling significantly differ between groups and seem able to contribute to characterize disease severity in children with ABI

Diastolic tolerance to systolic pressures closely reflects systolic performance in patients with coronary heart disease

In animal experiments, elevating systolic pressures induces diastolic dysfunction and may contribute to congestion, a finding not yet translated to humans. Coronary surgery patients (63 ± 8 years) were studied with left ventricular (LV) pressure (n = 17) or pressure-volume (n = 3) catheters, immediately before cardiopulmonary bypass. Single-beat graded pressure elevations were induced by clamping the ascending aorta. Protocol was repeated after volume loading (n = 7). Consecutive patients with a wide range of systolic function were included. Peak isovolumetric LV pressure (LVP(iso)) ranged from 113 to 261 mmHg. With preserved systolic function, LVP elevations neither delayed relaxation nor increased filling pressures. With decreasing systolic function, diastolic tolerance to afterload progressively disappeared: relaxation slowed and filling pressures increased (diastolic dysfunction). In severely depressed systolic function, filling pressures increased even with minor LVP elevations, suggesting baseline load-dependent elevation of diastolic pressures. The magnitude of filling pressure elevation induced in isovolumetric heartbeats was closely and inversely related to systolic performance, evaluated by LVP(iso) (r = -0.96), and directly related to changes in the time constant of relaxation τ (r = 0.95). The maximum tolerated systolic LVP (without diastolic dysfunction) was similarly correlated with LVP(iso) (r = 0.99). Volume loading itself accelerated relaxation, but augmented afterload-induced upward shift of filling pressures (7.9 ± 3.7 vs. 3.0 ± 1.5; P < 0.01). The normal human response to even markedly increased systolic pressures is no slowing of relaxation and preservation of normal filling pressures. When cardiac function deteriorates, the LV becomes less tolerant, responding with slowed relaxation and increased filling pressures. This increase is exacerbated by volume loading