title: Effect of intravenous nimodipine on blood pressure and outcome after acute stroke.
abstract: OBJECTIVE
  The Intravenous Nimodipine West European Stroke Trial (INWEST) found a correlation between nimodipine-induced reduction in blood pressure (BP) and an unfavorable outcome in acute stroke. We sought to confirm this correlation with and without adjustment for prognostic variables and to investigate outcome in subgroups with increasing levels of BP reduction.
  
  
  METHODS
  Patients with a clinical diagnosis of ischemic stroke (within 24 hours) were consecutively allocated to receive placebo (n=100), 1 mg/h (low-dose) nimodipine (n=101), or 2 mg/h (high-dose) nimodipine (n=94). The correlation between average BP change during the first 2 days and the outcome at day 21 was analyzed.
  
  
  RESULTS
  Two hundred sixty-five patients were included in this analysis (n=92, 93, and 80 for placebo, low dose, and high dose, respectively). Nimodipine treatment resulted in a statistically significant reduction in systolic BP (SBP) and diastolic BP (DBP) from baseline compared with placebo during the first few days. In multivariate analysis, a significant correlation between DBP reduction and worsening of the neurological score was found for the high-dose group (beta=0.49, P=0. 048). Patients with a DBP reduction of > or =20% in the high-dose group had a significantly increased adjusted OR for the compound outcome variable death or dependency (Barthel Index <60) (n/N=25/26, OR 10. 16, 95% CI 1.02 to 101.74) and death alone (n/N=9/26, OR 4.336, 95% CI 1.131 16.619) compared with all placebo patients (n/N=62/92 and 14/92, respectively). There was no correlation between SBP change and outcome.
  
  
  CONCLUSIONS
  DBP, but not SBP, reduction was associated with neurological worsening after the intravenous administration of high-dose nimodipine after acute stroke. For low-dose nimodipine, the results were not conclusive. These results do not confirm or exclude a neuroprotective property of nimodipine.
authors.affiliation: Karolinska Hospital, Stroke Research Unit, Department of Neurology, Stockholm, Sweden. niaz.ahmed@neuro.ks.se
authors.forename: N
authors.initials: N
authors.lastname: Ahmed
authors.forename: P
authors.initials: P
authors.lastname: Näsman
authors.forename: N G
authors.initials: NG
authors.lastname: Wahlgren
mesh_terms: D000208:Acute Disease; D000284:Administration, Oral; D001794:Blood Pressure / Q000187:drug effects*; D001925:Brain Damage, Chronic / Q000209:etiology / Q000517:prevention & control; D002545:Brain Ischemia / Q000150:complications / Q000188:drug therapy* / Q000401:mortality; D002121:Calcium Channel Blockers / Q000008:administration & dosage / Q000009:adverse effects / Q000627:therapeutic use*; D002560:Cerebrovascular Circulation / Q000187:drug effects; D003971:Diastole / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D005260:Female; D006801:Humans; D007022:Hypotension / Q000139:chemically induced / Q000150:complications; D007275:Injections, Intravenous; D008297:Male; D008875:Middle Aged; D018696:Neuroprotective Agents / Q000008:administration & dosage / Q000009:adverse effects / Q000627:therapeutic use*; D009553:Nimodipine / Q000008:administration & dosage / Q000009:adverse effects / Q000627:therapeutic use*; D012720:Severity of Illness Index; D016019:Survival Analysis; D013599:Systole / Q000187:drug effects; D016896:Treatment Outcome
chemical_list: D002121:Calcium Channel Blockers; D018696:Neuroprotective Agents; D009553:Nimodipine