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, R2 = 0.94) but underestimated wave reflection (correlation: 0.75, R2 = 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.
Original language | English |
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Pages (from-to) | H558-H567 |
Journal | American Journal of Physiology : Heart and Circulatory Physiology |
Volume | 313 |
Issue number | 3 |
DOIs | |
Publication status | Published - 1 Sept 2017 |
Funding
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.
Keywords
- Arterial model
- Arterial pressure
- Experimental model
- Hypertension
- Pressure amplification
- Pulse pressure
- Reflection
- Transducers, Pressure
- Pulse Wave Analysis
- Ventricular Function, Left
- Heart Ventricles/physiopathology
- Elastic Modulus
- Arterial Pressure
- Time Factors
- Cattle
- Computer Simulation
- Vascular Stiffness
- Silicones
- Aorta/physiopathology
- Models, Anatomic
- Myocardial Contraction
- Models, Cardiovascular
- Regional Blood Flow
- Hypertension/etiology
- Animals
- Blood Flow Velocity
- Ventricular Pressure