Impaired Clearance of Microemboli and Cerebrovascular Symptoms During Carotid Stenting Procedures

Abstract

Background: Transcranial Doppler monitoring shows a high prevalence of microemboli during carotid artery stenting (CAS); however, the occurrence of cerebrovascular symptoms (CVSs) does not seem to be related to the microembolic load. Objective: To evaluate embolic and hemodynamic transcranial Doppler monitoring findings and their relationships with the occurrence of procedural CVSs. Patients: Fifty-four patients who had carotid stenosis of more than 70% underwent a total of 57 CAS procedures during transcranial Doppler monitoring of mean blood flow velocity and microembolic signals in the middle cerebral artery. The occurrence of transient ischemic attack, transient monocular blindness, and stroke during the CAS procedure was considered CVSs. Results: Nine (15.8%) of the 57 patients had CVSs during the procedure (ie, 6 patients with transient ischemic attack, 1 with transient monocular blindness, 1 with a minor stroke, and 1 with a major stroke). The mean blood flow velocity median values were statistically significantly lower (PϽ.001) in the group of 9 patients with CVSs (36 cm/s; interquartile range, 32.3-38.5) compared with the 48 without CVSs (48 cm/s; interquartile range, 41.5-52). The median number of isolated microembolic signals was similar in the 2 groups (72; interquartile range, 66-81 vs 75; interquartile range, 67-83.5). The median number of microembolic signal showers (clusters of too many signals to be counted separately in one cardiac cycle) presented a nonsignificant prevalence in the patients with CVSs (9; interquartile range, 7.5-11.2) compared with the ones without CVSs (8.2; interquartile range, 7-9). Conclusion: The low flow velocity in the middle cerebral artery may impair the clearance of the microembolic load and should be considered a precursor of CVSs during the CAS procedure.

Intraoperative Microemboli and Low Middle Cerebral Artery Blood Flow Velocity Are Additive in Predicting Development of Cerebral Ischemic Events After Carotid Endarterectomy

“…Orlandi et al recently performed TCD monitoring during carotid artery stenting and also demonstrated that MCA median blood flow velocity values at the start of the procedure were significantly lower in patients with new postoperative neurological deficits than in those without. 8 The results of our multivariate analysis correspond with this finding and support the concept proposed by Caplan and Hennerici. 6 In the present study, among patients with at least one MES during carotid dissection, MCA MFV was better than the number of MES in terms of predicting new postoperative ischemic lesions on DWI.…”

“…Mean blood flow velocity (MFV) values were defined as diastolic flow velocity ϩone third (systolic flow velocity minus diastolic flow velocity; cm/s). 8 The MFV measured at the start of skin incision was defined as MFV during carotid dissection.…”

Transient neurological deficits mimicking left middle cerebral artery infarct after carotid artery stenting without associated imaging findings: A case report

“…Endothelium has been damaged and the inflammatory process has been activated because of these microembolus. Also low perfusion pressure distal to the stenosis affects the clearence of microembolus (7). Maybe we can talk about decreasing of cerebral clearance of contrast agent with a similar mechanism.…”

“…Further, ischemic lesions and hyperperfusion syndrome are well-known complications of CAS, and new cerebral microembolic lesions detected via diffusionweighted imaging (DWI) are observed in almost all patients after CAS (7,8). Fluid-attenuated inversion recovery (FLAIR) is very sensitive in detecting leptomeningeal hyperintensity (9), which has been noted to disappear after the symptoms resolve.…”

Mechanism of Ischemic Infarct in Spontaneous Cervical Artery Dissection

“…59 As recently suggested, border-zone infarcts might result from mixed mechanisms by impaired clearance of emboli in hypoperfused regions. 60 Indeed, during the constitution of the mural hematoma, only the embolic mechanism may explain the occurrence of an infarction, whereas the hemodynamic mechanism may appear progressively with the narrowing of the lumen due to the growth of the mural hematoma. Once the lumen is severely stenosed, hemodynamic impairment may encourage the formation of secondary clots in border-zone regions, impede the clearance of distal clots, and increase the impact on cerebral tissues.…”