Contact,Coagulation and Platelet Interaction with Heparin Treated Equipment during Heart Surgery

Abstract

Heparin coating of an extracorporeal device may reduce blood activation. To evaluate protein and platelet interaction with Duraflo II surface treatment of the cardiopulmonary bypass (CPB) circuit, thirty coronary artery bypass grafting patients were randomly divided into two groups (Duraflo II, n=15 or Control, n=15). Binding of antibodies against factor XII, antithrombin III (ATIII) and platelet receptor GpI_b were significantly higher (p<0.01) on the Duraflo II treated surface. Hageman Factor fragment (HFf or factor XIIf)^∗ activity observed in the fluid phase tended to be lower in the treated circuits, although complexes of factor XIIf-C1 inhibitor (C1INH) increased by the same extent in both groups. Thrombin was effectively bound on the Duraflo II surface while thrombin-antithrombin III formation was reduced during the first phase of CPB. As expected, this thrombin inhibiting capacity remained higher on the Duraflo II, although in the arterial line a reduction of 10% per hour was observed. This indicated loss of functional bound heparin of the Duraflo II surface. During the second phase of CPB, after release of the aortic crossclamp, factor XII and thrombin were strongly activated in both groups indicated by a sharp increase in concentrations of T/AT complex as well as FPA. Platelet numbers tended to increase more in the control group during CPB than in the Duraflo II group, likely by interaction of platelet Gpl_b receptors on the Duraflo II treated surface (p<0.01). However, platelet activation assessed by β-TG was similar in both groups of patients. It is concluded that Duraflo II treatment reduced intrinsic clotting activity during CPB by binding of factor XII and thrombin. In cardiac surgery this effect is attenuated after aortic crossclamp release by material-independent stimuli, but the heparin treatment remains functional for more than 3 hours.