Carotid Plaque on MR Angiography and Acute Ischemic Stroke
What is the association between nonstenosing, carotid artery plaque with intraplaque hemorrhage, and ischemic stroke?
The authors used data from a prospective stroke registry. Ischemic stroke types were classified using a standard scheme. Patients with ischemic stroke attributed to small vessel disease, cardioembolism, and cryptogenic causes in a carotid distribution who had a magnetic resonance imaging (MRI) brain and MR angiography (MRA) neck were included. Patients with stroke due to large-artery atherosclerosis and those with infarcts in multiple vascular distributions were excluded. Standard MR techniques were used to evaluate for intraplaque hemorrhage, defined as intraplaque high-intensity signal on axial images. Intrasubject comparisons regarding the presence of intraplaque hemorrhage were made between the carotid ipsilateral to the infarct and the contralateral carotid.
There were 109 patients included in the analyses. Twenty-two (20.2%) had <50% stenosis and intraplaque hemorrhage in the carotid ipsilateral to the infarction. There were only nine patients who had intraplaque hemorrhage in the carotid contralateral to the infarction (p = 0.01). Ipsilateral intraplaque hemorrhage was more common in patients with cryptogenic stroke (22%) than in patients with stroke attributed to cardioembolic (19%) or small vessel (18%) etiologies. Only in patients with cryptogenic stroke was there a difference in intraplaque hemorrhage rate between the ipsilateral and contralateral sides (22% vs. 0%; p = 0.0009).
Intraplaque hemorrhage may be a stroke etiology in patients with cryptogenic stroke and <50% carotid stenosis.
About one third of all ischemic strokes are classified as cryptogenic, where no clear etiology can be identified. Patients with <50% carotid stenosis ipsilateral to an infarct are considered cryptogenic (assuming no other cause can be identified). This study suggests that intraplaque hemorrhage in nonocclusive carotid atherosclerotic disease may be a risk factor for ischemic stroke. If this finding is confirmed in additional studies, it will allow better determination of stroke subtype and potentially more effective secondary prevention. This work is currently not a full manuscript, so caution is warranted in interpreting the results. It is unclear how many patients were screened to reach the 109 included in the study. The differences in intraplaque hemorrhage rates between the various subtypes are small and may be due to chance. Additionally, there are currently no evidence-based therapies for stroke due to large artery atherosclerotic disease with <50% stenosis beyond standard secondary prevention. While the results of this work could reduce the need for additional diagnostic testing, they may not lead to a change in management.
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