Open AccessReducing Hemostatic Activation During Cardiopulmonary Bypass: A Combined Approach
Author(s) -
Michael J. Eisses,
Kristy Seidel,
Gabriel S. Aldea,
Wayne L. Chandler
Publication year - 2004
Publication title -
anesthesia and analgesia/anesthesia and analgesia
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 1.404
H-Index - 201
eISSN - 1526-7598
pISSN - 0003-2999
DOI - 10.1213/01.ane.0000108489.88613.2c
Subject(s) - cardiopulmonary bypass , medicine , fibrin , heparin , tissue plasminogen activator , plasminogen activator , activated clotting time , fibrinolysis , anesthesia , t plasminogen activator , coagulation , thrombin , immunology , platelet
Interventions such as heparin-coated circuits, epsilon-aminocaproic acid, and reduced shed blood reinfusion have shown mixed results when applied individually for limiting hemostatic activation during cardiopulmonary bypass (CPB). We compared coagulation and fibrinolytic activation during conventional CPB (control) (CTRL) using noncoated circuits, no antifibrinolytics, and open cardiotomy with a combined strategy (HAC) that used heparin-coated circuits, epsilon-aminocaproic acid, and closed cardiotomy. Blood samples were drawn before, during, and after CPB for primary coronary bypass grafting surgery from 9 CTRL patients and 10 HAC patients. Thrombin-antithrombin complex and fibrinopeptide A levels (markers of thrombin and fibrin generation) were reduced in the HAC versus CTRL group after 30 min of CPB (P < 0.05). Average tissue plasminogen activator (tPA) levels were significantly lower in the HAC group by 30 min on CPB (P < 0.05), resulting in preservation of plasminogen activator inhibitor (PAI)-1 during CPB (P < 0.05). D-Dimer, a measure of intravascular fibrin formation and removal, was reduced in the HAC group during and after CPB (P < 0.005). Overall, the combined strategy was associated with a reduction in CPB-induced increases in markers of thrombin generation, fibrin formation, tPA release, and fibrin degradation and better preservation of PAI-1.