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Updated: Mar 29, 2026

Computerized Dynamic Posturography for Postural Control Assessment in Patients with Intermittent Claudication
Published on: December 11, 2013
Characterization of tibial velocities by duplex ultrasound in severe peripheral arterial disease and controls
Jeffrey D Crawford1, Nicholas G Robbins1, Lauren A Harry1
1Division of Vascular Surgery, Department of Surgery, Knight Cardiovascular Institute, Oregon Health & Science University, Portland, Ore.
Background:
The relationship between tibiopopliteal velocities and peripheral arterial disease (PAD) severity is not well understood. We sought to characterize tibiopopliteal velocities in severe PAD and non-PAD control patients.
Methods:
Patients with an arterial duplex ultrasound (DUS) examination with PAD evaluated during a 5-year period were retrospectively compared with non-PAD controls. Control DUS examinations were collected sequentially during a 6-month period, retrospectively. PAD patients included those with lifestyle-limiting intermittent claudication warranting revascularization and patients with critical limb ischemia, defined as ischemic rest pain, gangrene, or a nonhealing ischemic ulcer. For each, tibial and popliteal artery peak systolic velocity (PSV) was measured at the proximal, mid, and distal segment of each artery, and a mean PSV for each artery was calculated. Mean PSV, ankle-brachial indices, peak ankle velocity (PAV), average ankle velocity (AAV), mean tibial velocity (MTV), and ankle-profunda index (API) were compared between the two groups using independent t-tests. PAV is the maximum PSV of the distal peroneal, posterior tibial (PT), or anterior tibial (AT) artery; AAV is the average PSV of the distal peroneal, PT, and AT arteries; MTV is calculated by first averaging the proximal, mid, and distal PSV for each tibial artery and then averaging the three means together; API is the AAV divided by proximal PSV of the profunda.
Results:
DUS was available in 103 patients with PAD (68 patients with critical limb ischemia and 35 patients with intermittent claudication) and 68 controls. Mean ankle-brachial index in the PAD group was 0.64 ± 0.25 compared with 1.08 ± 0.09 in controls (P = .006). Mean PSVs were significantly lower in PAD patients than in controls at the popliteal (64.6 ± 42.2 vs 76.2 ± 29.6; P = .037), peroneal (34.3 ± 26.4 vs 53.8 ± 23.3; P < .001), AT (43.7 ± 31.4 vs 65.4 ± 25.0; P < .001), and PT (43.4 ± 42.3 vs 74.1 ± 30.6; P < .001) and higher at the profunda (131.5 ± 88.0 vs 96.2 ± 44.8; P = .001). Tibial parameters including PAV (52.6 ± 45.0 vs 86.9 ± 35.7; P < .001), AAV (37.4 ± 26.4 vs 64.5 ± 21.7; P < .001), MTV (41.7 ± 30.4 vs 65.4 ± 21.7; P < .001), and API (0.43 ± 0.45 vs 0.75 ± 0.30; P < .001) were significantly lower in the PAD group than in controls. Nonoverlapping 95% confidence interval reference ranges were established for severe PAD and non-PAD controls.
Conclusions:
This study aims to characterize lower extremity arterial PSVs and ankle parameters in severe PAD and non-PAD controls. These early criteria establish reference ranges to guide vascular laboratory interpretation and clinical decision-making.
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