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 (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 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. (Am Heart J 1998;136:398-405.)