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Atheroemboli to the brain: size threshold for causing acute neuronal cell death
1Division of Vascular Surgery and the Departments of Neurology and Radiology, The University of California, San Francisco, CA, USA.
Journal of Vascular Surgery
|July 6, 2000
Summary
Carotid angioplasty can dislodge plaque fragments, but the brain shows tolerance to acute microemboli. However, even small fragments can cause delayed neuronal ischemia, potentially leading to subtle long-term dysfunction.
Area of Science:
- Cerebrovascular disease research
- Interventional cardiology
- Neuropathology
Background:
- Carotid angioplasty is known to dislodge plaque fragments.
- Despite fragment dislodgement, neurologic complications are reported infrequently.
Purpose of the Study:
- To investigate the brain's tolerance to microemboli generated during carotid angioplasty.
- To correlate plaque fragment size and number with potential neurologic consequences.
Main Methods:
- Ex vivo human carotid plaques underwent simulated angioplasty procedures.
- Dislodged plaque fragments were collected, sized (<200 microm and 200-500 microm), and injected into rats.
- Brain tissue was analyzed for neuronal cell death and stress marker expression (HSP-72) at 1, 3, and 7 days.
Main Results:
- Angioplasty manipulations dislodged varying numbers of plaque fragments.
- Rats injected with 200-500 microm fragments showed acute neuronal cell death.
- Both small (<200 microm) and larger fragments induced scattered ischemic neurons by day 7.
Conclusions:
- The brain exhibits significant tolerance to acute microembolization.
- Small plaque fragments, even those less than 200 microm, can cause delayed neuronal ischemia.
- Periprocedural microemboli may contribute to subtle, late-onset neurologic dysfunction.