Our findings suggest the presence of diurnal variations in TF and TFPI concentrations in AMI patients, with the highest thrombotic risk in patients with high on-treatment platelet reactivity in the midmorning.
Reduced concentration of tissue factor pathway inhibitor is a risk factor for development of deep venous thrombosis, whereas elevated concentrations of tissue factor pathway inhibitor are observed in patients with acute myocardial infarction and disseminated intravascular coagulation.
FXa generation by monocytes of patients with AMI increased 53.6% +/- 9% in the presence of polyclonal antibodies to TFPI-1, indicating that cell-associated TFPI-1 inhibits monocyte TF activity.