Although ex vivo heparin dose-response technologies may identify patients who have a reduced sensitivity to conventional doses of heparin, these tests have limited ability to calculate correctly an optimal initial unfractio- nated heparin bolus dose. The observational study by Garvin and colleagues [6] demonstrated poor correlation of the calculated in vitro heparin dose response curve compared with the actual patient heparin dose response, resulting in a failure to reach therapeutic ACT values in nearly 17% of patients. During CPB, an overestimation of heparin concentration may occur when using the ACT assay alone. Falsely elevated ACT values may be observed under conditions of hypothermia, reduced he- moglobin concentration, hypo brinogenemia, and phar- macologic agents that are not associated with a concomitant increase in heparin concentration [9]. In a controlled, nonrandomized study of 42 patients, Machin and colleagues [10] demonstrated prolongation of ACT values during hypothermic CPB when compared with normothermic CPB. Leyvi and colleagues [11] reported similar ACT prolongation under conditions of both hy- pothermia and hemodilution using a number of ACT technologies while plasma antifactor Xa heparin level activity remained constant. Maintaining ACT values during CPB without heparin concentration monitoring may result in lower doses of heparin. These known sensitivity limitations in ACT monitoring may result in subclinical plasma coagulation occurring during CPB. Whole blood heparin concentration assays are statisti- cally more closely correlated with plasma anti-Xa levels than the ACT [12]. Clinically, heparin concentration tests are performed alongside a functional test of clotting, such as an ACT, because a therapeutic functional con rmation of anticoagulation provides important safety data. 