Heparin Binding Protein in Adult Heart Surgery.

BACKGROUND: Heparin binding protein (HBP) is released from neutrophilic secretory vesicles upon neutrophil adhesion on the endothelium. HBP mediates capillary hyperpermeability experimentally. In sepsis, HBP predicts organ dysfunction. Cardiopulmonary bypass induces both neutrophil activation and hyperpermeability. We hypothesized that in cardiopulmonary bypass, HBP is released in the reperfused coronary circulation concomitantly with neutrophil adhesion.

METHODS: In 30 patients undergoing aortic valve replacement, concomitant blood samples were drawn from the coronary sinus and arterial line before aortic crossclamping and 5 min after reperfusion to calculate transcoronary differences. Plasma HBP concentrations, neutrophil markers lactoferrin and myeloperoxidase, myocardial injury marker heart-type fatty acid binding protein (hFABP) and leukocyte differential counts were measured.

RESULTS: Arterial HBP was 4.1 (3.6-5.3) ng/ml preoperatively and 150.0 (108.2-188.6) ng/ml after aortic declamping. HBP increased 39-fold, lactoferrin 16-fold and myeloperoxidase 4-fold during cardiopulmonary bypass. Before cardiopulmonary bypass, there were marginal transcoronary differences in HBP [1.4 (-0.4-3.6) ng/ml, p=0.001] and hFABP [0.4 (-0.04-3.5) ng/ml, p=0.001] but not in the other parameters. During reperfusion, transcoronary HBP release [6.4 (1.8-13.7) ng/ml, p<0.001] was observed, concomitantly with transcoronary neutrophil sequestration [-0.14 (-0.28-0.01) x10ˆ9/l, p=0.001] and transcoronary hFABP release [6.9 (3.0-25.8) ng/ml, p<0.001]. There were no transcoronary differences in lactoferrin or myeloperoxidase during reperfusion.

CONCLUSIONS: CPB results in substantial increase in circulating HBP. HBP is also released from the reperfused coronary circulation, concomitantly with coronary neutrophil adhesion and myocardial injury. HBP may be one candidate for a humoral factor mediating capillary leak in cardiopulmonary bypass.