Anna Kopczak1, Andreas Schindler2, Anna Bayer-Karpinska3, Mia L Koch4, Dominik Sepp5, Julia Zeller6, Christoph Strecker7, Johann-Martin Hempel8, Chun Yuan9, Rainer Malik1, Frank A Wollenweber10, Tobias Boeckh-Behrens5, Clemens C Cyran11, Andreas Helck12, Andreas Harloff7, Ulf Ziemann6, Sven Poli6, Holger Poppert13, Martin Dichgans14, Tobias Saam15. 1. Institute for Stroke and Dementia Research, University Hospital, LMU Munich, Munich, Germany. 2. Department of Radiology, University Hospital, LMU Munich, Munich, Germany; Department of Radiology, Trauma Center Murnau, Murnau, Germany. 3. Institute for Stroke and Dementia Research, University Hospital, LMU Munich, Munich, Germany; Klinikum Fürstenfeldbruck, Neurology, Fürstenfeldbruck, Germany. 4. Department of Neurology, Klinikum rechts der Isar, Technical University of Munich (TUM), Munich, Germany. 5. Department of Neuroradiology, Klinikum rechts der Isar, Technical University of Munich (TUM), Munich, Germany. 6. Department of Neurology and Stroke, and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany. 7. Department of Neurology and Neurophysiology, Medical Center-University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany. 8. Department of Diagnostic and Interventional Neuroradiology, University of Tübingen, Tübingen, Germany. 9. Department of Radiology, University of Washington, Seattle, Washington. 10. Institute for Stroke and Dementia Research, University Hospital, LMU Munich, Munich, Germany; Department of Neurology, Helios Dr Horst-Schmidt-Kliniken, Wiesbaden, Germany. 11. Department of Radiology, University Hospital, LMU Munich, Munich, Germany. 12. Department of Radiology, University Hospital, LMU Munich, Munich, Germany; Radiology and Neuroradiology Zurich, Hirslanden/Klinik im Park, Zurich, Switzerland. 13. Department of Neurology, Klinikum rechts der Isar, Technical University of Munich (TUM), Munich, Germany; Department of Neurology, Helios Klinikum München West, Munich, Germany. 14. Institute for Stroke and Dementia Research, University Hospital, LMU Munich, Munich, Germany; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany; German Center for Neurodegenerative Diseases (DZNE), Munich, Germany. Electronic address: martin.dichgans@med.uni-muenchen.de. 15. Department of Radiology, University Hospital, LMU Munich, Munich, Germany; Radiologisches Zentrum Rosenheim, Rosenheim, Germany.
Abstract
BACKGROUND: The underlying etiology of ischemic stroke remains unknown in up to 30% of patients. OBJECTIVES: This study explored the causal role of complicated (American Heart Association-lesion type VI) nonstenosing carotid artery plaques (CAPs) in cryptogenic stroke (CS). METHODS: CAPIAS (Carotid Plaque Imaging in Acute Stroke) is an observational multicenter study that prospectively recruited patients aged older than 49 years with acute ischemic stroke that was restricted to the territory of a single carotid artery on brain magnetic resonance imaging (MRI) and unilateral or bilateral CAP (≥2 mm, NASCET [North American Symptomatic Carotid Endarterectomy Trial] <70%). CAP characteristics were determined qualitatively and quantitatively by high-resolution, contrast-enhanced carotid MRI at 3T using dedicated surface coils. The pre-specified study hypotheses were that that the prevalence of complicated CAP would be higher ipsilateral to the infarct than contralateral to the infarct in CS and higher in CS compared with patients with cardioembolic or small vessel stroke (CES/SVS) as a combined reference group. Patients with large artery stroke (LAS) and NASCET 50% to 69% stenosis served as an additional comparison group. RESULTS: Among 234 recruited patients, 196 had either CS (n = 104), CES/SVS (n = 79), or LAS (n = 19) and complete carotid MRI data. The prevalence of complicated CAP in patients with CS was significantly higher ipsilateral (31%) to the infarct compared with contralateral to the infarct (12%; p = 0.0005). Moreover, the prevalence of ipsilateral complicated CAP was significantly higher in CS (31%) compared with CES/SVS (15%; p = 0.02) and lower in CS compared with LAS (68%; p = 0.003). Lipid-rich and/or necrotic cores in ipsilateral CAP were significantly larger in CS compared with CES/SVS (p < 0.05). CONCLUSIONS: These findings substantiate the role of complicated nonstenosing CAP as an under-recognized cause of stroke. (Carotid Plaque Imaging in Acute Stroke [CAPIAS]; NCT01284933).
BACKGROUND: The underlying etiology of ischemic stroke remains unknown in up to 30% of patients. OBJECTIVES: This study explored the causal role of complicated (American Heart Association-lesion type VI) nonstenosing carotid artery plaques (CAPs) in cryptogenic stroke (CS). METHODS: CAPIAS (Carotid Plaque Imaging in Acute Stroke) is an observational multicenter study that prospectively recruited patients aged older than 49 years with acute ischemic stroke that was restricted to the territory of a single carotid artery on brain magnetic resonance imaging (MRI) and unilateral or bilateral CAP (≥2 mm, NASCET [North American Symptomatic Carotid Endarterectomy Trial] <70%). CAP characteristics were determined qualitatively and quantitatively by high-resolution, contrast-enhanced carotid MRI at 3T using dedicated surface coils. The pre-specified study hypotheses were that that the prevalence of complicated CAP would be higher ipsilateral to the infarct than contralateral to the infarct in CS and higher in CS compared with patients with cardioembolic or small vessel stroke (CES/SVS) as a combined reference group. Patients with large artery stroke (LAS) and NASCET 50% to 69% stenosis served as an additional comparison group. RESULTS: Among 234 recruited patients, 196 had either CS (n = 104), CES/SVS (n = 79), or LAS (n = 19) and complete carotid MRI data. The prevalence of complicated CAP in patients with CS was significantly higher ipsilateral (31%) to the infarct compared with contralateral to the infarct (12%; p = 0.0005). Moreover, the prevalence of ipsilateral complicated CAP was significantly higher in CS (31%) compared with CES/SVS (15%; p = 0.02) and lower in CS compared with LAS (68%; p = 0.003). Lipid-rich and/or necrotic cores in ipsilateral CAP were significantly larger in CS compared with CES/SVS (p < 0.05). CONCLUSIONS: These findings substantiate the role of complicated nonstenosing CAP as an under-recognized cause of stroke. (Carotid Plaque Imaging in Acute Stroke [CAPIAS]; NCT01284933).
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