Comparison of laboratory and ambulatory measures of central blood pressure and pulse wave reflection: hitting the target or missing the mark?

2018 ◽  
Vol 12 (4) ◽  
pp. 275-284 ◽  
Author(s):  
Matthew J. Burns ◽  
Jeremy D. Seed ◽  
Anthony V. Incognito ◽  
Connor J. Doherty ◽  
Karambir Notay ◽  
...  
2021 ◽  
Vol 143 ◽  
pp. 111146
Author(s):  
Catarina de Andrade Barboza ◽  
Eliezer Guimarães Moura ◽  
Gabriela Ministro ◽  
Javier Bedoya Castaño ◽  
Gabriela C. Silva Santos ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Paulo Farinatti ◽  
Alex da Silva Itaborahy ◽  
Tainah de Paula ◽  
Walace David Monteiro ◽  
Mário F. Neves

AbstractThe acute effects of exercise modes on pulse wave reflection (PWR) and their relationship with autonomic control remain undefined, particularly in individuals with elevated blood pressure (BP). We compared PWR and autonomic modulation after acute aerobic (AE), resistance (RE), and concurrent exercise (CE) in 15 men with stage-1 hypertension (mean ± SE: 34.7 ± 2.5 years, 28.4 ± 0.6 kg/m2, 133 ± 1/82 ± 2 mmHg). Participants underwent AE, RE, and CE on different days in counterbalanced order. Applanation tonometry and heart rate variability assessments were performed before and 30-min postexercise. Aortic pressure decreased after AE (− 2.4 ± 0.7 mmHg; P = 0.01), RE (− 2.2 ± 0.6 mmHg; P = 0.03), and CE (− 3.1 ± 0.5 mmHg; P = 0.003). Augmentation index remained stable after RE, but lowered after AE (− 5.1 ± 1.7%; P = 0.03) and CE (− 7.6 ± 2.4% P = 0.002). Systolic BP reduction occurred after CE (− 5.3 ± 1.9 mmHg). RR-intervals and parasympathetic modulation lowered after all conditions (~ 30–40%; P < 0.05), while the sympathovagal balance increased after RE (1.2 ± 0.3–1.3 ± 0.3 n.u., P < 0.05). Changes in PWR correlated inversely with sympathetic and directly with vagal modulation in CE. In conclusion, AE, RE, and CE lowered central aortic pressure, but only AE and CE reduced PWR. Overall, those reductions related to decreased parasympathetic and increased sympathetic outflows. Autonomic fluctuations seemed to represent more a consequence than a cause of reduced PWR.


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.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
S Yu ◽  
J Teliewubai ◽  
X Fan ◽  
C Chi ◽  
H Ji ◽  
...  

Abstract Background Peripheral artery disease (PAD) is prevalent and substantially contributes to cardiovascular mortality particularly in the elderly, although the pathophysiological impact of PAD on heart itself still needs further investigation. In theory, PAD can increase pulse wave reflection which is an important determinant of subendocardial viability ratio (SEVR), a valuable estimate of myocardial perfusion as indicated by previous invasive studies. Thus, we hypothesize that PAD impairs myocardial perfusion through increasing pulse wave reflection. In this study, we aim to test this hypothesis in a large cohort from the Northern Shanghai Study. Methods A total of 2947 community-dwelling elderly Chinese (43.6% male, mean age: 71.3±5.9 years) were recruited. Ankle-brachial index were measured with the VP1000 device and used to diagnose PAD. Pulse wave reflection was estimated as aortic augmentation pressure (AP). Aortic BP, AP and SEVR were assessed by radial applanation tonometry. Multiple linear regression with SEVR and AP as dependent variable and PAD as independent variable, meanwhile adjusted for other covariates, were performed, respectively. Results 375 (12.7%) participants presented PAD. Compared to subjects without PAD, those with PAD showed significantly lower SEVR (126 vs. 132, P&lt;0.001) but higher AP (19 vs. 17 mmHg, P&lt;0.001). Multiple regression analysis revealed that both SEVR (regression coefficient [B] = −1.69, P=0.04, R2=0.61) and AP (B=1.19, P=0.04, R2=0.56) significantly associated with PAD, respectively. However, the association between SEVR and PAD was abolished when further adjusted for AP (B=−0.49, P=0.52). Similar results were obtained when inter-leg systolic BP difference was used to diagnose PAD. Conclusions PAD significantly and independently associates with myocardial perfusion; moreover, this association is mediated by increased pulse wave reflection. These findings provide a new dimension for understanding the pathophysiological mechanisms of cardiac damage of PAD. Funding Acknowledgement Type of funding source: None


