Amplification Of Pressure Pulse Research Articles

Arterial pulse pressure amplification described by means of a nonlinear wave model: characterization of human aging

The representation of blood pressure pulse as a combination of solitons captures many of the phenomena observed during its propagation along the systemic circulation. The aim of this work is to analyze the applicability of a compartmental model for propagation regarding the pressure pulse amplification associated with arterial aging. The model was applied to blood pressure waveforms that were synthesized using solitons, and then validated by waveforms obtained from individuals from differentiated age groups. Morphological changes were verified in the blood pressure waveform as a consequence of the aging process (i.e. due to the increase in arterial stiffness). These changes are the result of both a nonlinear interaction and the phenomena present in the propagation of nonlinear mechanic waves.

Pressure Wave Propagation in Full-body Arterial Models: A Gateway to Exploring Aging and Hypertension

It is now widely recognized that changes in arterial wall properties have a significant impact on hemodynamic indices such as pressure pulse amplification and pulse wave velocity. It is also becoming increasingly evident that changes in wall mechanics may progress both spatially and temporally (e.g., in age-related arterial stiffening and hypertension). Modeling studies can help delineate how local changes in stiffness affect global hemodynamics. Previously, several modeling studies have investigated blood and pressure in full-body scale arterial trees using one-dimensional formulations. In this paper, we work towards the goal of deepening our understanding of arterial pulse propagation phenomena while incorporating detailed information on localized hemodynamics. To this end, we present the first multi-scale simulation of unsteady blood flow and pressure within a three-dimensional deformable full-body arterial network. This simulation framework builds upon previous advances in fluid-structure interaction, multi-scale outflow boundary conditions, and perivascular tissue support modeling. We consider application examples featuring realistic distributions of spatially and temporally varying mechanical properties. Simulations successfully demonstrate realistic pressure and flow waveforms, regional blood flow distribution, pressure pulse amplification and pulse wave velocity.

Importance of Pressure Pulse Amplification in the Association of Resting Heart Rate and Arterial Stiffness

The study by Whelton et al1 shows that resting heart rate is independently associated with arterial stiffness. Arterial stiffness was quantified as distensibility and determined from ultrasound measurements of carotid diameter and MRI measurements of aortic diameter. Distensibility, computed from the relative change in carotid diameter and relative change in aortic area for a cardiac cycle divided by the brachial pulse pressure, was related to heart rate that spanned an average range of 50.9 to 78.1 bpm between the first and the last quintile, respectively (Table 1 …

Response to Importance of Pressure Pulse Amplification in the Association of Resting Heart Rate and Arterial Stiffness

HomeHypertensionVol. 62, No. 6Response to Importance of Pressure Pulse Amplification in the Association of Resting Heart Rate and Arterial Stiffness Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBResponse to Importance of Pressure Pulse Amplification in the Association of Resting Heart Rate and Arterial Stiffness Seamus P. Whelton and Michael J. Blaha Seamus P. WheltonSeamus P. Whelton Division of Cardiology, Johns Hopkins School of Medicine, Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore, MD Search for more papers by this author and Michael J. BlahaMichael J. Blaha Division of Cardiology, Johns Hopkins School of Medicine, Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore, MD Search for more papers by this author Originally published21 Oct 2013https://doi.org/10.1161/HYPERTENSIONAHA.113.02263Hypertension. 2013;62:e47Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2013: Previous Version 1 In our analysis, demonstrating an independent and inverse association between resting heart rate and arterial distensibility in the Multi-Ethnic Study of Atherosclerosis (MESA) study, distensibility was measured using the noninvasive imaging modalities of carotid ultrasound and cardiac MRI.1 On the basis of these measurements, we calculated carotid and aortic distensibility using well-known equations that incorporate pulse pressure as measured from the routine resting brachial artery blood pressure. Avolio et al2 point out that this peripheral measurement of pulse pressure may be an overestimate of the central aortic pulse pressure, especially at higher heart rates. They propose the use of a model derived from pulse wave analysis work by Wilkinson et al3 to correct for differences in pulse pressure between the peripheral and the central arteries. Using this model, they think that the association between resting heart rate and distensibility would disappear for the carotid artery and would reverse for the aorta (higher heart rate would be associated with greater distensibility [less stiffness]).We agree that it would be ideal to measure the pulse pressure directly within the carotid and the aortic arteries. However, this would require invasive measurement techniques that are not feasible in a large population-based study and is a recognized limitation of these distensibility measurements. Pulse wave analysis is indeed an interesting novel methodology that uses peripheral wave forms and a generalized transfer function to estimate the central aortic pressures. However, it is important to note that in the study by Wilkinson et al,3 pulse wave analysis is conducted at different heart rates using a permanent pacemaker transiently to alter heart rate. A distinction should be drawn here between epidemiologically derived resting heart rate and near-term variability in heart rate. An individual who likely has a chronically elevated resting heart rate may over time develop structural changes to their vasculature that are not reflected in the measurements derived from short-term increases in heart rate.The pulse wave analysis derived estimates of central pulse pressure, and their effects on the association between resting heart rate and arterial distensibility proposed by Avolio et al2 are an interesting concept but not without their own limitations, including well-documented differences according to sex and an inverse relationship with height.4 We encourage further research investigating this association to determine whether these estimates of central amplification accurately predict directly measured values at differing physiological resting heart rates.Seamus P. WheltonMichael J. BlahaDivision of CardiologyJohns Hopkins School of MedicineJohns Hopkins Ciccarone Center for the Prevention of Heart DiseaseBaltimore, MDDisclosuresNone.

