MRI characteristics in acute ischemic stroke patients with preceding direct oral anticoagulant therapy as compared to vitamin K antagonists.
Administration, Oral
Aged
Aged, 80 and over
Anticoagulants
/ therapeutic use
Brain Ischemia
/ diagnostic imaging
Cohort Studies
Female
Fibrinolytic Agents
/ therapeutic use
Humans
Intracranial Hemorrhages
/ epidemiology
Magnetic Resonance Imaging
Male
Prospective Studies
Stroke
/ diagnostic imaging
Vitamin K
/ antagonists & inhibitors
Acute ischemic stroke
Anticoagulation
DOAC
Hemorrhagic transformation
Infarction size
Large vessel occlusion
VKA
Journal
BMC neurology
ISSN: 1471-2377
Titre abrégé: BMC Neurol
Pays: England
ID NLM: 100968555
Informations de publication
Date de publication:
11 Mar 2020
11 Mar 2020
Historique:
received:
04
12
2019
accepted:
06
03
2020
entrez:
13
3
2020
pubmed:
13
3
2020
medline:
14
7
2020
Statut:
epublish
Résumé
Despite the utility of neuroimaging in the diagnostic and therapeutic management of patients with acute ischemic stroke (AIS), imaging characteristics in patients with preceding direct oral anticoagulants (DOAC) compared to vitamin K antagonists (VKA) have hardly been described. We aimed to determine presence of large vessel occlusion (LVO), thrombus length, infarction diameter, and occurrence of hemorrhagic transformation in AIS patients with preceding DOAC as compared to VKA therapy. Using a prospectively collected cohort of AIS patients, we performed univariate and multivariable regression analyses regarding imaging outcomes. Additionally, we provide a sensitivity analysis for the subgroup of patients with confirmed therapeutic anticoagulation. We included AIS in patients with preceding DOAC (N = 75) and VKA (N = 61) therapy, median age 79 (IQR 70-83), 39% female. Presence of any LVO between DOAC and VKA patients (29.3% versus 37.7%, P = 0.361), and target LVO for endovascular therapy (26.7% versus 27.9%, P = 1.0) was equal with a similar occlusion pattern. DOAC as compared to VKA were associated with a similar rate of target LVO for EVT (aOR 0.835, 95% CI 0.368-1.898). The presence of multiple lesions and characteristics of the thrombus were similar in DOAC and VKA patients. Acute ischemic lesion diameter in real world patients was equal in patients taking DOAC as compared to VKA. Lesion diameter in VKA patients (median 13 mm, IQR 6-26 versus median 20 mm, IQR 7-36, P = 0.001), but not DOAC patients was smaller in the setting of confirmed therapeutic VKA. The frequency of radiological hemorrhagic transformation and symptomatic intracranial hemorrhage in OAC patients was low. Sensitivity analysis considering only patients with confirmed therapeutic anticoagulation did not change any of the results. Preceding DOAC treatment showed equal rates of LVO and infarct size as compared to VKA in AIS patients. This study adds to the knowledge of imaging findings in AIS patients with preceding anticoagulation.
Sections du résumé
BACKGROUND
BACKGROUND
Despite the utility of neuroimaging in the diagnostic and therapeutic management of patients with acute ischemic stroke (AIS), imaging characteristics in patients with preceding direct oral anticoagulants (DOAC) compared to vitamin K antagonists (VKA) have hardly been described. We aimed to determine presence of large vessel occlusion (LVO), thrombus length, infarction diameter, and occurrence of hemorrhagic transformation in AIS patients with preceding DOAC as compared to VKA therapy.
METHODS
METHODS
Using a prospectively collected cohort of AIS patients, we performed univariate and multivariable regression analyses regarding imaging outcomes. Additionally, we provide a sensitivity analysis for the subgroup of patients with confirmed therapeutic anticoagulation.
RESULTS
RESULTS
We included AIS in patients with preceding DOAC (N = 75) and VKA (N = 61) therapy, median age 79 (IQR 70-83), 39% female. Presence of any LVO between DOAC and VKA patients (29.3% versus 37.7%, P = 0.361), and target LVO for endovascular therapy (26.7% versus 27.9%, P = 1.0) was equal with a similar occlusion pattern. DOAC as compared to VKA were associated with a similar rate of target LVO for EVT (aOR 0.835, 95% CI 0.368-1.898). The presence of multiple lesions and characteristics of the thrombus were similar in DOAC and VKA patients. Acute ischemic lesion diameter in real world patients was equal in patients taking DOAC as compared to VKA. Lesion diameter in VKA patients (median 13 mm, IQR 6-26 versus median 20 mm, IQR 7-36, P = 0.001), but not DOAC patients was smaller in the setting of confirmed therapeutic VKA. The frequency of radiological hemorrhagic transformation and symptomatic intracranial hemorrhage in OAC patients was low. Sensitivity analysis considering only patients with confirmed therapeutic anticoagulation did not change any of the results.
CONCLUSION
CONCLUSIONS
Preceding DOAC treatment showed equal rates of LVO and infarct size as compared to VKA in AIS patients. This study adds to the knowledge of imaging findings in AIS patients with preceding anticoagulation.
Identifiants
pubmed: 32160909
doi: 10.1186/s12883-020-01678-4
pii: 10.1186/s12883-020-01678-4
pmc: PMC7065352
doi:
Substances chimiques
Anticoagulants
0
Fibrinolytic Agents
0
Vitamin K
12001-79-5
Types de publication
Comparative Study
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
86Références
Eur J Neurol. 2018 May;25(5):747-e52
pubmed: 29360254
N Engl J Med. 2003 Sep 11;349(11):1019-26
pubmed: 12968085
Stroke. 2015 Oct;46(10):2981-6
pubmed: 26330447
J Stroke. 2018 Sep;20(3):321-331
pubmed: 30309227
J Clin Neurosci. 2019 Jun;64:127-133
pubmed: 30929960
Eur Heart J. 2016 Oct 7;37(38):2893-2962
pubmed: 27567408
Lancet Neurol. 2009 Feb;8(2):165-74
pubmed: 19161908
Clin Ther. 2017 Jul;39(7):1456-1478.e36
pubmed: 28668628
J Stroke Cerebrovasc Dis. 2018 Feb;27(2):338-345
pubmed: 29033229
Vasc Health Risk Manag. 2017 Dec 13;13:457-467
pubmed: 29263674
Ann Neurol. 2008 Nov;64(5):499-506
pubmed: 18661516
J Neurol. 2019 Sep;266(9):2263-2272
pubmed: 31165232
J Am Heart Assoc. 2018 Sep 4;7(17):e009507
pubmed: 30371159
J Thromb Haemost. 2018 Feb;16(2):209-219
pubmed: 29193737
Lancet. 2014 Mar 15;383(9921):955-62
pubmed: 24315724
Stroke. 2001 Jun;32(6):1318-22
pubmed: 11387493
Neurosurg Focus. 2014 Jan;36(1):E3
pubmed: 24380480
Stroke. 2015 Jun;46(6):1453-61
pubmed: 25944319
Ann Neurol. 2018 Mar;83(3):451-459
pubmed: 29394504
Stroke. 2019 Apr;50(4):873-879
pubmed: 30852963
Pathology. 2016 Dec;48(7):712-719
pubmed: 27780603
Eur Neurol. 2014;72(5-6):309-16
pubmed: 25323674