| Summary: | Despite central pressure’s predictive power of cardiovascular risk, brachial pressure is the clinical standard. However, amplified brachial systolic pressure varies significantly with age, and during therapy. Our aim was to modulate individual arterial and ventricular parameters in an experimental model of the cardiovascular system, to quantify each parameter’s contribution to arterial pressure and its amplification.
A piston driven ventricle provided computer-controlled flow waveforms into various silicone arterial trees. Silicone tubes diameters (20, 15, 10mm), wall thicknesses (0.5, 0.7, 1.0, 1.5mm), lengths (30–400cm), taper (20mm inlet to 20, 15, 10 and 5mm outlets), were each applied with various ventricular stroke profiles (sawtooth to sinewave). Intravascular pressure-tip wires and ultrasonic flow probes measured pressure and flow. MAP, flow and HR were maintained between tests for comparison.
Ventricular stroke profile independently augmented pressure amplification from 16% to 82% between sinewave and sawtooth ejections profiles. As expected for any arterial model, the transfer function from central to distal pressure measurement sites remained constant. Decreasing taper, wall thickness, and length, and increasing diameter each increased amplification by shifting the peak of the amplifying transfer function towards the more prominent lower frequencies, (1–3Hz). However, the amplification variation between all vascular parameters was <30%.
Despite the arterial tree dictating how the ventricular pulse will propagate, the ventricle provides the wave packet of frequencies with which to be amplified. These findings correlate well with observations of decreasing amplification with age as the native inotropy decreases, and increasing amplification associated with decreased LV mass during hypertensive drug therapy.
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