The classic contact activation coagulation system emerges as a potentially important mechanism in arterial thrombosis. Recent studies not only indicate that coagulation factor (F) XII is associated with atherothrombotic coronary disease, but also that it contributes to clot formation via activation of downstream FXI. The time course of contact activation after an acute myocardial infarction (AMI), has not been studied. In addition, its relevance for arterial thrombosis has not been addressed in prospective studies. We measured the plasma concentrations of activated FXII (FXIIa), FXIa and Kallikrein in complex with their natural inhibitors in 135 consecutive patients with a documented first AMI (chest pain between 30 minutes and 24 hours accompanied by ST-segment elevation on ECG and/or elevated plasma levels of creatine kinase and troponin T). FXIIa-C1 inhibitor, kallikrein-C1 inhibitor, FXIa-C1 inhibitor and FXIa-antitrypsin complexes were measured in established homemade ELISAs (
Disclosure:Research Funding: The study was supported by grants from the Profileringsfonds of the Academic Hospital Maastricht and by an unrestricted grant from Pfizer.