BACKGROUND AND PURPOSE: The main purpose of carotid endarterectomy (CEA) for neurologically symptomatic high-grade extracranial carotid artery stenosis is to remove the suspected source of cerebral microemboli. Transcranial Doppler (TCD) ultrasonography has the potential for detecting solid microemboli in the basal cerebral arteries. Therefore, TCD monitoring provides the opportunity to assess the rate of microemboli to the brain in patients with symptomatic high-grade carotid artery stenosis and to verify whether these phenomena have ceased after CEA. METHODS: TCD monitoring was performed in 41 patients to detect high-intensity transient signals indicating microemboli in the middle cerebral artery before and after CEA. In the event that, within 1 week after CEA, TCD monitoring revealed ongoing cerebral microemboli on the side of surgery, the examination was repeated 3 months later. RESULTS: High-intensity transient signals were detected preoperatively on the side of the affected carotid artery in 22 patients (54%; mean, 10.2 per hour; range, 1 to 88). Linear regression analysis demonstrated a trend toward an inverse relationship between the number of high-intensity transient signals per hour and the time interval since the last episode of neurological symptoms (P < .1). CEA resulted in a significant reduction in the number of high-intensity transient signals per hour 7 days after surgery (mean, 6.0 versus 0.4 per hour; median, 0 versus 0; n = 37; P < .005) and 3 months later (mean, 6.3 versus 0 per hour; median, 1.3 versus 0; n = 41; P < .0001). CONCLUSIONS: Clearly, TCD monitoring can be helpful in assessing the effect of CEA in removing the suspected source of cerebral microemboli. Ongoing microemboli to the brain should prompt reassessment of the operated carotid artery or a search for other potential sources of cerebral embolism. Carotid artery plaques seem to produce cerebral microemboli for a limited period, which implies that the prophylactic effect of CEA might decrease if the operation is delayed.
BACKGROUND AND PURPOSE: The main purpose of carotid endarterectomy (CEA) for neurologically symptomatic high-grade extracranial carotid artery stenosis is to remove the suspected source of cerebral microemboli. Transcranial Doppler (TCD) ultrasonography has the potential for detecting solid microemboli in the basal cerebral arteries. Therefore, TCD monitoring provides the opportunity to assess the rate of microemboli to the brain in patients with symptomatic high-grade carotid artery stenosis and to verify whether these phenomena have ceased after CEA. METHODS:TCD monitoring was performed in 41 patients to detect high-intensity transient signals indicating microemboli in the middle cerebral artery before and after CEA. In the event that, within 1 week after CEA, TCD monitoring revealed ongoing cerebral microemboli on the side of surgery, the examination was repeated 3 months later. RESULTS: High-intensity transient signals were detected preoperatively on the side of the affected carotid artery in 22 patients (54%; mean, 10.2 per hour; range, 1 to 88). Linear regression analysis demonstrated a trend toward an inverse relationship between the number of high-intensity transient signals per hour and the time interval since the last episode of neurological symptoms (P < .1). CEA resulted in a significant reduction in the number of high-intensity transient signals per hour 7 days after surgery (mean, 6.0 versus 0.4 per hour; median, 0 versus 0; n = 37; P < .005) and 3 months later (mean, 6.3 versus 0 per hour; median, 1.3 versus 0; n = 41; P < .0001). CONCLUSIONS: Clearly, TCD monitoring can be helpful in assessing the effect of CEA in removing the suspected source of cerebral microemboli. Ongoing microemboli to the brain should prompt reassessment of the operated carotid artery or a search for other potential sources of cerebral embolism. Carotid artery plaques seem to produce cerebral microemboli for a limited period, which implies that the prophylactic effect of CEA might decrease if the operation is delayed.
Authors: Martin A Ritter; Ralf Dittrich; Niels Thoenissen; E Bernd Ringelstein; Darius G Nabavi Journal: J Neurol Date: 2008-05-06 Impact factor: 4.849