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

Date Published: September 1, 2017

Publisher: American Physiological Society

Author(s): Nicholas Gaddum, Jordi Alastruey, Phil Chowienczyk, Marcel C. M. Rutten, Patrick Segers, Tobias Schaeffter.


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.

Partial Text

We constructed an experimental cardiovascular model including a programmable ventricular stroke profile, various arterial models, and venous return to investigate important contributions to arterial pressure. The specific aim of this study was to characterize the relative contributions of geometric and mechanical properties of the arteries, bifurcations, and the ventricular stroke profile on arterial pressure and pressure amplification. Comparisons were made by maintaining the flow rate, mean arterial pressure, and heart rate constant at 3.8 l/min, 96 mmHg, and 60 beats/min for all tests. The experimental model allowed ventricular and arterial parameters to be modulated in isolation to observe their distinct contributions to the pressure wave and its propagation.

N. Gaddum, J. Alastruey, and S. Schaeffter acknowledge funding from the Engineering and Physical Sciences Research Council (EPSRC; Project Grant EP/K031546/1), the Centre of Excellence in Medical Engineering (funded by the Wellcome Trust and EPSRC under Grant WT 088641/Z/09/Z), support from the National Institute for Health Research (NIHR) Biomedical Research Centre award to Guy’s and St Thomas’ National Health Service (NHS) Foundation Trust in partnership with King’s College London, and the NIHR Healthcare Technology Co-operative for Cardiovascular Disease at Guy’s and St Thomas’ NHS Foundation Trust. The views expressed are those of the authors and not necessarily those of the NHS, NIHR, or Department of Health.

No conflicts of interest, financial or otherwise, are declared by the author(s).

N.G., M.C.R., P.S., and T.S. conceived and designed research; N.G. performed experiments; N.G. analyzed data; N.G., J.A., P.S., and T.S. interpreted results of experiments; N.G. prepared figures; N.G. drafted manuscript; N.G., J.A., P.C., M.C.R., P.S., and T.S. edited and revised manuscript; N.G., J.A., P.S., and T.S. approved final version of manuscript.




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