The effect of carotid artery stenting on capillary transit time heterogeneity in patients with carotid artery stenosis

Abstract

Introduction: Carotid revascularisation improves haemodynamic compromise in cerebral circulation as an additional benefit to the primary goal of reducing future thromboembolic risk. We determined the effect of carotid artery stenting on cerebral perfusion and oxygenation using a perfusion-weighted MRI algorithm that is based on assessment of capillary transit-time heterogeneity together with other perfusion and metabolism-related metrics. Patients and methods: A consecutive series of 33 patients were evaluated by dynamic susceptibility contrast perfusion-weighted MRI prior to and within 24 h of the endovascular procedure. The level of relative change induced by stenting, and relationship of these changes with respect to baseline stenosis degree were analysed. Results: Stenting led to significant increase in cerebral blood flow (p < 0.001), and decrease in cerebral blood volume (p ¼ 0.001) and mean transit time (p < 0.001); this was accompanied by reduction in oxygen extraction fraction (p < 0.001) and capillary transit-time heterogeneity (p < 0.001), but an overall increase in relative capillary transittime heterogeneity (RTH: CTH divided by MTT; p ¼ 0.008). No significant change was observed with respect to cerebral metabolic rate of oxygen. The median volume of tissue with MTT > 2s decreased from 24 ml to 12 ml (p ¼ 0.009), with CTH > 2s from 29 ml to 19 ml (p ¼ 0.041), and with RTH < 0.9 from 61 ml to 39 ml (p ¼ 0.037) following stenting. These changes were correlated with the baseline degree of stenosis. Discussion: Stenting improved the moderate stage of haemodynamic compromise at baseline in our cohort. The decreased relative transit-time heterogeneity, which increases following stenting, is probably a reflection of decreased functional capillary density secondary to chronic hypoperfusion induced by the proximal stenosis. Conclusion: Carotid artery stenting, is not only important for prophylaxis of future vascular events, but also is critical for restoration of microvascular function in the cerebral tissue.

URB597 protects against NLRP3 inflammasome activation by inhibiting autophagy dysfunction in a rat model of chronic cerebral hypoperfusion

“…A substantial amount of evidence indicates that chronic cerebral hypoperfusion (CCH), a state of chronic cerebral blood flow reduction, is associated with several cerebrovascular and neurodegenerative disorders including Alzheimer's disease (AD), carotid stenosis/occlusion, cerebral arteriovenous malformation, dural arteriovenous fistula, moyamoya disease and cerebral small vessel disease [1][2][3][4][5][6]. In our previous study [7][8][9][10][11], we found that CCH may contribute to neuronal apoptosis, cognitive impairment, chronic neuroinflammatory responses and abnormal excessive autophagy in the frontal cortex and hippocampus of rats, resulting in cerebral ischemic damage.…”

Blood flow, capillary transit times, and tissue oxygenation: the centennial of capillary recruitment

“…To address this question further, new diagnostic methods and biomarkers must be developed to allow easy assessment of capillary function and tissue oxygenation across organs (72). Thus far, findings support the hypothesis that capillary transit time effects play a role in vascular disease pathology (4,6,11,14,41), as well as in conditions less associated with vascular disease pathology (35), including AD (15,18,42,43) and cancer (10,59).…”

“…stenosis is indeed accompanied by downstream capillary flow disturbances (6) that partly account for regionally impaired brain oxygenation (increased OEF) (69). Carotid revascularization, however, seems to normalize both blood flow and capillary flow patterns in the affected tissue (6) (Fig. 6).…”

Relevance of Distal Arterial Collapse in Stenting of Atherosclerotic Near-Occlusion of the Carotid Artery

“…The limitations of our study include the retrospective nature of the study and the lack of mid-and long-term follow-up periods for the treated patients. In addition, it would have been ideal to perform routine postprocedure cross-sectional imaging dedicated to hyperperfusion syndrome or perfusion 31 or to obtain postprocedure TCD measurements in all patients.…”