title: The clinical use of flow cytometry for assessing platelet activation in acute coronary syndromes. TIMI-III Thrombosis and Anticoagulation Group.
abstract: BACKGROUND
  Unstable angina signals a sudden transition from stable to unstable atherosclerotic coronary artery disease. Although assessment of platelet activity has been shown to provide diagnostic and prognostic information, most available methods lack sufficient sensitivity or specificity for them to be useful in clinical practice. In recent years, fluorescently labeled antibodies and flow cytometry have permitted the detection of activation proteins on individual platelets. The purpose of the present study was to assess the ability of flow cytometry to detect platelet activation in patients with unstable angina and non-Q-wave myocardial infarction.
  
  
  METHODS
  Platelet activation before treatment was determined from whole-blood samples in 19 patients participating in the Thrombolysis in Myocardial Ischemia (TIMI)-IIIB study and in nine healthy volunteers (total of 24 samples) using flow cytometry and a monoclonal antibody (clone 1E3) to the activation-dependent, surface-expressed protein P-Selectin.
  
  
  RESULTS
  Among healthy volunteers, a small percentage of platelets were activated (2.0 +/- 2.5%). In contrast, 15 out of 19 (79%) patients with suspected myocardial ischemia at rest had 10.4 +/- 11.1% activated platelets (95% confidence interval 4.9-15.9%; P < 0.01). Seven patients (37%) were found to have more than 10% activated platelets. The degree of platelet activation did not differ significantly between patients with unstable angina and those with elevated creatine kinase levels (non-Q-wave myocardial infarction).
  
  
  CONCLUSIONS
  Whole-blood flow cytometric techniques can minimize the artifactual platelet activation often seen with other techniques and therefore offer distinct advantages in the investigation of patients with thrombotic coronary syndromes. In TIMI-III, patients with unstable angina and non-Q-wave myocardial infarction had clear evidence of platelet activation. An ongoing study will examine the correlation between platelet activation assessed using flow cytometry and clinical events in a larger patient cohort.
authors.affiliation: Thrombosis Research Center, University of Massachusetts Medical School, Worcester 01655.
authors.forename: R C
authors.initials: RC
authors.lastname: Becker
authors.forename: R P
authors.initials: RP
authors.lastname: Tracy
authors.forename: E G
authors.initials: EG
authors.lastname: Bovill
authors.forename: K G
authors.initials: KG
authors.lastname: Mann
authors.forename: K
authors.initials: K
authors.lastname: Ault
mesh_terms: D000208:Acute Disease; D000789:Angina, Unstable / Q000097:blood* / Q000503:physiopathology; D001792:Blood Platelets / Q000737:chemistry; D015815:Cell Adhesion Molecules / Q000032:analysis; D005069:Evaluation Studies as Topic; D005434:Flow Cytometry; D006801:Humans; D009203:Myocardial Infarction / Q000097:blood* / Q000503:physiopathology; D019007:P-Selectin; D015539:Platelet Activation; D010980:Platelet Membrane Glycoproteins / Q000032:analysis
chemical_list: D015815:Cell Adhesion Molecules; D019007:P-Selectin; D010980:Platelet Membrane Glycoproteins