Microemboli at the Different Stages of Percutaneous Transluminal Carotid Angioplasty and Stenting in Patients with Post–carotid Endarterectomy Restenosis Compared to Primary Stenosis

Microembolization to cerebral arteries during percutaneous transluminal carotid angioplasty (PTCA) and stenting is well described, as well as different mural pathology in primary versus post–carotid endarterectomy (CEA) restenosis lesions. The purpose of this study is to investigate possible different patterns of embolization in regards to number and distribution of microembolic signals (high-intensity transient signals (HITS)) in patients with primary carotid stenosis and restenosis after CEA. We used transcranial Doppler (TCD) to monitor the ipsilateral middle cerebral artery (MCA) of 13 patients (13 procedures) with restenosis after CEA and six patients (seven procedures) with primary stenosis of the internal carotid artery (ICA) during PTCA and stenting. All the procedures were performed without protection devices. The total number of HITS recorded in all patients was 2692, including 1563 microemboli in patients with restenosis and 1129 in patients with primary stenosis. The mean number of microemboli per procedure was 120.2 ± 65 and 161.3 ± 70 (p = 0.05) respectively. The average number of microembolic signals during the various stages of PTCA and stenting in the two groups was as follows: 1. Crossing the stenotic region with the guidewire and positioning the balloon inside the stenosis 33 ± 6.9 and 73.4 ± 9.4 (restenosis patients versus primary–stenosis patients, respectively, (p = 0.011); 2. angioplasty, balloon inflation and deflation, 19.l ± 6.9 and 38.9 ± 9.4 (restenosis versus primary lesions, respectively, p = 0.09); 3. stent deployment, 39.5 ± 6.9 and 27.3 ± 9.4 (restenosis versus primary lesions, respectively, p = 0.3); and 4. Post-stent dilatation, 29 ± 6.9 and 21.7 ± 9.4 (restenosis versus primary lesions, respectively, p = 0.53). Microembolic signals are detected through all stages of PTCA and stenting in patients with primary or post-CEA-restenosis lesions. The number of HITS was significantly higher in patients with primary stenosis than with restenosis of ICA in stages prior to stenting. This probably stems from the difference in pathomorphologic structure between the lesions. There was no significant difference between groups during stent deployment and post-stent dilatation. The clinical significance of the phenomenon of microembolism during carotid stenting is still not clear, but our results suggest the importance of using protection devices to reduce the incidence of these events in both primary and post-CEA lesions.