Background Pipeline embolization devices (PEDs) are commonly used for endovascular treatment of cerebral aneurysms but can be associated with delayed ipsilateral intraparenchymal hemorrhage. Although intra-aneurysmal hemodynamic changes have been studied, parent vessel and intracranial hemodynamics after PED use are unknown. We examine the impact of flow diversion on parent artery and distal intracranial hemodynamics. Method Patients with internal carotid cerebral aneurysms treated with PED who had flow volume rate, flow velocities, pulsatility index, resistance index, Lindegaard ratio, and wall shear stress (WSS) obtained after treatment using quantitative magnetic resonance angiography were reviewed. Means were compared between ipsilateral and contralateral internal carotid artery (ICA) and middle cerebral artery (MCA) using paired t tests. Results A total of 18 patients were included. Mean flow volume rate was lower in the ipsilateral versus contralateral ICA ( p = 0.04) but tended to be higher in the ipsilateral versus contralateral MCA ( p = 0.08). Lindegaard ratio was higher ipsilateral to the PED in diastole ( p = 0.05). Although there was no significant difference in flow velocities, pulsatility or resistance indices, and WSS, the two cases in our cohort with hemorrhagic complications did display significant changes in MCA flows and MCA WSS. Conclusion PED placement appears to alter the elasticity of the stented ICA segment, with lower flows in the ipsilateral versus contralateral ICA. Conversely, MCA flows and MCA WSS are higher in the ipsilateral MCA among patients with hemorrhage after PED placement, suggesting the role of disrupted distal hemodynamics in delayed ipsilateral intraparenchymal hemorrhage.

A-Vt and iFlow transit times on DSA correlate with cerebral AVM flow measured using QMRA. Thus, these parameters may be used to indirectly estimate AVM flow before and after embolization during angiography in real time.

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Resting-state functional magnetic resonance imaging (rs-fMRI) is frequently used to study brain function; but, it is unclear whether BOLD-signal fluctuation amplitude and functional connectivity are associated with vascular factors, and how vascularhealth factors are reflected in rs-fMRI metrics in the healthy population. As arterial stiffening is a known age-related cardiovascular risk factor, we investigated the associations between aortic stiffening (as measured using pulse-wave velocity [PWV]) and rs-fMRI metrics. We used cardiac MRI to measure aortic PWV (an established indicator of whole-body vascular stiffness), as well as dual-echo pseudo-continuous arterial-spin labeling to measure BOLD and CBF dynamics simultaneously in a group of generally healthy adults. We found that: (1) higher aortic PWV is associated with lower variance in the resting-state BOLD signal; (2) higher PWV is also associated with lower BOLD-based resting-state functional connectivity; (3) regions showing lower connectivity do not fully overlap with those showing lower BOLD variance with higher PWV; (4) CBF signal variance is a significant mediator of the above findings, only when averaged across regions-of-interest. Furthermore, we found no significant association between BOLD signal variance and systolic blood pressure, which is also a known predictor of vascular stiffness. Age-related vascular stiffness, as measured by PWV, provides a unique scenario to demonstrate the extent of vascular bias in rs-fMRI signal fluctuations and functional connectivity. These findings suggest that a substantial portion of age-related rs-fMRI differences may be driven by vascular effects rather than directly by brain function. K E Y W O R D Saging, aortic stiffness, arterial stiffening, blood pressure, blood-oxygenation level dependent signal (BOLD), BOLD signal amplitude, functional connectivity, functional MRI (fMRI), phasecontrast imaging, pulse wave velocity, resting-state fMRI

After PED, ipsilateral MCA mean flow velocity increases more in patients with DIPH. These flow velocity changes suggest the possible role of altered distal intracranial hemodynamics in DIPH after PED treatment of cerebral aneurysms. Further data are required to confirm this observation.