Circulating microemboli in 33 patients with intracranial arterial stenosis
Dirk W Droste1, Katja Junker, Tjark Hansberg
1Department of Neurology, University of Münster, Germany.
Insights
Microembolic signals are detected in symptomatic patients with high-grade intracranial arterial stenosis (> or =210 cm/s peak systolic flow velocity). Anticoagulation did not prevent microemboli formation in these high-risk stroke patients.
Area of Science:
- Neurology
- Vascular Medicine
- Diagnostic Ultrasound
Background:
- Intracranial arterial stenosis is an uncommon cause of stroke in Caucasian populations.
- Transcranial Doppler sonography is being explored for detecting silent microemboli in carotid artery disease to stratify stroke risk.
Purpose of the Study:
- To investigate the presence of microembolic signals in patients with intracranial arterial stenosis.
- To correlate microembolic signals with stenosis severity and clinical symptoms.
Main Methods:
- 33 patients with intracranial arterial stenosis underwent 1-hour microembolus detection downstream to the stenosis.
- Stenosis severity was assessed using transcranial Doppler and duplex ultrasound.
- Patients included those with internal carotid, middle cerebral, posterior cerebral, and basilar artery stenosis.
Main Results:
- Microembolic signals (3-25 events/h) were observed in 5 recently symptomatic patients with peak systolic flow velocity > or =210 cm/s.
- These 5 patients showed embolic lesion patterns on CT/MRI.
- No microembolic signals were detected in asymptomatic patients (n=15) or those with velocities between 160 to <210 cm/s (n=13).
Conclusions:
- Microembolic signals are associated with high-grade intracranial arterial stenosis (peak systolic velocity > or =210 cm/s) in symptomatic patients.
- Anticoagulation therapy was insufficient to inhibit microemboli formation in this patient group.
Background:
Intracranial arterial stenosis is a rare cause of stroke in Caucasians. Detection of clinically silent circulating microemboli by transcranial Doppler sonography is now widely investigated in patients with carotid artery disease in the hope to identify patients at increased risk for stroke.
Methods:
In 33 patients with intracranial internal carotid (n = 12), middle cerebral (n = 18), posterior cerebral (n = 2), or basilar artery stenosis (n = 1), we performed a 1-hour microembolus detection downstream to the stenosis in the middle or in the posterior cerebral artery, respectively. The stenosis was assessed by transcranial Doppler and duplex ultrasound. 18 patients had been symptomatic in the dependent territory.
Results:
Five patients with ischaemic symptoms within the last 8 days and with a peak systolic flow velocity of > or =210 cm/s in the stenosis showed microembolic signals at a rate of 3-25 events/h, despite effective anticoagulation. All these 5 patients had a lesion pattern on cranial CT or MRI scan suggesting embolic origin. All the asymptomatic patients (n = 15) and all the patients with a peak systolic intrastenostic velocity of 160 to <210 cm/s (n = 13) did not show microembolic signals at all.
Conclusion:
Microembolic signals occur in recently symptomatic patients with high-grade intracranial arterial stenosis indicated by a sonographically measured stenotic peak flow velocity of > or =210 cm/s. Therapeutic anticoagulation was not sufficient to suppress microemboli formation.
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