Antiplatelet and anticoagulant prophylaxis and postoperative blood loss in cardiac surgery.

Abstract

To the Editor: We read with interest the article by Pothula et al. (1) investigating effects had by preoperative ADP antagonists with or without heparin on postoperative blood loss after cardiac surgery. This is an important issue because anesthesiologists are increasingly confronted with patients on platelet-active drugs. The authors found that patients receiving ADP antagonists and additional low-dose heparin exhibited a significantly minor blood loss as compared with the control group and the group receiving only ADP antagonists. This result was explained by a possible beneficial effect of heparin in preventing formation of microemboli and thus preserving coagulation factors until the postoperative period. This assumption is interesting, since exogenous heparin or endogenous heparinoids are usually associated with increased bleeding and all patients were on full heparin dosage during CBP. Furthermore, with the exception of fibrinogen, no coagulation factor was measured pre- or postoperatively. In addition, the authors made no attempt to measure platelet function preoperatively, which seems necessary to guarantee that groups are comparable. Clopidogrel is six times more potent than ticlopidine and shows linear pharmacokinetics, while ticlopidine does not (2). However, clopidogrel-induced platelet inhibition exhibits considerable individual heterogeneity (3). Furthermore, it is not clear how many patients in each group received clopidogrel or ticlopidine or whether patients received one single or repeated doses, which influences half-life, especially for ticlopidine. Why did 13% of patients in the treatment groups receive aprotinin and 4.3% the combination of aprotinin and ε-aminocaproic acid, while this was true for 9% and 0% of control patients, respectively? Data from animal experiments show that aprotinin partially reverses effects of thienopyridines in a dose-dependent manner (4). Lastly, concentrations of fibrinogen already varied considerably between groups at baseline. Although differences in aortic cross-clamping time and extracorporeal circulation time were investigated as possible confounders, the obvious difference in preoperative fibrinogen concentrations did not correlate with the amount of blood loss. Since intraoperative blood loss was equal in all groups, it was to be expected that postoperative concentrations of fibrinogen would correlate well with preoperative values in all groups (5), provided that fluid therapy, which itself influences hemostasis, was also comparable between groups. Consequently, the causal relationship between platelet antagonists with or without heparin therapy and the reported postoperative blood loss seems quite questionable. Moreover, since several confounders cannot be excluded, results should be interpreted with caution. Dietmar Fries, MD Corinna Velik-Salchner, MD Petra Innerhofer, MD Department of Anaesthesiology and Critical Care Medicine University Hospital Innsbruck Innsbruck, Austria