Factors associated with therapeutic anticoagulation status in patients with ischemic stroke and atrial fibrillation.
Aged
Aged, 80 and over
Anticoagulants
/ administration & dosage
Atrial Fibrillation
/ diagnosis
Blood Coagulation
/ drug effects
Brain Ischemia
/ diagnosis
Drug Monitoring
Female
Humans
International Normalized Ratio
Intracranial Arteriosclerosis
/ epidemiology
Male
Recurrence
Registries
Retrospective Studies
Risk Assessment
Risk Factors
Stroke
/ diagnosis
Time Factors
Treatment Outcome
United States
/ epidemiology
Warfarin
/ administration & dosage
Anticoagulation
Atrial fibrillation
Predictors
Recurrence
Stroke
Journal
Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association
ISSN: 1532-8511
Titre abrégé: J Stroke Cerebrovasc Dis
Pays: United States
ID NLM: 9111633
Informations de publication
Date de publication:
Jul 2020
Jul 2020
Historique:
received:
02
03
2020
revised:
09
04
2020
accepted:
12
04
2020
pubmed:
18
5
2020
medline:
21
10
2020
entrez:
17
5
2020
Statut:
ppublish
Résumé
Understanding factors associated with ischemic stroke despite therapeutic anticoagulation is an important goal to improve stroke prevention strategies in patients with atrial fibrillation (AF). We aim to determine factors associated with therapeutic or supratherapeutic anticoagulation status at the time of ischemic stroke in patients with AF. The Initiation of Anticoagulation after Cardioembolic stroke (IAC) study is a multicenter study pooling data from stroke registries of eight comprehensive stroke centers across the United States. Consecutive patients hospitalized with acute ischemic stroke in the setting of AF were included in the IAC cohort. For this study, we only included patients who reported taking warfarin at the time of the ischemic stroke. Patients not on anticoagulation and patients who reported use of a direct oral anticoagulant were excluded. Analyses were stratified based on therapeutic (INR ≥2) versus subtherapeutic (INR <2) anticoagulation status. We used binary logistic regression models to determine factors independently associated with anticoagulation status after adjustment for pertinent confounders. In particular, we sought to determine whether atherosclerosis with 50% or more luminal narrowing in an artery supplying the infarct (a marker for a competing atherosclerotic mechanism) and small stroke size (≤ 10 mL; implying a competing small vessel disease mechanism) related to anticoagulant status. Of the 2084 patients enrolled in the IAC study, 382 patients met the inclusion criteria. The mean age was 77.4 ± 10.9 years and 52.4% (200/382) were women. A total of 222 (58.1%) subjects presented with subtherapeutic INR. In adjusted models, small stroke size (OR 1.74 95% CI 1.10-2.76, p = 0.019) and atherosclerosis with 50% or more narrowing in an artery supplying the infarct (OR 1.96 95% CI 1.06-3.63, p = 0.031) were independently associated with INR ≥2 at the time of their index stroke. Small stroke size (≤ 10 ml) and ipsilateral atherosclerosis with 50% or more narrowing may indicate a competing stroke mechanism. There may be important opportunities to improve stroke prevention strategies for patients with AF by targeting additional ischemic stroke mechanisms to improve patient outcomes.
Sections du résumé
BACKGROUND AND PURPOSE
OBJECTIVE
Understanding factors associated with ischemic stroke despite therapeutic anticoagulation is an important goal to improve stroke prevention strategies in patients with atrial fibrillation (AF). We aim to determine factors associated with therapeutic or supratherapeutic anticoagulation status at the time of ischemic stroke in patients with AF.
METHODS
METHODS
The Initiation of Anticoagulation after Cardioembolic stroke (IAC) study is a multicenter study pooling data from stroke registries of eight comprehensive stroke centers across the United States. Consecutive patients hospitalized with acute ischemic stroke in the setting of AF were included in the IAC cohort. For this study, we only included patients who reported taking warfarin at the time of the ischemic stroke. Patients not on anticoagulation and patients who reported use of a direct oral anticoagulant were excluded. Analyses were stratified based on therapeutic (INR ≥2) versus subtherapeutic (INR <2) anticoagulation status. We used binary logistic regression models to determine factors independently associated with anticoagulation status after adjustment for pertinent confounders. In particular, we sought to determine whether atherosclerosis with 50% or more luminal narrowing in an artery supplying the infarct (a marker for a competing atherosclerotic mechanism) and small stroke size (≤ 10 mL; implying a competing small vessel disease mechanism) related to anticoagulant status.
