Vasodilation in Spontaneous Cervical Artery Dissection

Abstract

Cervical artery dissection (CAD) accounts for 10-20% of ischemic strokes in young adults. Although trauma and pre-existing disorders of the arterial wall are the main predisposing factors, most CAD are considered as 'spontaneous'. We hypothesized that CAD could originate in a systemic vascular disease, bound to the intima-media interface, with no clinical sign. If this hypothesis is true, the endothelium-dependent vasodilation would be impaired in response to physiological stimulus such as blood flow increase. Flow-mediated arterial dilation was studied in 65 consecutive patients with spontaneous CAD: 26 with internal carotid artery dissection (ICAD), and 39 with vertebral artery dissection (VAD) were included. CAD patients with vascular risk factors, trivial or obvious cervical trauma, or connective tissue disease were excluded. Twenty-three patients with ischemic stroke of unknown cause were included as controls. Using high-resolution ultrasonography, brachial artery diameter was measured at rest, during postischemic hyperemia (flow-mediated endotheliumdependent dilation), and after sublingual glyceryl trinitrate spray (endothelium-independent dilation). The means (SD) of flow-mediated vasodilation index were 5.7% (6.2) in ICAD, 5.0% (9.3) in VAD, and 13.2% (6.5) in controls (p < 0.0005), without any difference between ICAD and VAD; endothelium-independent dilation means were 21.5% (9.5) in ICAD, 25.1% (12.5) in VAD, and 20.8% (8.4) in controls, without significant difference between groups (p = 0.49). These results give evidence for an impaired endotheliumdependent vasodilation in CAD patients that is not the consequence of stroke and suggest that an underlying abnormality of the arterial wall layers may predispose to CAD.