Associations between heart rate asymmetry expression and asymmetric detrended fluctuation analysis results.

The relation between recently established asymmetry in Asymmetric Detrended Fluctuation Analysis (ADFA) and Heart Rate Asymmetry is studied. It is found that the ADFA asymmetric exponents are related both to the overall variability and to its asymmetric components at all studied time scales. We find that the asymmetry in scaling exponents, i.e., [Formula: see text] is associated with both variance-based and runs-based types of asymmetry. This observation suggests that the physiological mechanisms of both types are similar, even though their origins and mathematical methods are very different. The graphical abstract demonstrates strong, nonlinear association between the expression of Heart Rate Asymmetry measured using relative descriptors and the Asymmetric Detrended Fluctuation Analysis results. It is clear that there is a strong relation between the two theoretically disparate approaches to signal analysis. The technique to demonstrate the association is loess fit.

Testing heart rate asymmetry in long, nonstationary 24 hour RR-interval time series.

OBJECTIVE: Heart rate asymmetry is a phenomenon in which the contribution of heart rate decelerations to short-term heart rate variability is greater than that of accelerations, and the contribution of accelerations to long-term and total variability is greater than that of decelerations. This has been established for short, stationary recordings, so our aim is to do it for long recordings. APPROACH: In this paper, we analyze heart rate asymmetry in 87 long, 24 h electrocardiogram Holter recordings from healthy people. We show that in the whole recording all types of asymmetry are observable, clear and highly statistically significant. To analyze the local changes of asymmetry in time, we analyzed the recordings by disjoint jumping windows of 300 beats. MAIN RESULTS: This analysis revealed that the local, averaged measures of all types of asymmetry also demonstrate its presence which is highly statistically significant. Additionally, we introduce in this paper a statistical test for asymmetry in a single long recording, as opposed to the current approach in which whole groups are tested. We do this by introducing the proportion of time spent in asymmetry for each recording and using it in the binomial tests. SIGNIFICANCE: We found that for all the recordings most of the time is spent in asymmetry.

Gray matter volume in relation to cardio-vascular stiffness.

BACKGROUND: Hemodynamic disturbances are associated with aging as well as the chronic process of left ventricular and arterial stiffening. This process can influence gray matter volume and thereby contribute to brain atrophy. We performed a comprehensive assessment of left ventricular and arterial function as well as central hemodynamics. These data were correlated with gray matter volume (GMV) as evaluated by magnetic resonance imaging (MRI). METHODS: GMV and aortic stiffness were estimated using MRI. Left ventricular end-systolic elastance or stiffness (Ees), arterial elastance (Ea) and total arterial compliance (TAC) were determined by echocardiography. Central hemodynamics were assessed using pulse wave analysis. RESULTS: Seventy-five healthy subjects (42 women, 33 men, mean age of 58 years) were recruited. The clinical analyses showed that GMV correlates significantly and inversely with age (r=-0.37, P=0.001), end-systolic LV stiffness (r=-0.39, P=0.0009), augmentation pressure (r=-0.48, P<0.0001), arterial elastance (r=-0.27, P=0.02) and aortic stiffness (r=-0.23, P=0.04), as determined by aortic pulse wave velocity (aPWV). GMV correlated significantly with total arterial compliance (r=0.23, P=0.04). Stepwise forward multiple regression analysis revealed that 35% of variance (P<0.0001) in GMV is attributed to aPWV, Ees and AP. CONCLUSIONS: Left ventricular end-systolic stiffness, augmentation of central arterial pressure and aortic stiffness are associated independently and negatively with GMV. These associations suggested that brain atrophy is influenced by hemodynamic factors.

Arterial stiffness in relation to subclinical atherosclerosis.

BACKGROUND: Increased arterial stiffness or arteriosclerosis, represents a physiological part of ageing. Atherosclerosis is a process that does not affect the arterial bed uniformly but has a variable local distribution and is frequently superimposed on stiffened vessels. We therefore addressed the question of whether any correlation exists between the general characteristics of arterial stiffness or wave reflection and subclinical atherosclerosis as assessed by carotid intima-media thickness (IMT) in a sample of healthy subjects. METHODS: A total of 116 healthy subjects (mean age 55 years, 43 female) were evaluated. Arterial stiffness and wave reflection was assessed with the use of digital volume pulse analysis (DVP) and pulse wave analysis (PWA). Subclinical atherosclerosis was assessed by measurement of IMT. RESULTS: Stiffness Index (SI(DVP)), the measure of general arterial stiffness correlated significantly with IMT (r = 0.37, P < 0.01). IMT correlated significantly with age (r = 0.5, P < 0.0001), waist to hip ratio (WHR) (r = 0.39, P < 0.0001) and mean blood pressure (BPmean) (r = 0.4, P < 0.0001). IMT did not correlate with measures of wave reflection. SI(DVP) correlated significantly with age (r = 0.32, P < 0.005), WHR (r = 0.36, P < 0.0001), BPmean (r = 0.36, P < 0.0001) and measurements of wave reflection. However analysis of a model which included variables that significantly influenced SI(DVP) and IMT, such as age, WHR and mean BP showed that arterial stiffness is not independently associated with subclinical atherosclerosis. CONCLUSIONS: The indices of subclinical atherosclerosis, arterial stiffness and wave reflection, indicate different aspects of vascular status in otherwise healthy subjects.

Augmentation index, pulse pressure amplification and superoxide anion production in patients with coronary artery disease.

BACKGROUND: Free oxygen radicals appear to be involved in several processes that contribute to atherogenesis and increased arterial stiffness. METHODS: The aim of our study was to evaluate arterial stiffness and the production of superoxide anions by activated polymorphonuclear neutrophils (PMN) obtained from patients with stable coronary artery disease (CAD). Thirty four consecutive patients were studied (21 men, 13 women, mean age 58 years) who underwent coronary angiography. Arterial stiffness was assessed by pulse wave analysis using a validated system (Sphygmocor Mx, AtCor Medical). Superoxide anion production by activated neutrophils was determined by a spectrophotometric method involving the measurement of cytochrome C reduction. The extent of coronary narrowing was estimated by calculation of the Gensini score. RESULTS: Superoxide anion production by stimulated PMN showed a significant positive correlation with the augmentation index (AIx) and a significant negative correlation with pulse pressure amplification (PPA), (r=0.4, p=0.02; r=-0.5 and p=0.0026 respectively). In multivariable analyses, after adjustment for age, gender and Gensini score, superoxide anions and BMI were significant predictors of AIx (R2=57.37%, p=0.001) and PPA (R2=49.04%, p=0.008). Superoxide anion production was significantly higher in the middle (52.0+/-5.8 nmol O2-/2.5x10(6) PMN/30 min) and upper teriles (62.7+/-5.6) of AIx in comparison with the first tertile 31.8+/-4.1 (p< or =0.05, p< or =0.001). Moreover, superoxide anion production in the highest tertile of PPA was significantly lower (35.6+/-4.3 nmol O2-/2.5x10(6) PMN/30 min) than that in the tertile (60.8+/-6.2, p< or =0.05). Neither the augmentation index nor pulse pressure amplification correlate with the severity of coronary atherosclerosis as indicated by the Gensini score. CONCLUSIONS: markers of arterial stiffness, AIx and pulse pressure amplification correlate with superoxide anion production but not with the severity of atherosclerosis in coronary arteries.