RESULTS
RESULTS
Of the 2084 patients enrolled in the IAC study, 382 patients met the inclusion criteria. The mean age was 77.4 ± 10.9 years and 52.4% (200/382) were women. A total of 222 (58.1%) subjects presented with subtherapeutic INR. In adjusted models, small stroke size (OR 1.74 95% CI 1.10-2.76, p = 0.019) and atherosclerosis with 50% or more narrowing in an artery supplying the infarct (OR 1.96 95% CI 1.06-3.63, p = 0.031) were independently associated with INR ≥2 at the time of their index stroke.
CONCLUSION
CONCLUSIONS
Small stroke size (≤ 10 ml) and ipsilateral atherosclerosis with 50% or more narrowing may indicate a competing stroke mechanism. There may be important opportunities to improve stroke prevention strategies for patients with AF by targeting additional ischemic stroke mechanisms to improve patient outcomes.
Identifiants
pubmed: 32414583
pii: S1052-3057(20)30287-1
doi: 10.1016/j.jstrokecerebrovasdis.2020.104888
pmc: PMC8207529
mid: NIHMS1708365
pii:
doi:
Substances chimiques
Anticoagulants
0
Warfarin
5Q7ZVV76EI
Types de publication
Journal Article
Multicenter Study
Langues
eng
Sous-ensembles de citation
IM
Pagination
104888Subventions
Organisme : NINDS NIH HHS
ID : R44 NS076272
Pays : United States
Organisme : NINDS NIH HHS
ID : K23 NS107643
Pays : United States
Organisme : NINDS NIH HHS
ID : K08 NS091499
Pays : United States
Organisme : NINDS NIH HHS
ID : K23 NS113858
Pays : United States
Organisme : NINDS NIH HHS
ID : K23 NS105924
Pays : United States
Informations de copyright
Copyright © 2020 Elsevier Inc. All rights reserved.
Références
JAMA. 1995 May 10;273(18):1421-8
pubmed: 7723155
Stroke. 2017 Dec;48(12):e343-e361
pubmed: 29097489
J Stroke Cerebrovasc Dis. 2014 Apr;23(4):618-24
pubmed: 23800503
Curr Neurol Neurosci Rep. 2010 Jan;10(1):14-20
pubmed: 20425221
N Engl J Med. 2005 Mar 31;352(13):1305-16
pubmed: 15800226
Ann Neurol. 2008 Nov;64(5):499-506
pubmed: 18661516
BMJ. 2017 Nov 28;359:j5058
pubmed: 29183961
Stroke. 2018 Dec;49(12):2933-2944
pubmed: 30571400
J Stroke Cerebrovasc Dis. 2018 Jan;27(1):192-197
pubmed: 28918087
Cerebrovasc Dis. 2009;27(5):502-8
pubmed: 19342826
Stroke. 2011 Aug;42(8):e464-540
pubmed: 21282493
Ann Intern Med. 2007 Jun 19;146(12):857-67
pubmed: 17577005
Lancet. 1994 Mar 19;343(8899):687-91
pubmed: 7907677
N Engl J Med. 2011 Mar 3;364(9):806-17
pubmed: 21309657
Stroke. 2014 Jul;45(7):2160-236
pubmed: 24788967
N Engl J Med. 1998 Nov 12;339(20):1415-25
pubmed: 9811916
Eur J Echocardiogr. 2006 Mar;7(2):79-108
pubmed: 16458610
Stroke. 2007 Nov;38(11):2979-84
pubmed: 17901381
Neurology. 2009 Jun 16;72(24):2104-10
pubmed: 19528517
Stroke. 2014 May;45(5):1248-57
pubmed: 24699050
JAMA Neurol. 2016 Apr;73(4):396-401
pubmed: 26926383
Lancet. 2013 Aug 10;382(9891):507-15
pubmed: 23726159
Eur Heart J. 2014 Jun 7;35(22):1457-65
pubmed: 24302269
JAMA Neurol. 2014 Sep;71(9):1181-5
pubmed: 25069522
N Engl J Med. 2001 Nov 15;345(20):1444-51
pubmed: 11794192
Neurology. 2017 Jan 24;88(4):379-385
pubmed: 28003500
Stroke. 1993 Jan;24(1):35-41
pubmed: 7678184
Neurology. 1978 Oct;28(10):973-7
pubmed: 570666