Estimation of pressure pulse amplification between aorta and brachial artery using stepwise multiple regression models

The pressure pulse is amplified between the aorta and peripheral sites. This study compares two methods to estimate pressure pulse amplification (PPA) between the aorta and the brachial artery. Method 1: PPA was determined from a multi-parameter linear regression of subject parameters (gender, age, height, weight, heart rate (HR), brachial systolic pressure (BSP), diastolic pressure (BDP), mean pressure (MP)). Method 2: PPA was calculated from central aortic pressure waveforms (CW) estimated from the same subject parameters. The sample population (1421 male, 992 female) was selected from a database where aortic pressure was estimated by mathematical transformation of a peripheral (radial) pulse calibrated to sphygmomanometric BSP and BDP. The two methods were consistent in showing HR and MP as the most important parameters to estimate PPA. Correlation coefficients (R2) of 0.48 (method 1) and 0.44 (method 2) were obtained using height, weight, HR, BSP, BDP and age. Inclusion of MP increased R2 to 0.77 (method 1) and 0.71 (method 2). This study shows that databases containing peripheral and central aortic pressure waveforms can be used to construct multiple regression models for PPA estimation. These models could be applied to studies of similar subject groups where peripheral waveforms may not be available.

Pressure-flow relationships of the canine iliac periphery and systemic hemodynamics: effects of sodiumnitroprusside and adenosine.

It has been reported that sodiumnitroprusside (SNP) decreases mean systemic pressure and simultaneously increases pressure pulse amplification towards the iliac periphery (Kenner and van Zwieten 1982). This unexpected finding was suggested to be due to a decrease in iliac peripheral resistance but an increase in iliac differential resistance. In order to investigate this apparent contradiction, the iliac periphery was hemodynamically isolated from the rest of the circulation and perfused with the dog's own blood by means of a pump. Perfusion pressure (P) and flow (F), femoral venous pressure (Pv), systemic pressure (Ps) and cardiac output (CO) were measured. Steady state pressure-flow relations of the isolated bed were obtained during control and during various i.v. infusion rates of SNP and adenosine (ADS) and were found to be straight (mean r = 0.99). Their slope (delta P/delta F) was defined as differential resistance (Rd). Peripheral resistance (Rp) of the iliac bed was defined as Rp = (P-Pv)/F, calculated at the flow value where perfusion pressure equalled the prevailing systemic pressure. Total peripheral resistance (TPR) was defined as TPR = Ps/CO. The changes of Rd, Rp, Ps, CO and TPR with respect to control show that during low SNP infusion rates Rd and Rp were both increased while TPR was decreased. During all infusion rates of SNP CO did not change while Ps decreased. During low infusion rates of adenosine CO increased while Ps, Rd and Rp did not change and TPR decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

Pressure Wave Generation in a Fissioning Gas, III: Amplification of the Pressure Pulse with Helium 3 as Driver

Use of He3 is associated with highest specific energy released in gaseous fission, but amplitude of resulting pressure wave is small. This can be ameliorated by use of heavier gases in driven section, yielding interesting means for amplification of pressure pulse.