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Determining cardiac and arterial contributions to central Pulse Pressure

Research output: Contribution to journalPoster abstract

Original languageEnglish
Article numberP32
Pages (from-to)88-89
JournalArtery Research
Volume24
Early online date4 Dec 2018
DOIs
Publication statusPublished - Dec 2018
EventARTERY18 - Guimaraes, Portugal
Duration: 18 Oct 201820 Oct 2018
http://www.arterysociety.org/our-activities/our-conference/

King's Authors

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.

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