2018 ◽  
Vol 50 (5S) ◽  
pp. 186-187
Author(s):  
Kathryn Geither ◽  
Leslie Sensibello ◽  
Jason C. Parks ◽  
Erica M. Marshall ◽  
Yu Lun Tai ◽  
...  

Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Brianna K Bruggeman ◽  
Katharine E Storo ◽  
Haley M Fair ◽  
Andrew J Wommack ◽  
James M Smoliga ◽  
...  

Intro: Glutathione is endogenous within human plasma, erythrocyte lysate and is also bound to the protein within plasma. Glutathione mediates redox chemistry and prevents oxidative damage within and around cellular components via reduction of reactive species (e.g. reactive oxygen, nitrogen, or sulfur species). Polyphenols and antioxidants have been shown to improve NO bioavailability which may reduce long term incidence of endothelial dysfunction. Less is known about whether changes in antioxidant capacity augments the risk of developing hypertension. Hypothesis: We hypothesized that acute glutathione supplementation would decrease arterial stiffness and reduce both brachial (bBP) and central blood pressure (cBP) in healthy male and female volunteers. Methods: Six males and six females (25 ± 3 and 22 ± 1 years, respectively) participated in a randomized, double blind, placebo controlled, crossover protocol. On two visits separated by 1 week, following a 12-hour fast, participants consumed either a placebo or glutathione (negligible and 200 mg, respectively) supplement via 90 second sublingual absorption which was then swallowed. Concentrations of oxidized (GSSG) and reduced glutathione (GSH) were spectrophotometrically measured in plasma (protein-bound) and erythrocyte lysate using a kinetic, enzymatic assay. Arterial stiffness was measured via pulse wave velocity (PWV) using applanation tonometry, and cBP was determined non-invasively using pulse wave analysis. All data were recorded before supplementation (baseline) and at 10, 30, 60 and 120 minutes post-consumption. Results: Linear mixed effect models revealed a significant (p<0.01) increase in total glutathione (GSH+GSSG) in the supplement group compared to placebo across all post-supplementation time points with the greatest increase occurring at 120 minutes (mean 99.0; 95%CI: 7.9,190.1). At 120 minutes post-consumption, no difference was present between glutathione and placebo groups for PWV (5.86 ± 1.19 and 6.08 ± 1.25 m/s, respectively; p=0.43), resting heart rate (52.95 ± 3.55 and 55.83 ± 6.36, respectively; p=0.16), systolic bBP (123.05 ± 12.75 and 123.13 ± 14.52 mmHg; p=0.22), diastolic bBP (71.81 ± 7.87 and 74.21 ± 6.53; p=0.48), systolic cBP (108.05 ± 10.45 and 108.68 ± 11.14 mmHg, respectively; p=0.11) and diastolic cBP (72.03 ± 7.82 and 74.94 ± 6.42 mmHg, respectively; p=0.46). Conclusion: Young healthy males and females experienced an increase in circulating humoral antioxidants in response to glutathione supplementation. However, supplementation had minimal effects on resting hemodynamics. Future research should examine glutathione supplementation’s effect in participants with decreased antioxidant capacity and increased oxidative stress including patients with known disease such as hypertension or peripheral artery disease.


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