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To the Editor:
I read with interest the recent paper by Hakan Posacioglu and colleagues, “Carotid Endarterectomy versus Carotid Artery Stenting: Findings in Regard to Neuroclinical Outcomes and Diffusion-Weighted Imaging,”1 in the Texas Heart Institute Journal. The authors' thorough review of carotid endarterectomy versus carotid stenosis contains some inconsistencies and definitions that require clarification. For example, their abstract states that the difference in stroke rate between carotid artery endarterectomy (CAE) and carotid artery stenting was reportedly “due chiefly to nonischemic lesions such as hemorrhage and watershed ischemia.” In my view, watershed ischemia is ischemia. Perhaps the authors intended to say that watershed ischemia is not embolic infarction, but rather is ischemia of hemodynamic origin. Embolism to distal branches and hemodynamic ischemia are both significant sequelae of surgery.
Another confusing comment differentiates ischemic infarction from embolic infarction. Ischemic infarctions are frequently of embolic origin, and embolic infarctions are ischemic by definition. It is possible that the 4 hemorrhagic “lesions” noted post-CAE were hemorrhagic infarctions with complete recovery and without clinical symptoms.
A 3rd issue is whether cognitive dysfunction might be present in patients who have abnormal MRI scans. The authors cite a reference titled “Neuropsychological dysfunction in the absence of structural evidence for cerebral ischemia after uncomplicated carotid endartectomy.”2 Consequently, the authors' statement that there is “no correlation between DW MRI [diffusion-weighted magnetic resonance imaging] findings and neurocognitive dysfunction of CAE” is misleading. The main question is whether cognitive dysfunction occurs when there is structural disease documented by MRI, which describes the status of many of the cases reviewed in this paper.
I believe that, had a neurologist been a co-author of this paper, these points would have been appropriately addressed.