title: Lp(a) lipoprotein and plasminogen activity in patients with different etiology of ischemic stroke.
abstract: OBJECTIVE
  Lp(a) lipoprotein plays an important part in atherothrombogenesis and is considered an independent risk factor for coronary heart disease. However, its role in cerebrovascular disease remains unclear, in particular because of the heterogeneous nature of strokes. We investigated whether elevated Lp(a) is more frequent in ischemic stroke related to atherothrombosis than in other etiologies of stroke. Because of the close structural homology between Lp(a) and plasminogen, we also studied the role of plasminogen in different stroke subtypes and whether there is a dependency on Lp(a) plasma levels.
  
  
  METHODS
  Lp(a) levels and plasminogen activity were measured in 253 consecutive patients with acute ischemic stroke and in 63 controls (CS). Subtypes of stroke were established according to the TOAST criteria.
  
  
  RESULTS
  Median Lp(a) levels were found to be higher in the total cerebral infarction group and in patients with large artery atherosclerosis (LAA) when compared with CS (20.9 and 22.0 mg/dl, respectively, vs. 16.0 mg/dl; p < 0.05). In addition, elevated Lp(a) levels >30 mg/dl were more frequent among the LAA subgroup than among CS (39.4 vs. 11.1%; p < 0.001). Mean plasminogen activity was lower in the total cerebral infarction group (110.8 vs. 120.3%; p < 0.001) and in patients with cardioembolic stroke (109.8 vs. 120.3%; p < 0.05) when compared with CS. There was no correlation between Lp(a) levels and plasminogen activity.
  
  
  CONCLUSIONS
  Our results support the hypothesis that elevated Lp(a) is a risk factor for ischemic stroke and especially for strokes caused by LAA. Low plasminogen activity may play a role in the pathogenesis of cerebrovascular disease, especially for the development of cardioembolic stroke.
authors.affiliation: Department of Neurology, Christian-Albrechts University, Kiel, Germany. n.petersen@neurologie.uni-kiel.de
authors.forename: Nils H
authors.initials: NH
authors.lastname: Petersen
authors.forename: Alexander B
authors.initials: AB
authors.lastname: Schmied
authors.forename: Jörn A
authors.initials: JA
authors.lastname: Zeller
authors.forename: Hansjörg
authors.initials: H
authors.lastname: Plendl
authors.forename: Günther
authors.initials: G
authors.lastname: Deuschl
authors.forename: Peter
authors.initials: P
authors.lastname: Zunker
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D050197:Atherosclerosis / Q000150:complications; D002545:Brain Ischemia / Q000097:blood* / Q000209:etiology*; D016022:Case-Control Studies; D005260:Female; D006331:Heart Diseases / Q000150:complications; D006801:Humans; D020766:Intracranial Embolism / Q000150:complications; D017270:Lipoprotein(a) / Q000097:blood*; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D010958:Plasminogen / Q000378:metabolism*; D012307:Risk Factors; D020521:Stroke / Q000097:blood* / Q000209:etiology*
chemical_list: D017270:Lipoprotein(a); D010958:Plasminogen