LAUSR

IN THIS ISSUE of Journal of Cardiothoracic and Vascular Anesthesia, Fang et al present results of a retrospective observational study aimed at identifying associations between thromboelastographic (TEG) variables and heparin resistance in a cohort of children and adults with congenital heart disease. Nearly a quarter of patients in the cohort exhibited heparin resistance, defined as failure to achieve an activated clotting time (ACT) of at least 480 seconds after weight-based dosing of heparin. Logistic regression modeling illustrated that patients with TEG K variable r1.3 minutes was associated with 3.7 greater odds of heparin resistance after weight-based dosing; the K variable is a measure of clot propagation and indicates the time to achieve a certain level of clot strength (an amplitude of 20 mm). The authors’ conclusion is that preoperative TEG indices indicating hypercoagulability are associated with altered heparin response and potentially inadequate anticoagulation on bypass. They propose that patients be screened for hypercoagulability instead of or in addition of standard coagulation testing. The authors completed a thorough descriptive retrospective analysis of the TEG variables as it relates to heparin resistance in congenital heart patients having cardiac surgery. Heparin resistance and hypercoagulability have been associated with increased morbidity and mortality in both children and adults; however, it is unclear what further conclusions can be drawn from this current retrospective data. The authors’ definition of heparin resistance as an ACT below 480 seconds after weight-based dosing of only 300 U/kg is problematic. Though inter-institutional variability exists, 300 U/kg is significantly less than the doses of heparin commonly administered; 400 U/kg has become a more standard dose since the United States Food and Drug Administration changed the heparin formulation to be more in line with World Health Organization potency standards. Neonates may require even doses exceeding 400 U/kg to achieve effective thrombin inhibition. This is not surprising given the principles of developmental hemostasis that guide our understanding of changing levels of coagulation factors throughout infancy into childhood.