Procoagulant triggers during cardiopulmonary bypass.

Recently, Boisclair et all has given us an important clue to show the main trigger to coagulation activity during cardiopulmonary bypass (CPB). They observed the increase of factor IX activation peptide during CPB, which shows a strong correlation with the increase of prothrombin fragment F1 + 2. In contrast, they found no significant increase in factor XIIa levels during CPB. This activation pattern in the clotting cascade indicates that the clotting activity during CPB is not mainly triggered from the contact activation to the surface of the extracorporeal circuit, but from the tissue factor-factor VIIa mechanism, which Boisclair et al suggested to be generated from the subendothelial surfaces exposed as a result of surgical damage to blood vessels. However, their speculation seems rather unlikely. We cannot imagine that the major surgical insult of opening the thorax, which is completed before CPB, contributes to the clotting activation during CPB after an interval of more than 60 minutes. Moreover, if the surgical insult is the main procoagulant trigger, other major surgical procedures without CPB should manifest a much more profound procoagulant activity in the systemic blood that is not or to a lesser extent anticoagulated. Alternatively, Boisclair’s result appears to us to imply other triggers to coagulation via the extrinsic pathway during CPB. Our recent study* showed that the blood shed into the pericardial cavity and afterwards returning through cardiotomy suction during CPB is highly activated, quite contrasting with the activation of blood exposed to the low thrombogenic surfaces of modern extracorporeal circuits. Our supporting in vitro experiment using rabbit pericardium* showed that the conventional dose of heparin could not prevent the clotting activity triggered by tissue factor of the pericardium. However, we miss the description in Boisclair’s report of whether they used cardiotomy suction during CPB as usual practice. If they avoided using cardiotomy suction in their study model, the observed clotting activity in their study seems to indicate another trigger. Endothelial cells and monocytes have been shown to express tissue factor activity upon exposure to agonists such as tumor necrosis factor or endot~xin,’,~ which had increased activity observed during CPB.5 Because the clinical contribution of this procoagulant pathway has not been shown, Boisclair’s report would be a strong support for this hypothesis. In conclusion, the nicely performed study of Boisclair et all would give us an important clue to speculate the major procoagulant trigger during CPB, if the information is provided whether they used cardiotomy suction in their study.