Abstract
Much like the ebb and tide of the seas, most physiologic functions are observed to operate in balance; a constant yin and yang of biology operates to maintain the body in careful equilibrium, yet the realm of vascular biology has focused mostly on the ability of vessels to dilate in an effort to improve the supply of flow to demanding tissues. It is only fitting and appropriately balanced that new data now support the concept of the endothelium and vascular wall directing constriction to low-flow territories. Moreover, we just might be able to harness the ability of vessels to appropriately constrict as a measure of endothelial health. Despite the fact that the notion of low-flow mediated constriction (L-FMC) has been intermittently studied over the past decades,1,2 and recently been reprised in the cardiac literature,3 relatively little is known regarding the mechanisms behind this phenomenon, let alone their potential clinical implications. In this issue of Circulation: Cardiovascular Interventions , Dawson et al4 present new data showing that vascular injury—potentially secondary to denudation of the endothelium or smooth-muscle cell injury—following a radial access approach impairs both endothelial-dependent dilation and L-FMC, and moreover, that this can be ameliorated with subsequent isometric handgrip exercise training. This complex study design and provocative set of results not only implicates a potential mechanism for L-FMC, but also provides a relatively safe and easy treatment for an increasingly common complication seen in interventional practice. Article see p 713 The present study by Dawson et al essentially combines 2 separate experiments to effectively underscore the importance of the endothelium in L-FMC. The first experiment follows 32 patients immediately before a radial approach to percutaneous coronary intervention and then 1 day after, to measure vascular reactivity to reactive hyperemia in both the catheterized arm and …
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