Heterogeneity of platelet aggregation and major surface receptor expression in patients with acute myocardial infarction

Background: Platelets play an important role in the natural history of acute myocardial infarction (AMI). Methods and 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 μmol/L adenosine 5'-diphosphate, 10 μmol/L ADP, 1 μg/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 (CD41 b), 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 μmol/L ADP (64.1 ± 12.7 vs 52.0 ± 6.7; P = .04), by 10 μmol/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.