Relative Contributions from the Ventricle and Arterial Tree to Arterial Pressure and its Amplification: An Experimental Study

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 characterise 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 were measured and compared to theory, varying parent/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 was 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 non-invasive assessment of ventricular health.