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      Relative contributions from the ventricle and arterial tree to arterial pressure and its amplification: an experimental study

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          Abstract

          The present study distinguishes contributions from cardiac and arterial parameters to elevated blood pressure and pressure amplification. Most importantly, it offers the first evidence that ventricular inotropy, an indicator of ventricular function, is an independent determinant of pressure amplification and could be measured with such established devices such as the SphygmoCor.

          Abstract

          Arterial pressure is an important diagnostic parameter for cardiovascular disease. However, relative contributions of individual ventricular and arterial parameters in generating and augmenting pressure are not understood. Using a novel experimental arterial model, our aim was to characterize individual parameter contributions to arterial pressure and its amplification. A piston-driven ventricle provided programmable stroke profiles into various silicone arterial trees and a bovine aorta. Inotropy was varied in the ventricle, and arterial parameters modulated included wall thickness, taper and diameter, the presence of bifurcation, and a native aorta (bovine) versus silicone. Wave reflection at bifurcations was measured and compared with theory, varying parent-to-child tube diameter ratios, and branch angles. Intravascular pressure-tip wires and ultrasonic flow probes measured pressure and flow. Increasing ventricular inotropy independently augmented pressure amplification from 17% to 61% between the lower and higher systolic gradient stroke profiles in the silicone arterial network and from 10% to 32% in the bovine aorta. Amplification increased with presence of a bifurcation, decreasing wall thickness and vessel taper. Pulse pressure increased with increasing wall thickness (stiffness) and taper angle and decreasing diameter. Theoretical predictions of wave transmission through bifurcations werre similar to measurements (correlation: 0.91, R 2 = 0.94) but underestimated wave reflection (correlation: 0.75, R 2 = 0.94), indicating energy losses during mechanical wave reflection. This study offers the first comprehensive investigation of contributors to hypertensive pressure and its propagation throughout the arterial tree. Importantly, ventricular inotropy plays a crucial role in the amplification of peripheral pressure wave, which offers opportunity for noninvasive assessment of ventricular health.

          NEW & NOTEWORTHY The present study distinguishes contributions from cardiac and arterial parameters to elevated blood pressure and pressure amplification. Most importantly, it offers the first evidence that ventricular inotropy, an indicator of ventricular function, is an independent determinant of pressure amplification and could be measured with such established devices such as the SphygmoCor.

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          Most cited references28

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          An analysis of the relationship between central aortic and peripheral upper limb pressure waves in man.

          Amplification of the pressure pulse between central and peripheral arteries renders pressure values in the upper limb an inaccurate measure of ascending aortic (AA) pressure. Accuracy could be improved by allowance for such amplification. Transfer functions (TF) for pressures between AA and brachial artery (BA):(BATF) and between AA and radial artery (RA):(RATF) were derived from high-fidelity pressure recordings obtained at cardiac catheterization in 14 patients under control conditions, and after sublingual nitroglycerine 0.3 mg. There was no significant difference in BATF under control conditions and with nitroglycerine; hence results were pooled. Control and nitroglycerine results were also pooled to obtain a single RATF. BATF and RATF moduli peaked at 5 Hz and 4 Hz, reaching 2.5 and 2.8 times the value at zero frequency respectively. Frequency-dependent changes in modulus and phase of BATF and RATF were attributable to wave travel and reflection in the upper limb. BATF and RATF were compared to published transfer functions and those derived from analysis of aortic and brachial or radial pressure waves in previous publications. Results were similar. Our BATF and RATF were used to synthesize AA pressure waves from published peripheral pulses. Correspondence was close, especially for systolic pressure which differed by 2.4 +/- 1.0 (mean +/- SEM) mmHg, whereas recorded systolic pressure differed by 20.4 +/- 2.6 (mean +/- SEM) mmHg between central and peripheral sites. Results indicate that in adult humans a single generalized TF can be used with acceptable accuracy to determine central from peripheral pressure under different conditions.(ABSTRACT TRUNCATED AT 250 WORDS)
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            Role of pulse pressure amplification in arterial hypertension: experts' opinion and review of the data.

