Reactive Hyperemia and Cardiovascular Risk

Since the description of the classical cardiovascular risk factors by the Framingham group some 50 years ago,1 more recent efforts have explored the utility of biomarkers to further refine risk stratification. Although vascular imaging and biochemical markers have shown considerable promise,2 assessment of vascular function has particular appeal. Endothelial dysfunction is an attendant feature of established atherosclerosis3 and a precursor when only risk factors for atherosclerosis are present.4 It is thought in large part to reflect decreased nitric oxide bioavailability in the vasculature. As such it has been suggested that endothelial dysfunction plays a central pathophysiological role in the development and clinical expression of cardiovascular disease, making it well suited as a surrogate marker of risk.See p 2113 Endothelial function has been generally assessed by measuring vasomotion of conduit vessels or regional increases in blood flow, reflecting microvascular/resistance vessel function, in the coronary or peripheral circulation. Although coronary endothelial function remains a “gold standard,” its complexity and invasive requirements do not permit extensive use. Flow-mediated dilation of the peripheral circulation (FMD) has evolved as a popular marker because of the relative simplicity, a belief that it largely reflects nitric oxide–dependent endothelial function, its correlation with coronary reactivity, and modulation by risk factors or their treatment. What is often underappreciated, however, is that the relationship between vascular risk factors and FMD is rather poor. In addition, the correlation between measures of conduit vessel and microvascular function is weak and ultimately it is microvascular function that controls blood flow and oxygen transport.Impaired coronary reactivity has been shown to predict subsequent cardiac events in several small studies.5,6 …