Arjen Lindenholz

173 MRI Vessel Wall Imaging after Intra-Arterial Treatment for Acute Ischemic Stroke 7 showed that 3T MRI vessel wall imaging can also detect most vessel wall lesions. 17,18 Furthermore, previous 3T MRI studies assessing vessel wall enhancement after treatment with stent-retriever devices have comparable findings. 10-13,24 Second, the observed vessel wall enhancement may be a result of the former occluding thrombus on the arterial vessel wall that causes reactive, inflammatory changes or a local ‘scarring’ of the vessel wall. This is supported by studies that showed an increased level of inflammatory markers after an ischemic stroke. 27,28 A third, more hypothetical explanation for the higher number of ipsilateral foci of contrast enhancement is the presence of pre-existent intracranial atherosclerotic lesions, possibly with active inflammation, in the revascularized segment. 29 However, the absence of a significant difference in enhancement between the ipsi- and contralateral arteries in our non-IAT group suggests that not all of the observed enhancing foci can be explained by pre-existent atherosclerotic lesions. Furthermore, atherosclerotic lesions often have a more eccentric configuration, which is in contrast to the high number of concentric type of enhancing foci seen in our study and might indicate an inflammatory state of the whole vessel wall rather than an eccentric atherosclerotic plaque. 22 It is unknown how long contrast enhancement of the arterial vessel wall persists after IAT in patients with stroke. In our study we used a relatively long time interval between thrombectomy and MR imaging (up to three months) compared with previously published papers (range 1–11 days). 10,11 Our results indicate that vessel wall enhancement persists also in the subacute-to-chronic phase. This study has limitations. First, because local areas of ischemia appear as hypointense parenchymal lesions on the T 1 -weighted vessel wall sequences, we were unable to blind the observers to the side of thrombectomy in the IAT- group or side of infarction in the non-IAT group (left or right). Second, IAT was introduced in our center as standard clinical care during the study inclusion period, after the successful international IAT trials. Therefore, the first 28 patients in the non-IAT group did not have IAT as a treatment option. Retrospectively, 10 of all 35 patients without IAT had a proximal occlusion (ICA, M1 or M2) similar to the IAT patients. In the remaining 25 patients without IAT no acute occlusion and a better overall NIHSS score was recorded in the final reports ( Supplemental table 1 ). This result may have led to a selection bias in the non-IAT group with the inclusion of lesser affected patients that may have biased the true results. Nevertheless, we feel that the comparison of the ipsilateral to contralateral side in the IAT-group is most relevant because in this comparison, all potential individual risk factors are the similar. Third, the number of IAT patients enrolled in this study is relatively low. Including more patients would benefit the statistical power and enable the possibility of additional analyses. Fourth, for most patients without IAT, the time window between symptom onset and 7T MRI was shorter.