title: Heterogeneity of platelet aggregation and major surface receptor expression in patients with acute myocardial infarction.
abstract: BACKGROUND
  Platelets play an important role in the natural history of acute myocardial infarction (AMI).
  
  
  RESULTS
  Platelet aggregation and receptor expression were studied in 23 patients with AMI before reperfusion therapy and compared with 10 healthy control subjects. Platelet aggregation was induced with 5 micromol/L adenosine 5'-diphosphate, 10 micromol/L ADP, 1 microg/mL collagen, 1 mg/mL thrombin, and 1.25 mg/mL ristocetin. Receptor expression was measured by flow cytometry with monoclonal antibodies to p24 (CD9), Ib (CD42b), IIb (CD41b), IIIa (CD61), IIb/IIIa (CD41b/CD61), very late antigen-2 (CD49b), P-selectin (CD62p), platelet/endothelial cell adhesion molecule-1 (CD31); and vitronectin (CD51/CD61). The percentage of platelet aggregation was higher in patients with AMI when induced by 5 micromol/L ADP (64.1+/-12.7 vs 52.0+/-6.7; P=.04), by 10 micromol/L ADP (71.7+/-13.0 vs 59.2+/-7.2, P=.003), by thrombin (75.8+/-10.9 vs 60.5+/-6.9, P=.01), and by ristocetin (92.5+/-7.8 vs 71.3+/-7.4, P=.0001). Collagen-induced platelet aggregation did not differ between groups. Expression of P-selectin (log amplification of fluorescence intensity) (31.5+/-5.0 vs 25.1+/-2.6, P=.003) and platelet/endothelial cell adhesion molecule-1 (56.8+/-17.7 vs 44.5+/-3.7, P=.04) were significantly increased in patients with AMI. The expression of IIb (28.4+/-2.5 vs 37.2+/-1.7, P=.0001) and Ib (103.6+/-29.9 vs 133.8+/-8.0, P=.007) were reduced in patients with AMI.
  
  
  CONCLUSIONS
  Platelets are not necessarily systemically activated during the prereperfusion phase of AMI. For each agonist used and surface antigen measured, there was a cohort of patients with AMI within the normal or even below normal range of platelet status.
authors.affiliation: Center for Thrombosis Research, Sinai Hospital, Baltimore, MD 21215, USA.
authors.forename: V L
authors.initials: VL
authors.lastname: Serebruany
authors.forename: P A
authors.initials: PA
authors.lastname: Gurbel
authors.forename: A R
authors.initials: AR
authors.lastname: Shustov
authors.forename: E M
authors.initials: EM
authors.lastname: Ohman
authors.forename: E J
authors.initials: EJ
authors.lastname: Topol
mesh_terms: D000244:Adenosine Diphosphate; D000368:Aged; D000911:Antibodies, Monoclonal; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism*; D016022:Case-Control Studies; D003094:Collagen; D005260:Female; D005434:Flow Cytometry; D006490:Hemostatics; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000378:metabolism*; D019007:P-Selectin; D010974:Platelet Aggregation / Q000187:drug effects; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D011956:Receptors, Cell Surface / Q000187:drug effects / Q000378:metabolism*; D016024:Receptors, Cytoadhesin / Q000187:drug effects / Q000378:metabolism*; D012310:Ristocetin; D013917:Thrombin
chemical_list: D000911:Antibodies, Monoclonal; D006490:Hemostatics; D019007:P-Selectin; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D011956:Receptors, Cell Surface; D016024:Receptors, Cytoadhesin; D012310:Ristocetin; D000244:Adenosine Diphosphate; D003094:Collagen; D013917:Thrombin