title: Symptomatic intracranial hemorrhage in the ALIAS Multicenter Trial: relationship to endovascular thrombolytic therapy.
abstract: BACKGROUND
  In the ALIAS (Albumin in Acute Stroke) Part 2 Multicenter Trial, 85% of subjects received standard-of-care intravenous tissue plasminogen activator, and 21% received some form of endovascular thrombolysis. The overall rate of symptomatic intracranial hemorrhage was within the expected range but was higher in albumin-treated subjects than in saline-treated subjects.
  
  
  OBJECTIVE
  Using the trial's Public Use Dataset, we analyzed factors contributing to symptomatic and asymptomatic intracranial hemorrhage in the 'safety sample' of 830 subjects.
  
  
  RESULTS
  Four hundred sixteen subjects received albumin therapy, and 414 received saline. Intravenous tissue plasminogen activator was given to 68.2%; intravenous tissue plasminogen activator plus endovascular intervention in 16.4%; and endovascular therapy alone in 43%. Symptomatic intracranial hemorrhage occurred in 41 subjects - within the first 12 h in one-third of cases, and within the first day in ∼60%. Intravenous tissue plasminogen activator had been used in 78% of symptomatic intracranial hemorrhage subjects - no higher than in the overall cohort. In contrast, 48.8% of subjects with symptomatic intracranial hemorrhage had received endovascular therapy - a rate markedly higher than the 20.7% rate for the entire cohort (P = 0.0001). Sixty-eight point three percent of subjects with symptomatic intracranial hemorrhage had received albumin, and 31.7% saline (risk ratio 2.14, P = 0.025). Other factors associated with symptomatic intracranial hemorrhage were baseline NIHSS and ASPECTS scores and the SEDAN score. Forty-one point four percent of subjects with symptomatic intracranial hemorrhage died. The odds ratio for symptomatic intracranial hemorrhage was 3.89 (95% confidence interval 2.04-7.41) with endovascular therapy and 2.15 (confidence interval 1.08-4.25) with albumin.
  
  
  CONCLUSIONS
  Endovascular thrombolysis was the major factor predisposing to symptomatic intracranial hemorrhage, and albumin contributed to this predisposition. The latter may be mediated by albumin's influence on platelet aggregation or collateral perfusion.
authors: Department of Neurology, University of Miami Miller School of Medicine, Miami, FL, USA.
authors: Myron D
authors: MD
authors: Ginsberg
authors: Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta, Canada.
authors: Michael D
authors: MD
authors: Hill
mesh_terms: D061605:Administration, Intravenous; D000368:Aged; D000369:Aged, 80 and over; D000418:Albumins / Q000627:therapeutic use*; D015331:Cohort Studies; D066264:Datasets as Topic; D057510:Endovascular Procedures; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D006801:Humans; D020300:Intracranial Hemorrhages / Q000209:etiology / Q000401:mortality / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D012720:Severity of Illness Index; D020521:Stroke / Q000150:complications / Q000401:mortality / Q000628:therapy; D015912:Thrombolytic Therapy; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use*; D016896:Treatment Outcome
chemical_list: D000418:Albumins; D005343:Fibrinolytic Agents; D010959:Tissue Plasminogen Activator
keywords: albumin; endovascular therapy; intracranial hemorrhage; ischemic stroke; neuroprotection; thrombolysis