Flow-mediated dilation: An evolving method.

Abstract

Endothelial dysfunction embodies roles of precursor and perpetuator of systemic atherosclerotic disease. Identifying and quantifying its impact would therefore provide insight on the genesis of atherosclerosis initiation and progression. However, endothelial dysfunction comprises a broad spectrum of impaired functionsdranging from vascular tone regulation to plaque stabilizing propertiesdand available clinical methods effectively estimate only singular aspects of the underlying condition. Functionally, vasomotor regulation reflects endothelial function and its regulation occurs at the macrovascular [1] and microvascular [2] levels. Substantial evidence indicates that impairment in vasomotor function signalizes subsequent atherosclerotic disease [3e5] and recurrence of cardiovascular events [6,7]. However, this discriminator is not an effective surrogate indicator in all populations [2,8]. Some studies suggest that microvascular dysfunction predicts risk more reliably in healthier and younger populations as opposed to patients with established systemic, macrovascular atherosclerosis [9]. Flow mediated dilation methods (FMD) provide a surrogate endpoint to evaluate the potential dilatatory response of a conduit (macrovascular) artery stimulated by reactive hyperemia. This observed response generally mimics the increase in myocardial blood flow to accommodate local metabolic demands, known as coronary flow reserve [10,11]. Arterial flow and vessel wall shear stress variables (stimulus for FMD) are not traditionally assessed;