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Minor stroke due to large artery occlusion. When is intravenous thrombolysis not enough? Results from the SITS International Stroke Thrombolysis Register

MV. Mazya, C. Cooray, KR. Lees, D. Toni, GA. Ford, M. Bar, S. Frol, T. Moreira, L. Sekaran, V. Švigelj, N. Wahlgren, N. Ahmed,

. 2018 ; 3 (1) : 29-38. [pub] 20171129

Jazyk angličtina Země Anglie, Velká Británie

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/bmc19029109

Purpose: Beyond intravenous thrombolysis, evidence is lacking on acute treatment of minor stroke caused by large artery occlusion. To identify candidates for additional endovascular therapy, we aimed to determine the frequency of non-haemorrhagic early neurological deterioration in patients with intravenous thrombolysis-treated minor stroke caused by occlusion of large proximal and distal cerebral arteries. Secondary aims were to establish risk factors for non-haemorrhagic early neurological deterioration and report three-month outcomes in patients with and without non-haemorrhagic early neurological deterioration. Method: We analysed data from the SITS International Stroke Thrombolysis Register on 2553 patients with intravenous thrombolysis-treated minor stroke (NIH Stroke Scale scores 0-5) and available arterial occlusion data. Non-haemorrhagic early neurological deterioration was defined as an increase in NIH Stroke Scale score ≥4 at 24 h, without parenchymal hematoma on follow-up imaging within 22-36 h. Findings: The highest frequency of non-haemorrhagic early neurological deterioration was seen in 30% of patients with terminal internal carotid artery or tandem occlusions (internal carotid artery + middle cerebral artery) (adjusted odds ratio: 10.3 (95% CI 4.3-24.9), p < 0.001) and 17% in extracranial carotid occlusions (adjusted odds ratio 4.3 (2.5-7.7), p < 0.001) versus 3.1% in those with no occlusion. Proximal middle cerebral artery-M1 occlusions had non-haemorrhagic early neurological deterioration in 9% (adjusted odds ratio 2.1 (0.97-4.4), p = 0.06). Among patients with any occlusion and non-haemorrhagic early neurological deterioration, 77% were dead or dependent at three months. Conclusions: Patients with minor stroke caused by internal carotid artery occlusion, with or without tandem middle cerebral artery involvement, are at high risk of disabling deterioration, despite intravenous thrombolysis treatment. Acute vessel imaging contributes usefully even in minor stroke to identify and consider endovascular treatment, or intensive monitoring at a comprehensive stroke centre, for patients at high risk of neurological deterioration.

Citace poskytuje Crossref.org

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$a Mazya, Michael V $u 1Department of Neurology, Karolinska University Hospital, Solna, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
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$a Minor stroke due to large artery occlusion. When is intravenous thrombolysis not enough? Results from the SITS International Stroke Thrombolysis Register / $c MV. Mazya, C. Cooray, KR. Lees, D. Toni, GA. Ford, M. Bar, S. Frol, T. Moreira, L. Sekaran, V. Švigelj, N. Wahlgren, N. Ahmed,
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$a Purpose: Beyond intravenous thrombolysis, evidence is lacking on acute treatment of minor stroke caused by large artery occlusion. To identify candidates for additional endovascular therapy, we aimed to determine the frequency of non-haemorrhagic early neurological deterioration in patients with intravenous thrombolysis-treated minor stroke caused by occlusion of large proximal and distal cerebral arteries. Secondary aims were to establish risk factors for non-haemorrhagic early neurological deterioration and report three-month outcomes in patients with and without non-haemorrhagic early neurological deterioration. Method: We analysed data from the SITS International Stroke Thrombolysis Register on 2553 patients with intravenous thrombolysis-treated minor stroke (NIH Stroke Scale scores 0-5) and available arterial occlusion data. Non-haemorrhagic early neurological deterioration was defined as an increase in NIH Stroke Scale score ≥4 at 24 h, without parenchymal hematoma on follow-up imaging within 22-36 h. Findings: The highest frequency of non-haemorrhagic early neurological deterioration was seen in 30% of patients with terminal internal carotid artery or tandem occlusions (internal carotid artery + middle cerebral artery) (adjusted odds ratio: 10.3 (95% CI 4.3-24.9), p < 0.001) and 17% in extracranial carotid occlusions (adjusted odds ratio 4.3 (2.5-7.7), p < 0.001) versus 3.1% in those with no occlusion. Proximal middle cerebral artery-M1 occlusions had non-haemorrhagic early neurological deterioration in 9% (adjusted odds ratio 2.1 (0.97-4.4), p = 0.06). Among patients with any occlusion and non-haemorrhagic early neurological deterioration, 77% were dead or dependent at three months. Conclusions: Patients with minor stroke caused by internal carotid artery occlusion, with or without tandem middle cerebral artery involvement, are at high risk of disabling deterioration, despite intravenous thrombolysis treatment. Acute vessel imaging contributes usefully even in minor stroke to identify and consider endovascular treatment, or intensive monitoring at a comprehensive stroke centre, for patients at high risk of neurological deterioration.
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$a Cooray, Charith $u 1Department of Neurology, Karolinska University Hospital, Solna, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
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$a Lees, Kennedy R $u 3Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK.
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$a Toni, Danilo $u Department of Neurology and Psychiatry, University of Rome - 'La Sapienza', Rome, Italy.
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$a Ford, Gary A $u Acute Stroke Service, Oxford University Hospitals NHS Foundation Trust, Oxford, UK.
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$a Bar, Michal $u 6Department of Neurology, University Hospital and Faculty of Medicine, University of Ostrava, Ostrava, Czech Republic.
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$a Frol, Senta $u Department of Vascular Neurology and Neurological Intensive Care, University Medical Center Ljubljana, Ljubljana, Slovenia.
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$a Moreira, Tiago $u 1Department of Neurology, Karolinska University Hospital, Solna, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
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$a Sekaran, Lakshmanan $u Luton & Dunstable NHSFT University Hospital, Luton, UK.
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$a Švigelj, Viktor $u Department of Vascular Neurology and Neurological Intensive Care, University Medical Center Ljubljana, Ljubljana, Slovenia.
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$a Wahlgren, Nils $u 1Department of Neurology, Karolinska University Hospital, Solna, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
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$a Ahmed, Niaz $u 1Department of Neurology, Karolinska University Hospital, Solna, Sweden. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
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