title: Platelet hyperaggregability persists even after the improvement of increased blood coagulation and impaired fibrinolysis with the stabilization of symptoms in patients with unstable angina.
abstract: BACKGROUND
  Platelet aggregation, blood coagulation, and fibrinolysis play a pivotal role in the pathogenesis of unstable angina.
  
  
  METHODS
  Platelet aggregability was examined on admission and after 2 weeks of treatment in 22 patients with unstable angina, in particular with regard to small-sized platelet aggregates, plasma tissue factor (TF) antigen levels as a marker of blood coagulation, and plasma plasminogen activator inhibitor (PAI) activity levels as an indicator of fibrinolysis. We also examined the same parameters in 19 patients with stable exertional angina and 17 patients with chest pain syndrome.
  
  
  RESULTS
  The number of small-sized platelet aggregates increased more significantly in the unstable angina group than in the stable exertional angina and chest pain syndrome groups. In the unstable angina group, the number of small-sized platelet aggregates decreased significantly after 2 weeks of treatment, but was still higher than that in the stable exertional angina and chest pain syndrome groups. Plasma TF antigen and PAI activity were higher in the unstable angina group than in the stable exertional angina and chest pain syndrome groups. TF and PAI activity decreased to normal ranges after 2 weeks of treatment in the unstable angina group. There were significant positive correlations among the three parameters on admission.
  
  
  CONCLUSIONS
  It was demonstrated that small-sized platelet aggregates, plasma TF antigen and PAI activity levels increased concomitantly in the unstable angina group. While the blood coagulation and fibrinolytic parameters decreased after stabilization of the clinical symptoms, platelet hyperaggregability still persisted. These results suggest that continuous antiplatelet therapy is essential for the treatment of unstable angina.
authors.affiliation: Department of Cardiovascular Medicine, Kumamoto University School of Medicine, 1-1-1 Honjo, Kumamoto City 860-8556,, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Miyamoto
authors.forename: H
authors.initials: H
authors.lastname: Ogawa
authors.forename: T
authors.initials: T
authors.lastname: Sakamoto
authors.forename: H
authors.initials: H
authors.lastname: Soejima
authors.forename: K
authors.initials: K
authors.lastname: Takazoe
authors.forename: H
authors.initials: H
authors.lastname: Shimomura
authors.forename: I
authors.initials: I
authors.lastname: Kajiwara
authors.forename: M
authors.initials: M
authors.lastname: Yoshimura
authors.forename: K
authors.initials: K
authors.lastname: Kugiyama
authors.forename: S
authors.initials: S
authors.lastname: Nakamura
authors.forename: Y
authors.initials: Y
authors.lastname: Ozaki
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000789:Angina, Unstable / Q000097:blood* / Q000188:drug therapy; D015415:Biomarkers / Q000097:blood; D001777:Blood Coagulation / Q000502:physiology*; D003328:Coronary Thrombosis / Q000150:complications*; D005260:Female; D005342:Fibrinolysis / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D015849:Plasminogen Inactivators / Q000097:blood*; D010974:Platelet Aggregation / Q000502:physiology*; D013925:Thromboplastin / Q000276:immunology
chemical_list: D015415:Biomarkers; D015849:Plasminogen Inactivators; D013925:Thromboplastin