King's College London

Research portal

Determining cardiac and arterial contributions to central Pulse Pressure

Research output: Contribution to journalPoster abstract

Standard

Determining cardiac and arterial contributions to central Pulse Pressure. / Vennin, Samuel Michel Laurent; Li, Ye; Willemet, Marie; Fok, Henry; Gu, Haotian; Charlton, Peter Harcourt; Alastruey-Arimon, Jordi; Chowienczyk, Philip Jan.

In: Artery Research, Vol. 24, P32, 12.2018, p. 88-89.

Research output: Contribution to journalPoster abstract

Harvard

Vennin, SML, Li, Y, Willemet, M, Fok, H, Gu, H, Charlton, PH, Alastruey-Arimon, J & Chowienczyk, PJ 2018, 'Determining cardiac and arterial contributions to central Pulse Pressure', Artery Research, vol. 24, P32, pp. 88-89. https://doi.org/10.1016/j.artres.2018.10.085

APA

Vennin, S. M. L., Li, Y., Willemet, M., Fok, H., Gu, H., Charlton, P. H., Alastruey-Arimon, J., & Chowienczyk, P. J. (2018). Determining cardiac and arterial contributions to central Pulse Pressure. Artery Research, 24, 88-89. [P32]. https://doi.org/10.1016/j.artres.2018.10.085

Vancouver

Vennin SML, Li Y, Willemet M, Fok H, Gu H, Charlton PH et al. Determining cardiac and arterial contributions to central Pulse Pressure. Artery Research. 2018 Dec;24:88-89. P32. https://doi.org/10.1016/j.artres.2018.10.085

Author

Vennin, Samuel Michel Laurent ; Li, Ye ; Willemet, Marie ; Fok, Henry ; Gu, Haotian ; Charlton, Peter Harcourt ; Alastruey-Arimon, Jordi ; Chowienczyk, Philip Jan. / Determining cardiac and arterial contributions to central Pulse Pressure. In: Artery Research. 2018 ; Vol. 24. pp. 88-89.

Bibtex Download

@article{fce50e49b3cd401987bc1ef4d0914153,
title = "Determining cardiac and arterial contributions to central Pulse Pressure",
abstract = "We examined the ability of a simple reduced model comprising a proximal characteristic impedance linked to a Windkessel element to accurately predict central Pulse Pressure (PP) from aortic blood flow, verified that parameters of the model corresponded to physical properties, and applied the model to examine PP dependence on cardiac and vascular properties. PP obtained from the reduced model was compared with theoretical values obtained in silico and measured values in vivo. Theoretical values were obtained using a distributed multisegment model in a population of virtual (computed) subjects in which cardiovascular properties were varied over the pathophysiological range (n = 3,095). In vivo measurements were in normotensive subjects during modulation of physiology with vasoactive drugs (n = 13) and in hypertensive subjects (n = 156). Central PP derived from the reduced model agreed with theoretical values (mean difference ±SD, -0.09 ± 1.96 mmHg) and with measured values (means differences -1.95 ± 3.74 and -1.18 ± 3.67 mmHg for normotensive and hypertensive subjects, respectively). Parameters extracted from the reduced model agreed closely with theoretical and measured physical properties. Central PP was seen to be determined mainly by total arterial compliance (inversely associated with central arterial stiffness) and ventricular dynamics: the blood volume ejected by the ventricle into the aorta up to time of peak pressure and blood flow into the aorta (corresponding to the rate of ventricular ejection) up to this point. Increased flow and volume accounted for 20.1 mmHg (52%) of the 39.0 mmHg difference in PP between the upper and lower tertiles of the hypertensive subjects.",
author = "Vennin, {Samuel Michel Laurent} and Ye Li and Marie Willemet and Henry Fok and Haotian Gu and Charlton, {Peter Harcourt} and Jordi Alastruey-Arimon and Chowienczyk, {Philip Jan}",
year = "2018",
month = dec,
doi = "10.1016/j.artres.2018.10.085",
language = "English",
volume = "24",
pages = "88--89",
journal = "Artery Research",
issn = "1872-9312",
publisher = "Elsevier BV",
note = "ARTERY18 ; Conference date: 18-10-2018 Through 20-10-2018",
url = "http://www.arterysociety.org/our-activities/our-conference/",

