Endothelium function dependence of acute changes in pulse wave velocity and flow-mediated slowing

Figures

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  Figure 1.. Experimental set-up. To measure PWV at baseline, and then the minimum PWV during reactive hyperemia (FMS), arterial pressure waveforms were simultaneously captured at proximal (A) and distal (B) sites using an oscillometric device. Duplex Doppler ultrasound was used to measure brachial artery FMD, and to capture pulsed Doppler waveforms (C) at baseline (0 mmHg) and during the ED protocol (75 mmHg). Ante, antegrade; ED, endothelial dysfunction; FMD, flow-mediated dilation; FMS, flow-mediated slowing; Osc, oscillatory; PWV, pulse wave velocity; Retro, retrograde.

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  Figure 2.. Example traces of FMD (A) and FMS (B) data recorded before and after the ED protocol. (A) Diameters were recorded at 30 Hz for 2 min at baseline, during the 5 min of occlusion, and for 3 min following occlusion release. The diameters were analyzed offline using specialized image analysis software. FMD was calculated as (Dmax – Dbase)/Dbase * 100. (B) PWV was automatically recorded every 3.5 s by the Vicorder device. For PWVbase, PWV was recorded continuously for 2 min and then averaged. For PWVmin, the minimum PWV following occlusion release was automatically detected and then manually confirmed. Dbase, baseline brachial diameter; Dmax, maximum brachial diameter during reactive hyperemia r; ED, endothelial dysfunction; FMD, flow-mediated dilation; FMS, flow-mediated slowing; PWV, pulse wave velocity; PWVbase, PWV at baseline; PWVmin, minimum PWV during reactive hyperemia.

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  Figure 3.. Intra-individual (pre- vs post-endothelial dysfunction) associations between FMD with PWV (A) and PWVmin (B) (n = 22 repeated measures). FMD, flow-mediated dilation; PWV, pulse wave velocity; PWVmin, minimum pulse wave velocity.