Severity of leukoaraiosis, leptomeningeal collaterals, and clinical outcomes after intra-arterial therapy in patients with acute ischemic stroke.
OBJECTIVE
Leukoaraiosis (LA) is defined as ischemic white matter lesions associated with increased stroke risk and poor post-stroke outcomes. These lesions are likely the result of diffuse angiopathic changes affecting the cerebral small vessels. We investigated whether pre-existing LA burden is associated with outcomes in patients with large cerebral artery occlusion undergoing intra-arterial therapy (IAT) for acute ischemic stroke (AIS).


METHODS
We analyzed consecutive AIS subjects undergoing IAT from the institutional Get With The Guidelines-Stroke database enrolled between January 1, 2007 and June 30, 2009, who had National Institutes of Health Stroke Scale scores of ≥ 8, baseline diffusion weighted imaging volume ≤ 100 mL, and evidence of proximal artery occlusion (PAO) on pre-IAT computed tomography angiography (CTA). LA volume (LAv) was assessed on fluid attenuated inversion recovery MRI using a validated semi-automated protocol. We used CTA for collateral grade, post-IAT angiogram for recanalization status (Thrombolysis in Cerebral Infarction score ≥ 2b), and the 24 h head CT for symptomatic intracranial hemorrhage. Logistic regression was used to determine independent predictors of 90 day post-stroke good functional outcome (modified Rankin Scale score ≤ 2) and mortality.


RESULTS
Increasing LAv independently reduced the odds of good collateral grade (OR 0.85, 95% CI 0.73 to 0.98). Good functional outcome was independently predicted by intravenous tissue plasminogen activator use (OR 12.86, 95% CI 2.20 to 76.28), and recanalization status (OR 6.94, 95% CI 1.56 to 30.86). Mortality was independently associated with recanalization status (OR 0.08, 95% CI 0.01 to 0.51), age (OR 1.08, 95% CI 1.01 to 1.15), and antecedent use of hypoglycemic agents (OR 6.55, 95% CI 1.58 to 54.01).


CONCLUSIONS
Severity of LA is linked to poor collateral grade in AIS patients undergoing IAT for PAO; however, greater LAv appears not to be a contraindication for acute intervention.
Stroke Service, Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA Stroke Institute, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA.
Dan-Victor
http://orcid.org/0000-0002-8065-6821
DV
Giurgiutiu
Neuroendovascular Service, Massachusetts General Hospital, Boston, Massachusetts, USA.
Albert J
AJ
Yoo
Stroke Service, Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA.
Kaitlin
K
Fitzpatrick
Neuroendovascular Service, Massachusetts General Hospital, Boston, Massachusetts, USA.
Zeshan
Z
Chaudhry
Stroke Service, Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA Neuroendovascular Service, Massachusetts General Hospital, Boston, Massachusetts, USA.
Thabele
T
Leslie-Mazwi
Stroke Service, Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA.
Lee H
LH
Schwamm
Stroke Service, Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA.
Natalia S
NS
Rost
D000368:Aged; D000369:Aged, 80 and over; D002545:Brain Ischemia / Q000188:drug therapy; D002560:Cerebrovascular Circulation / Q000502:physiology*; D005260:Female; D005343:Fibrinolytic Agents / Q000008:administration & dosage / Q000494:pharmacology*; D006801:Humans; D007261:Infusions, Intra-Arterial; D049292:Leukoaraiosis / Q000473:pathology*; D008297:Male; D008578:Meninges / Q000098:blood supply*; D008875:Middle Aged; D017063:Outcome Assessment, Health Care; D012720:Severity of Illness Index; D020521:Stroke / Q000188:drug therapy*; D010959:Tissue Plasminogen Activator / Q000008:administration & dosage / Q000494:pharmacology*
D005343:Fibrinolytic Agents; D010959:Tissue Plasminogen Activator