Summary
There is growing evidence that the tissue factor/factor VIIa pathway of coagulation
is enhanced during cardiopulmonary bypass. Hitherto, available evidence has suggested
that upregulated monocyte bound tissue factor is made available, either in the blood
collected from the site of surgery or on circulating cells. However, cellular upregulation
is slow, while generation of factor VIIa in blood collected from the pericardial cavity
is rapid. We have therefore investigated the possibility of an alternative source
of tissue factor, plasma (as opposed to cellular) tissue factor in blood samples taken
from the central vein catheter (systemic circulation) and collected from the pericardial
cavity during cardiopulmonary bypass. Six patients undergoing first time cardiopulmonary
bypass grafting were studied. Tissue factor antigen was found to be rapidly elevated
(by 15 min) in the pericardial plasma, ∼5-fold above systemic levels (p <0.004). Similar
elevations were found in markers of coagulation activation, factor VIIa antigen (p
= 0.066), prothrombin fragment F1+2 (p <0.003) and thrombin-antithrombin complex (p <0.03). To explore whether plasma
tissue factor was (or had been) functionally active, factor VIIa was measured also
with the soluble tissue factor functional assay after removal of heparin. Functional
factor VIIa activity fell significantly in the systemic circulation, probably due
to the heparin-induced increase (∼15-fold) in tissue factor pathway inhibitor (TFPI),
but was elevated in pericardial blood compared with that taken from the central line
catheter (p <0.006). These results demonstrate that both components of the activation
complex for the extrinsic pathway of coagulation are rapidly generated in pericardial
blood during bypass.
Keywords
Tissue factor - factor VIIa - cardiopulmonary bypass - tissue factor pathway inhibitor
- heparin