}

RIS (suitable for import to EndNote) Download

TY - JOUR

T1 - Determining cardiac and arterial contributions to central Pulse Pressure

AU - Vennin, Samuel Michel Laurent

AU - Li, Ye

AU - Willemet, Marie

AU - Fok, Henry

AU - Gu, Haotian

AU - Charlton, Peter Harcourt

AU - Alastruey-Arimon, Jordi

AU - Chowienczyk, Philip Jan

PY - 2018/12

Y1 - 2018/12

N2 - We examined the ability of a simple reduced model comprising a proximal characteristic impedance linked to a Windkessel element to accurately predict central Pulse Pressure (PP) from aortic blood flow, verified that parameters of the model corresponded to physical properties, and applied the model to examine PP dependence on cardiac and vascular properties. PP obtained from the reduced model was compared with theoretical values obtained in silico and measured values in vivo. Theoretical values were obtained using a distributed multisegment model in a population of virtual (computed) subjects in which cardiovascular properties were varied over the pathophysiological range (n = 3,095). In vivo measurements were in normotensive subjects during modulation of physiology with vasoactive drugs (n = 13) and in hypertensive subjects (n = 156). Central PP derived from the reduced model agreed with theoretical values (mean difference ±SD, -0.09 ± 1.96 mmHg) and with measured values (means differences -1.95 ± 3.74 and -1.18 ± 3.67 mmHg for normotensive and hypertensive subjects, respectively). Parameters extracted from the reduced model agreed closely with theoretical and measured physical properties. Central PP was seen to be determined mainly by total arterial compliance (inversely associated with central arterial stiffness) and ventricular dynamics: the blood volume ejected by the ventricle into the aorta up to time of peak pressure and blood flow into the aorta (corresponding to the rate of ventricular ejection) up to this point. Increased flow and volume accounted for 20.1 mmHg (52%) of the 39.0 mmHg difference in PP between the upper and lower tertiles of the hypertensive subjects.

AB - We examined the ability of a simple reduced model comprising a proximal characteristic impedance linked to a Windkessel element to accurately predict central Pulse Pressure (PP) from aortic blood flow, verified that parameters of the model corresponded to physical properties, and applied the model to examine PP dependence on cardiac and vascular properties. PP obtained from the reduced model was compared with theoretical values obtained in silico and measured values in vivo. Theoretical values were obtained using a distributed multisegment model in a population of virtual (computed) subjects in which cardiovascular properties were varied over the pathophysiological range (n = 3,095). In vivo measurements were in normotensive subjects during modulation of physiology with vasoactive drugs (n = 13) and in hypertensive subjects (n = 156). Central PP derived from the reduced model agreed with theoretical values (mean difference ±SD, -0.09 ± 1.96 mmHg) and with measured values (means differences -1.95 ± 3.74 and -1.18 ± 3.67 mmHg for normotensive and hypertensive subjects, respectively). Parameters extracted from the reduced model agreed closely with theoretical and measured physical properties. Central PP was seen to be determined mainly by total arterial compliance (inversely associated with central arterial stiffness) and ventricular dynamics: the blood volume ejected by the ventricle into the aorta up to time of peak pressure and blood flow into the aorta (corresponding to the rate of ventricular ejection) up to this point. Increased flow and volume accounted for 20.1 mmHg (52%) of the 39.0 mmHg difference in PP between the upper and lower tertiles of the hypertensive subjects.

U2 - 10.1016/j.artres.2018.10.085

DO - 10.1016/j.artres.2018.10.085

M3 - Poster abstract

VL - 24

SP - 88

EP - 89

JO - Artery Research

JF - Artery Research

SN - 1872-9312

M1 - P32

T2 - ARTERY18

Y2 - 18 October 2018 through 20 October 2018

ER -

View graph of relations

© 2018 King's College London | Strand | London WC2R 2LS | England | United Kingdom | Tel +44 (0)20 7836 5454