title: Plasma thioredoxin levels and platelet aggregability in patients with acute myocardial infarction.
abstract: BACKGROUND
  Oxidative stress is thought to play an important role in atherosclerotic vascular disease. Recently, it has become possible to quantitatively measure thioredoxin, a marker of oxidative stress in human plasma. A platelet aggregometer that uses laser-light scattering enables minimal changes in platelet aggregability to be monitored; however, the relationship between oxidative stress and platelet aggregability in vivo is not well understood.
  
  
  METHODS
  We investigated plasma thioredoxin levels and platelet aggregability, in particular small platelet aggregates, in 45 patients with acute myocardial infarction (AMI); we compared the results with 33 patients with stable exertional angina (SEA) and 30 patients with chest pain syndrome (CPS).
  
  
  RESULTS
  The plasma thioredoxin levels and the degree of small platelet aggregates were higher in the AMI group than in the SEA and the CPS groups: in the AMI group, at 4 weeks after admission, both of those parameters were significantly decreased (P <.01), but they were still higher (P <.05) than in the SEA or the CPS group. There was a significant positive correlation between small platelet aggregates and plasma thioredoxin levels (rho = 0.354, P =.0002). We divided the AMI patients into 2 groups according to the 75 percentile of plasma thioredoxin levels on admission. At the chronic phase, the left ventricular ejection fraction was significantly higher in the lower thioredoxin group than in the higher thioredoxin group.
  
  
  CONCLUSIONS
  We showed that plasma thioredoxin levels and platelet aggregability increased concomitantly in patients with AMI. In these patients, increased plasma thioredoxin was associated with platelet hyperaggregability and lower left ventricular ejection fraction.
authors.affiliation: Department of Cardiovascular Medicine, Kumamoto University School of Medicine, Kumamoto, Japan.
authors.forename: Shinzo
authors.initials: S
authors.lastname: Miyamoto
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Sakamoto
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Soejima
authors.forename: Hideki
authors.initials: H
authors.lastname: Shimomura
authors.forename: Ichiro
authors.initials: I
authors.lastname: Kajiwara
authors.forename: Sunao
authors.initials: S
authors.lastname: Kojima
authors.forename: Jun
authors.initials: J
authors.lastname: Hokamaki
authors.forename: Seigo
authors.initials: S
authors.lastname: Sugiyama
authors.forename: Michihiro
authors.initials: M
authors.lastname: Yoshimura
authors.forename: Yukio
authors.initials: Y
authors.lastname: Ozaki
authors.forename: Hajime
authors.initials: H
authors.lastname: Nakamura
authors.forename: Junji
authors.initials: J
authors.lastname: Yodoi
authors.forename: Hisao
authors.initials: H
authors.lastname: Ogawa
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000704:Analysis of Variance; D000787:Angina Pectoris / Q000097:blood / Q000503:physiopathology; D015415:Biomarkers / Q000097:blood; D002637:Chest Pain / Q000097:blood / Q000503:physiopathology; D005260:Female; D006801:Humans; D007834:Lasers; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000503:physiopathology; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology*; D010974:Platelet Aggregation / Q000187:drug effects; D010979:Platelet Function Tests / Q000295:instrumentation; D013318:Stroke Volume / Q000502:physiology; D013879:Thioredoxins / Q000097:blood*
chemical_list: D015415:Biomarkers; D013879:Thioredoxins