Related Experiment Video
Updated: Oct 7, 2026
Hemocompatibility Testing of Blood-Contacting Implants in a Flow Loop Model Mimicking Human Blood Flow
Published on: March 5, 2020
Heparin coating of extracorporeal circuits inhibits contact activation during cardiac operations
H te Velthuis1, C Baufreton, P G Jansen
1Department of Pathophysiology of Plasma Proteins, Central Laboratory of The Netherlands Red Cross Blood Transfusion Service, Amsterdam, The Netherlands.
Insights
Heparin-coated circuits significantly reduce contact system activation during heart surgery. This suggests coagulation and fibrinolysis during bypass are largely independent of the contact system.
Area of Science:
- Biomedical Engineering
- Cardiovascular Surgery
- Hematology
Background:
- Extracorporeal circuits are essential for cardiopulmonary bypass during cardiac surgery.
- Heparin coating is known to reduce complement activation on circuit surfaces.
- The effect of heparin coating on contact system activation during cardiac surgery requires further investigation.
Purpose of the Study:
- To investigate the impact of heparin-coated extracorporeal circuits on contact system activation in patients undergoing coronary artery bypass grafting.
- To compare contact system activation between patients using heparin-coated circuits and those using uncoated circuits.
Main Methods:
- A comparative study involving 30 patients undergoing coronary artery bypass grafting.
- Patients were divided into two groups: heparin-coated circuit (n=15) and uncoated circuit (n=15).
- Plasma markers for contact (kallikrein-C1-inhibitor complexes), coagulation (prothrombin fragments F1 + 2), and fibrinolysis (plasmin-alpha 2-antiplasmin complexes) were measured before and during surgery.
Main Results:
- Heparin-coated circuits significantly reduced the generation of kallikrein-C1-inhibitor complexes compared to uncoated circuits.
- Reductions in kallikrein-C1-inhibitor complexes were observed both after the onset and cessation of cardiopulmonary bypass.
- No significant intergroup differences were found in prothrombin fragments F1 + 2 or plasmin-alpha 2-antiplasmin complexes.
Conclusions:
- Heparin-coated extracorporeal circuits effectively reduce contact system activation during cardiac operations.
- The observed reduction in contact system activation does not appear to significantly impact coagulation or fibrinolysis during cardiopulmonary bypass.
- Thrombin and plasmin generation during cardiopulmonary bypass seem to occur independently of contact system activation.
Objective:
Heparin coating reduces complement activation on the surface of extracorporeal circuits. In this study we investigated its effect on activation of the contact system in 30 patients undergoing coronary artery bypass grafting with the use of a heparin-coated (Duraflo II, Baxter Healthcare Corp., Edwards Division, Santa Ana, Calif.; n = 15) or an uncoated extracorporeal circuit (n = 15).
Methods:
Plasma markers that reflect activation of contact (kallikrein-C1-inhibitor complexes), coagulation (prothrombin fragments F1 + 2), or fibrinolytic (plasmin-alpha 2-antiplasmin complexes) systems were determined before and during the operation. The generation of kallikrein-C1-inhibitor complexes was reduced by 62% (p = 0.06) after the onset of cardiopulmonary bypass and by 43% (p = 0.026) after the cessation of bypass in the group in which a heparin-coated circuit was used compared with the group in which the circuit was uncoated. Generation was reduced by 58% (p = 0.06) when the ratio of kallikrein-C1-inhibitor to prekallikrein after onset of bypass was considered. We detected significant increases in F1 + 2 levels in both groups and increases in plasmin-alpha 2-antiplasmin complexes in the heparin-coated group at cessation of bypass, but no intergroup differences were observed. Thus use of heparin-coated extracorporeal circuits during cardiac operations reduces formation of kallikrein-C1-inhibitor complexes when compared with use of uncoated circuits. The heparin coating is not accompanied by similar reductions in coagulation or fibrinolysis, suggesting that thrombin and plasmin formation during cardiopulmonary bypass occurs mainly independently of the contact system activation.
Related Concept Videos
01:19Depolarizing Blockers: Pharmocokinetics
01:30Anticoagulant Drugs: Low-Molecular-Weight Heparins
01:18Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
01:20Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
01:20Extrinsic and Intrinsic Pathways of Hemostasis
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...
01:28Cardiac Catheterization I: Pre-Procedure Overview