Absence of directional sensitivity of dynamic cerebral autoregulation in acute ischemic stroke.

Abstract

Dynamic cerebral autoregulation (dCA) is impaired in acute ischemic stroke (AIS) and this dysfunction has been associated with worse clinical outcomes. It has been demonstrated that the cerebral circulation responds differently to increases and decreases of mean arterial blood pressure (MAP). This phenomenon is known as directional sensitivity and has been characterized in healthy participants but is yet to be described in AIS. We hypothesize that directional sensitivity is impaired following AIS and may contribute to the altered dCA seen in stroke. Retrospective analysis of transcranial Doppler ultrasound recordings of middle cerebral artery blood velocity were analyzed in 34 patients with AIS (23 males) and 34 age-matched healthy controls (22 males). Following correction for differences in EtCO₂, directional sensitivity was observed in controls, but absent in patients with AIS. For example, median autoregulatory index measures during increases (ARI_+D) and decreases (ARI_-D) in MAP were impaired following AIS (affected hemisphere: ARI_+D 5.3 [IQR: 3.7, 6.3], ARI_-D 4.4 [IQR: 3.8, 6.1], P = 0.088; unaffected hemisphere: ARI_+D 5.3 [IQR: 4.1, 6.1], ARI_-D 4.2 [3.5, 6.1], P = 0.174) compared with control (right hemisphere: ARI_+D 6.6 [IQR: 5.3, 8.2], ARI_-D 5.7 [IQR: 3.6, 5.4], P = 0.007; left hemisphere: ARI_+D 6.4 [IQR: 5.0, 8.2], ARI_-D 5.5 [4.6, 6.9], P = 0.026). As AIS was associated with impaired responses to increases and decreases in MAP, dysfunction of vasoconstriction and vasodilation are suspected. These changes may relate to the effect of AIS on the endothelium, vascular smooth muscle, or piezo mechanosensitive ion channels.NEW & NOTEWORTHY Patients with AIS demonstrate significantly impaired dynamic cerebral autoregulation compared with controls. AIS was associated with lower autoregulation index parameters and absent directional sensitivity of the cerebral pressure-flow relationship. We speculate that these results are due to AIS-induced impairment to both cerebral vasoconstriction and vasodilation mechanisms.