Aging is associated with an earlier arrival of reflected waves without a distal shift in reflection sites

Background-Despite pronounced increases in central pulse wave velocity (PWV) with aging, reflected wave transit time (RWTT), traditionally defined as the timing of the inflection point (T-INF) in the central pressure waveform, does not appreciably decrease, leading to the controversial proposition of a "distal-shift" of reflection sites. T-INF, however, is exceptionally prone to measurement error and is also affected by ejection pattern and not only by wave reflection. We assessed whether RWTT, assessed by advanced pressure-flow analysis, demonstrates the expected decline with aging. Methods and Results-We studied a sample of unselected adults without cardiovascular disease (n=48; median age 48 years) and a clinical population of older adults with suspected/established cardiovascular disease (n=164; 61 years). We measured central pressure and flow with carotid tonometry and phase-contrast MRI, respectively. We assessed RWTT using wave-separation analysis (RWTTWSA) and partially distributed tube-load (TL) modeling (RWTTTL). Consistent with previous reports, T-INF did not appreciably decrease with age despite pronounced increases in PWV in both populations. However, aging was associated with pronounced decreases in RWTTWSA (general population -15.0 ms/decade, P<0.001; clinical population -9.07 ms/decade, P=0.003) and RWTTTL (general -15.8 ms/decade, P<0.001; clinical -11.8 ms/decade, P<0.001). There was no evidence of an increased effective reflecting distance by either method. TINF was shown to reliably represent RWTT only under highly unrealistic assumptions about input impedance. Conclusions-RWTT declines with age in parallel with increased PWV, with earlier effects of wave reflections and without a distal shift in reflecting sites. These findings have important implications for our understanding of the role of wave reflections with aging

Usefulness of bioelectrical impedance analysis for monitoring patients with refractory ascites

Background: bioelectrical impedance analysis is a technique for the determination of the hydropic component. The hydropic component, determined by blood volume, could be a reflection of the hemodynamic situation. This study aimed to evaluate the usefulness of peripheral bioelectrical impedance analysis (BIA) for the prediction of hemodynamic changes in large-volume paracentesis and prognosis. Methods: this was a proof-of-concept prospective study of 14 patients with liver cirrhosis and refractory ascites. Peripheral bioimpedance was measured three times using a portable device, IVOL®, before and after large-volume paracentesis, at different frequencies (5, 10, 20, 50, 100 and 200 kHz). Consequently, resistance, reactance and phase angle were obtained, both pre- and post-paracentesis (the difference between them was defined as Δ). Results: the mean age of patients was 62.2 ± 9.6 years, the Child-Pugh was 8.4 ± 1.3 and the MELD score was 15.2 ± 3.9. A direct correlation between the extraction of ascitic fluid and Δresistance (10 kHz [r = 0.722; n = 12; p = 0.008], 20 kHz [r = 0.658; n = 12; p = 0.020] and 50 kHz [r = 0.519; n = 14; p = 0.057]) was observed. The presence of edema was related to lower values of both pre-paracentesis resistance (10 Hz [23.9 ± 8 vs 32.2 ± 4; p = 0.043]) and phase angle (5 kHz [-1.9 ± 2.8 vs 5.9 ± 7.3; p = 0.032]). Pre-paracentesis phase angle was directly correlated with the decline in blood pressure after paracentesis at lower frequencies (5 kHz [r = 0.694; n = 13; p = 0.008] and 10 kHz [r = 0.661; n = 13; p = 0.014]). Lower frequencies of Δphase-angle impacted on patient prognosis (5 kHz [-8.6 ± 5 vs -2.5 ± 2.7; p = 0.021]), patients with Δphase-angle 5 kHz > -4 had a higher rate of mortality (83.3% [5/6] vs 0% [0/6]; logRank 7.306, p = 0.007). Δresistance values were associated with overt HE at six months (10 kHz [4.9 ± 2.5 vs -0.4 ± 4.7; p = 0.046]). Conclusions: in conclusion, a significant correlation between peripheral impedance and hemodynamic changes was found. Impedance was also significantly related to prognosis and overt hepatic encephalopathy

Cardiac electrical defects in progeroid mice and Hutchinson-Gilford progeria syndrome patients with nuclear lamina alterations

Hutchinson–Gilford progeria syndrome (HGPS) is a rare genetic disease caused by defective prelamin A processing, leading to nuclear lamina alterations, severe cardiovascular pathology, and premature death. Prelamin A alterations also occur in physiological aging. It remains unknown how defective prelamin A processing affects the cardiac rhythm. We show age-dependent cardiac repolarization abnormalities in HGPS patients that are also present in the Zmpste24-/- mouse model of HGPS. Challenge of Zmpste24-/- mice with the ß-adrenergic agonist isoproterenol did not trigger ventricular arrhythmia but caused bradycardia-related premature ventricular complexes and slow-rate polymorphic ventricular rhythms during recovery. Patch-clamping in Zmpste24-/- cardiomyocytes revealed prolonged calcium-transient duration and reduced sarcoplasmic reticulum calcium loading and release, consistent with the absence of isoproterenol-induced ventricular arrhythmia. Zmpste24-/- progeroid mice also developed severe fibrosis-unrelated bradycardia and PQ interval and QRS complex prolongation. These conduction defects were accompanied by overt mislocalization of the gap junction protein connexin43 (Cx43). Remarkably, Cx43 mislocalization was also evident in autopsied left ventricle tissue from HGPS patients, suggesting intercellular connectivity alterations at late stages of the disease. The similarities between HGPS patients and progeroid mice reported here strongly suggest that defective cardiac repolarization and cardiomyocyte connectivity are important abnormalities in the HGPS pathogenesis that increase the risk of arrhythmia and premature death.Peer ReviewedPostprint (published version

Aerospace medicine and biology: A continuing bibliography with indexes, supplement 128, May 1974

This special bibliography lists 282 reports, articles, and other documents introduced into the NASA scientific and technical information system in April 1974

Modeling the pulse signal by wave-shape function and analyzing by synchrosqueezing transform

We apply the recently developed adaptive non-harmonic model based on the wave-shape function, as well as the time-frequency analysis tool called synchrosqueezing transform (SST) to model and analyze oscillatory physiological signals. To demonstrate how the model and algorithm work, we apply them to study the pulse wave signal. By extracting features called the spectral pulse signature, {and} based on functional regression, we characterize the hemodynamics from the radial pulse wave signals recorded by the sphygmomanometer. Analysis results suggest the potential of the proposed signal processing approach to extract health-related hemodynamics features

General dynamics of the physical-chemical systems in mammals

Biodynamic regulator chain models for physical chemical systems in mammal