| Summary: | Background: Recent studies proposed that deceleration in pulse wave velocity (PWV) following hyperemia might reflect arterial distensibility and endothelial function. We therefore investigated methodological aspects and clinical determinants of newly proposed indexes of such flow-mediated slowing (FMS) in a community-based sample.
Methods: In 71 subjects (60.3±13.7 years; 50.7% women), we continuously assessed brachial- radial pulse wave velocity (PWV) using Vicorder® equipment at rest and after 3 or 5 minutes suprasystolic occlusion to induce reactive hyperemia. We calculated the relative change (Δ) in PWV per 30s post-occlusion intervals. We performed stepwise regression analyses to assess determinants of the PWV response.
Results: The decline in PWV during hyperemia was significantly stronger after 5 minutes of occlusion as compared to 3 minutes (effect sizes for 0–180s intervals: −3.58% to −0.1%; P≤0.0019). PWV declined significantly less with higher age during the 0–90s post-occlusion intervals (+1.61 to +3.99%; P≤0.023). On the other hand, we observed that, after 120s of hyperemic response, ΔPWV remained significantly lower in smokers (−4.28% to −5.37%) and subjects with high mean arterial pressure (−2.14% to −2.23%) and low pulse pressure (+2.06% to +2.07%; P≤0.046 for all). Hence, compared to non-smoking normotensives, subjects with cardiovascular risk factors exhibited a delayed age-adjusted recovery of PWV after 5 minutes of occlusion (P≤0.039).
Conclusions: Our findings confirm an occlusion time of 5 minutes for assessment of endothelial function by FMS. Whereas early FMS response might deteriorate with ageing, cardiovascular risk factors such as smoking and hypertension might impair the late recovery of PWV following reactive hyperemia.
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