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              Pressure amplification explains why pulse pressure is unrelated to risk in young subjects.

              Pulse pressure rather than diastolic pressure is the best predictor of coronary heart disease risk in older subjects, but the converse is true in younger subjects. We hypothesized that this disparity results from an age-related difference in pressure amplification from the aorta to brachial artery. Data from 212 subjects age or =50 years were abstracted from a community database. All subjects were free from cardiovascular disease, diabetes, and medication. Peripheral blood pressure was assessed by sphygmomanometry. Radial artery waveforms recorded noninvasively by applanation tonometry were used to derive central blood pressure. Pressure amplification (peripheral/central pulse pressure ratio) was linearly related to age (r=0.7; P<0.001). There was an inverse, linear relationship between amplification and diastolic pressure in the younger group (r=0.3; P<0.001) but not in older subjects (r=0.1; P=0.2). There was no relationship in either group when the amplification ratio was calculated with nonaugmented central pressure. Amplification is reduced in older subjects because of enhanced wave reflection. In younger, but not older, subjects, amplification declines as diastolic pressure rises. Therefore, peripheral pulse pressure underestimates the effect that diastolic pressure has on central pulse pressure in younger subjects. This may explain why diastolic pressure is a better predictor of risk in this age group and suggests that assessment of central pressure may improve risk stratification further.
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                Author and article information

                Journal
                Am J Physiol Heart Circ Physiol
                Am. J. Physiol. Heart Circ. Physiol
                ajpheart
                ajpheart
                AJPHEART
                American Journal of Physiology - Heart and Circulatory Physiology
                American Physiological Society (Bethesda, MD )
                0363-6135
                1522-1539
                1 September 2017
                3 June 2017
                3 June 2017
                : 313
                : 3
                : H558-H567
                Affiliations
                [1] 1Division of Imaging Sciences and Biomedical Engineering, King’s College London, St. Thomas' Hospital , London, United Kingdom;
                [2] 2King’s College London British Heart Foundation Centre, St. Thomas’ Hospital , London, United Kingdom;
                [3] 3Department of Biomedical Engineering, Technische Universiteit Eindhoven, Eindhoven, The Netherlands;
                [4] 4Ghent University, IBiTech-bioMMeda, iMinds Medical IT, Gent, Belgium; and
                [5] 5Physikalisch-Technische Bundesanstalt, Medical Physics and Metrological Information Technology, Berlin, Germany
                Author notes
                Address for reprint requests and other correspondence: N. Gaddum, Div. of Imaging Sciences and Biomedical Engineering, King’s College London, St. Thomas' Hospital, London SE1 7EH, UK (e-mail: nickgaddum@ 123456gmail.com ).
                Article
                H-00844-2016 H-00844-2016
                10.1152/ajpheart.00844.2016
                5625171
                28576835
                85e554d7-e569-4b46-afc1-8cfb9c26713b
                Copyright © 2017 the American Physiological Society

                Licensed under Creative Commons Attribution CC-BY 4.0: © the American Physiological Society.

                History
                : 3 January 2017
                : 15 May 2017
                : 31 May 2017
                Funding
                Funded by: http://doi.org/10.13039/501100000266 Engineering and Physical Sciences Research Council (EPSRC)
                Award ID: EP/K031546/1
                Funded by: Wellcome Trust and EPSRC
                Award ID: WT 088641/ Z/09/Z
                Funded by: Guy's and St Thomas' NHS Foundation Trust
                Funded by: King's College London
                Categories
                Research Article
                Integrative Cardiovascular Physiology and Pathophysiology

                Cardiovascular Medicine
                arterial pressure,hypertension,pulse pressure,pressure amplification,reflection,experimental model,arterial model

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