Hooman Kamel1, Gino Gialdini2, Hediyeh Baradaran3, Ashley E Giambrone4, Babak B Navi5, Michael P Lerario5, James K Min6, Costantino Iadecola5, Ajay Gupta7. 1. Feil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, New York; Department of Neurology, Weill Cornell Medicine, New York, New York. Electronic address: hok9010@med.cornell.edu. 2. Feil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, New York. 3. Department of Radiology, Weill Cornell Medicine, New York, New York. 4. Department of Radiology, Weill Cornell Medicine, New York, New York; Department of Healthcare Policy and Research, Weill Cornell Medicine, New York, New York. 5. Feil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, New York; Department of Neurology, Weill Cornell Medicine, New York, New York. 6. Department of Radiology, Weill Cornell Medicine, New York, New York; Dalio Institute of Cardiovascular Imaging, Weill Cornell Medicine, New York, New York. 7. Feil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, New York; Department of Radiology, Weill Cornell Medicine, New York, New York.
Abstract
OBJECTIVE: Because some cryptogenic strokes may result from large-artery atherosclerosis that goes unrecognized as it causes <50% luminal stenosis, we compared the prevalence of nonstenosing intracranial atherosclerotic plaques ipsilateral to cryptogenic cerebral infarcts versus the unaffected side using imaging biomarkers of calcium burden. METHODS: In a prospective stroke registry, we identified patients with cerebral infarction limited to the territory of one internal carotid artery (ICA). We included patients with stroke of undetermined etiology and, as controls, patients with cardioembolic stroke. We used noncontrast computed tomography to measure calcification in both intracranial ICAs, including qualitative calcium scoring and quantitative scoring utilizing the Agatston-Janowitz (AJ) calcium scoring. Within subjects, the Wilcoxon signed-rank sum test for nonparametric paired data was used to compare the calcium burden in the ICA upstream of the infarction versus the ICA on the unaffected side. RESULTS: We obtained 440 calcium measures from 110 ICAs in 55 patients. Among 34 patients with stroke of undetermined etiology, we found greater calcium in the ICA ipsilateral to the infarction (mean Modified Woodcock Visual Scale score, 6.7 ± 4.6) compared with the contralateral side (5.4 ± 4.1) (P = .005). Among 21 patients with cardioembolic stroke, we found no difference in calcium burden ipsilateral to the infarction (6.7 ± 5.9) versus the contralateral side (7.3 ± 6.3) (P = .13). The results were similar using quantitative calcium measurements, including the AJ calcium scores. CONCLUSION: In patients with strokes of undetermined etiology, the burden of calcified intracranial large-artery plaque was associated with downstream cerebral infarction.
OBJECTIVE: Because some cryptogenic strokes may result from large-artery atherosclerosis that goes unrecognized as it causes <50% luminal stenosis, we compared the prevalence of nonstenosing intracranial atherosclerotic plaques ipsilateral to cryptogenic cerebral infarcts versus the unaffected side using imaging biomarkers of calcium burden. METHODS: In a prospective stroke registry, we identified patients with cerebral infarction limited to the territory of one internal carotid artery (ICA). We included patients with stroke of undetermined etiology and, as controls, patients with cardioembolic stroke. We used noncontrast computed tomography to measure calcification in both intracranial ICAs, including qualitative calcium scoring and quantitative scoring utilizing the Agatston-Janowitz (AJ) calcium scoring. Within subjects, the Wilcoxon signed-rank sum test for nonparametric paired data was used to compare the calcium burden in the ICA upstream of the infarction versus the ICA on the unaffected side. RESULTS: We obtained 440 calcium measures from 110 ICAs in 55 patients. Among 34 patients with stroke of undetermined etiology, we found greater calcium in the ICA ipsilateral to the infarction (mean Modified Woodcock Visual Scale score, 6.7 ± 4.6) compared with the contralateral side (5.4 ± 4.1) (P = .005). Among 21 patients with cardioembolic stroke, we found no difference in calcium burden ipsilateral to the infarction (6.7 ± 5.9) versus the contralateral side (7.3 ± 6.3) (P = .13). The results were similar using quantitative calcium measurements, including the AJ calcium scores. CONCLUSION: In patients with strokes of undetermined etiology, the burden of calcified intracranial large-artery plaque was associated with downstream cerebral infarction.
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