Hour-to-hour and week-to-week variability and reproducibility of wave reflection indices derived by aortic pulse wave analysis: implications for studies with repeated measurements

2007 ◽  
Vol 25 (8) ◽  
pp. 1678-1686 ◽  
Author(s):  
Theodore G Papaioannou ◽  
Emmanouil N Karatzis ◽  
Kalliopi N Karatzi ◽  
Elias J Gialafos ◽  
Athanassios D Protogerou ◽  
...  
2014 ◽  
Vol 33 (3) ◽  
pp. 322-332 ◽  
Author(s):  
Michael A. Crilly ◽  
Kirsty M. Orme ◽  
Joan Henderson ◽  
Angela J. Allan ◽  
Sohinee Bhattacharya

2004 ◽  
Vol 287 (3) ◽  
pp. H1262-H1268 ◽  
Author(s):  
Brian A. Mullan ◽  
Ciaran N. Ennis ◽  
Howard J. P. Fee ◽  
Ian S. Young ◽  
David R. McCance

Mortality increases when acute coronary syndromes are complicated by stress-induced hyperglycemia. Early pulse wave reflection can augment central aortic systolic blood pressure and increase left ventricular strain. Altered pulse wave reflection may contribute to the increase in cardiac risk during acute hyperglycemia. Chronic ascorbic acid (AA) supplementation has recently been shown to reduce pulse wave reflection in diabetes. We investigated the in vivo effects of acute hyperglycemia, with and without AA pretreatment, on pulse wave reflection and arterial hemodynamics. Healthy male volunteers were studied. Peripheral blood pressure (BP) was measured at the brachial artery, and the SphygmoCor pulse wave analysis system was used to derive central BP, the aortic augmentation index (AIx; measure of systemic arterial stiffness), and the time to pulse wave refection ( Tr; measure of aortic distensibility) from noninvasively obtained radial artery pulse pressure (PP) waveforms. Hemodynamics were recorded at baseline and then every 30 min during a 120-min systemic hyperglycemic clamp (14 mmol/l). The subjects, studied on two separate occasions, were randomized in a double-blind, crossover manner to placebo or 2 g intravenous AA before the initiation of hyperglycemia. During hyperglycemia, AIx increased and Tr decreased. Hyperglycemia did not change peripheral PP but did magnify central aortic PP and diminished the normal physiological amplification of PP from the aorta to the periphery. Pulse wave reflection, as assessed from peripheral pulse wave analysis, is enhanced during acute hyperglycemia. Pretreatment with AA prevented the hyperglycemia-induced hemodynamic changes. By protecting hemodynamics during acute hyperglycemia, AA may have therapeutic use.


2021 ◽  
Vol 9 (18) ◽  
Author(s):  
Junjing Su ◽  
Ulf Simonsen ◽  
Soren Mellemkjaer ◽  
Luke S. Howard ◽  
Charlotte Manisty ◽  
...  

2010 ◽  
Vol 213 (2) ◽  
pp. 469-474 ◽  
Author(s):  
Catherine T. Prince ◽  
Aaron M. Secrest ◽  
Rachel H. Mackey ◽  
Vincent C. Arena ◽  
Lawrence A. Kingsley ◽  
...  

2014 ◽  
Vol 31 (1) ◽  
pp. 74-79 ◽  
Author(s):  
Simon Pecha ◽  
Samer Hakmi ◽  
Iris Wilke ◽  
Yalin Yildirim ◽  
Boris Hoffmann ◽  
...  

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Sagar Nagpal ◽  
Debduti Mukhopadhyay ◽  
Peter Osmond ◽  
Joseph E Schwartz ◽  
Joseph L Izzo

BP is highly variable within and between individuals but the impact of variation in underlying hemodynamic components is unknown. We tested the feasibility and clinical associations of quantitated variances in MAP and its hemodynamic components [heart rate (HR), stroke volume (SV) and total vascular resistance (TVR)] obtained by 24-hr ambulatory pulse wave analysis (PWA, Mobil-O-Graph, IEM, Stolzberg, DE). BP and PWA were measured every 20 min for 24 hrs. Indexed to body surface area, MAP = HR*[SV index (SVI)]*[TVR index (TVRI)]; ln(MAP) = ln(HR) + ln(SVI) + ln(TVRI); and total MAP variability = var [ln(MAP)] = covariance (cov)[ln(HR), ln(MAP)] + cov[ln(SVI), ln(MAP)] + cov[ln(TVRI), ln(MAP)]. Relative contributions to var[ln(MAP)] for each hemodynamic component (as %) were calculated and associations with demographic characteristics were analyzed by correlations and t-tests. We studied 152 people (49% women, 23% black); mean(SD): # readings 57(11), age 59(16) yr, BMI 29.9(6.5) kg/m 2 , systolic BP 135(18) and MAP 106(14) mmHg. Mean(SD) 24-hr values were: ln(MAP) 4.64 (0.13), ln(HR) 4.20 (0.15), ln(SVI) -3.32 (0.15), and ln(TVRI) 3.75 (0.18). Relative contributions of hemodynamic components to total 24-hr ln(MAP) variation were: TVRI 54(36)%, HR 33(38)%, and SVI 13(40)%. The large SDs of these relative contributions led to analysis of potential contributing factors: TVRI contribution was correlated with 24-hr mean MAP (r=0.24, p=0.003) and was higher (>54%) in males (p=0.03) and blacks (p=0.04); HR contribution was inversely related to MAP (r=-0.26, p=0.001), age (r=-0.29, p=0.0003) and BMI (r=-0.173 p=0.05) and was lower (<33%) in blacks (p=0.008); SVI contribution was correlated with age (r=0.31, p<0.0001) and BMI (r=0.23, p=0.005) and was higher (>13%) in women (p=0.03). We conclude that 24-hr ambulatory PWA can identify components of MAP variation within individuals and their associations with demographic factors. The relative contributions of hemodynamic components (HR, SV, TVR) to 24-hr variability in ln(MAP) varies systematically with 24-hr mean MAP, age, race, gender, and BMI. Theoretical clinical implications may include therapeutic adjustments for extremes of variation in HR (beta-blockers), TVR (vasodilators) or SV (diuretics).


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