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Published on: September 25, 2016
Anticoagulation and microembolus detection in a case of internal carotid artery dissection
Insights
Intravenous heparin reduced microembolic signals (MES) in a patient with internal carotid artery dissection. This suggests anticoagulation may help manage dissection-related embolic events.
Area of Science:
- Neurology
- Vascular Surgery
- Diagnostic Imaging
Background:
- Internal carotid artery dissection can lead to microembolic signals (MES), detected via transcranial Doppler (TCD).
- The impact of treatments on MES in arterial dissection remains unclear.
- This case examines MES changes following heparin initiation in carotid dissection.
Observation:
- A 37-year-old woman presented with headache and ischemic symptoms.
- MRI confirmed a right frontal ischemic infarct; angiography revealed right internal carotid artery dissection.
- Transcranial Doppler (TCD) monitored microembolic signals (MES) before and after treatment.
Findings:
- Initial TCD showed 39 MES per hour in the middle cerebral artery.
- Intravenous heparin reduced MES by 50% within 96 hours.
- No further MES were detected after 11 days of heparin anticoagulation.
Implications:
- Heparin anticoagulation may decrease microembolic signals in internal carotid artery dissection.
- This finding could inform treatment strategies for carotid artery dissection.
- Further research is warranted to confirm the efficacy of anticoagulation in reducing embolic events.
Background:
Microembolic signals (MES) have been demonstrated by transcranial Doppler (TCD) in cases of internal carotid artery dissection. The influence of treatment on MES in arterial dissection is uncertain. The authors here present a case of internal carotid artery dissection in which we detected a reduction of MES after the initiation of intravenous heparin.
Methods:
A 37-year-old woman developed a right temporal headache 10 days prior to admission. This was followed by episodes of left arm numbness and weakness. Magnetic resonance imaging (MRI) showed a right frontal and deep subcortical ischemic infarct. Catheter angiography confirmed a right internal carotid artery dissection with intracranial extension. She was then monitored with TCD for MES before and after intravenous heparin was started.
Results:
The first TCD, performed 12 days after symptom onset, showed 39 MES during 60 minutes of insonation of the right middle cerebral artery. Treatment with intravenous heparin resulted in a decline in MES by 50% after 96 hours. This decline continued and no further MES were detected after 11 days of anticoagulation.
Conclusion:
The authors were able to demonstrate a decline of MES with heparin anticoagulation in a case of internal carotid artery dissection.
