Acute myocardial infarction was associated with 20% more GPIIb-IIIa complexes on platelets and 7% greater platelet size compared with controls.
Case-Control (n=28)
Are platelet GPIIb-IIIa complex numbers and platelet size increased in patients immediately following acute myocardial infarction compared to controls?
Patients with acute myocardial infarction have larger platelets with increased GPIIb-IIIa complexes, suggesting a potential causal relationship between these highly reactive platelets and AMI.
Effect estimate: 20% more
Platelet aggregation, which plays an important role in acute myocardial infarction (AMI), is mediated by fibrinogen binding to the platelet membrane glycoprotein (GP)IIb-IIIa (CD41). This study measured the relative number of GPIIb-IIIa complexes on platelets from patients immediately following AMI (n = 14) compared with those from controls (n = 14). Flow cytometry was used to demonstrate that there were, on average, 20% more GPIIb-IIIa complexes on platelets after AMI compared with controls. Platelet size was also 7% greater in AMI and it is known that larger platelets are more reactive. Since platelet size and protein content are determined at thrombopoiesis the majority of these platelets must have been circulating prior to AMI. Larger platelets, with more GPIIb-IIIa may, therefore, be causally related to AMI.
Giles et al. (Sat,) conducted a case-control in Acute myocardial infarction (n=28). Acute myocardial infarction vs. Controls was evaluated on Relative number of GPIIb-IIIa complexes on platelets (20% more). Acute myocardial infarction was associated with 20% more GPIIb-IIIa complexes on platelets and 7% greater platelet size compared with controls.