Peripheral vascular dysfunction in migraine: a review

Abstract

Numerous studies have indicated an increased risk of vascular disease among migraineurs. Alterations in endothelial and arterial function, which predispose to atherosclerosis and cardiovascular diseases, have been suggested as an important link between migraine and vascular disease. However, the available evidence is inconsistent. We aimed to review and summarize the published evidence about the peripheral vascular dysfunction of migraineurs.We systematically searched in BIOSIS, the Cochrane database, Embase, Google scholar, ISI Web of Science, and Medline to identify articles, published up to April 2013, evaluating the endothelial and arterial function of migraineurs.Several lines of evidence for vascular dysfunction were reported in migraineurs. Findings regarding endothelial function are particularly controversial since studies variously indicated the presence of endothelial dysfunction in migraineurs, the absence of any difference in endothelial function between migraineurs and non-migraineurs, and even an enhanced endothelial function in migraineurs. Reports on arterial function are more consistent and suggest that functional properties of large arteries are altered in migraineurs.Peripheral vascular function, particularly arterial function, is a promising non-invasive indicator of the vascular health of subjects with migraine. However, further targeted research is needed to understand whether altered arterial function explains the increased risk of vascular disease among patients with migraine.

Figure 1

Flow-mediated dilation. Flow-mediated dilation (FMD) measures endothelial function by inducing a temporary ischemia in a brachial artery and observing the amount of vasodilation following the stressor event. After a baseline measurement of the artery diameter via an ultrasound probe, a sphygmomanometer blood pressure cuff is positioned on the right forearm 2 cm below the elbow and inflated to 250 mmHg to produce ischemia in the forearm. The cuff is deflated after some minutes, usually 5, thus causing a reactive hyperemia which in turn produces a shear stress stimulus that induces the endothelium to release nitric oxide as a vasodilator. FMD is considered as diameter after reactive hyperemia - basal diameter/basal diameter × 100. The figure shows the diameter (upper part) and shear rate (lower part) of brachial artery during FMD before (grey-shaded part on the left), during (black-shaded part), and after (grey-shaded part on the right) ischemia.

Figure 2

Carotid-Femoral Pulse Wave Velocity. Increased arterial stiffness leads to increased velocity of the pulse wave generated in the arteries by the contraction of the left ventricle. Pulse wave velocity (PWV) consists in measuring pulse wave profiles by tonometry at two distant locations (carotid and femoral) and measuring the delay in the onset of the wave between those two locations. PWV is calculated as the distance traveled by the wave divided by the time taken to travel that distance. Surface distance between the two recording sites and simultaneously recorded electrocardiograms are used to calculate wave transit time. The figure shows tonometric (white lines) recordings of the carotid (above) and femoral (below) artery waves according with simultaneous electrocardiographic (yellow lines) ‘R’ wave of the electrocardiogram as a timing reference.

Figure 3

Augmentation Index. The interaction between the incident pulse wave and the reflected pulse wave, which is generated by the arterial resistance, is expressed by the augmentation index, which is the amount of pulse wave induced only by arterial resistance. In the figure, the upper arrow indicates the first systolic peak (incident wave), while the lower arrow indicates the second systolic peak (reflected wave). The ratio between the reflected wave/incident wave × 100 is the augmentation index.