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Ann Thorac Surg 2001;72:320-321
© 2001 The Society of Thoracic Surgeons
e-mail: elijah.muriithi{at}gstt.sthames.nhs.uk
To the Editor
Nakajima and colleagues [1] studied the effects of two heparin doses on platelets during cardiopulmonary bypass while using heparin-bonded circuits. They observed that the lower heparin dose preserved platelet numbers without improving platelet function. Although their findings are interesting, their investigations failed to target the platelet functional changes that occur during cardiopulmonary bypass. The platelet function defect associated with cardiopulmonary bypass is the inability to form large stable aggregates (macroaggregates) in response to stimulation by weak agonists [2]; the initial responses of platelets to stimulation by weak agonists, up to and including the formation of small aggregates (microaggregates), are well preserved [2]. Heparin, as they quote, has a dose-dependent stimulatory action on platelets. We have demonstrated that, although heparinization induces microaggregation [3], it also has an indirect action that selectively inhibits platelet macroaggregation [4]. This indirect action is independent of heparin at doses more than 30 U/kg [4]. Therefore, reducing heparin dosage to 200 U/kg as used by Nakajima and colleagues [1] is unlikely to improve platelet hemostatic function.
The contrasting effects of heparin on early and late platelet responses to stimuli limit the use of markers of platelet activation as measures of platelet function. ß-Thromboglobulin is a relatively nonspecific measure of the platelet activation state as it is released both during the primary and secondary phases of aggregation [5]. Membrane receptor expression changes that occur in the early stages of platelet activation similarly give little information on the ability of the platelets to form macroaggregates. Plasma platelet factor-4 levels are difficult to interpret in heparinized patients as overwhelming quantities of this molecule are released from the endothelium by heparin [6].
With regard to platelet counts, unfortunately it is not stated at which stages of cardiopulmonary bypass platelet counts were significantly different between the groups. The in vitro anticoagulant used for platelet counting is also not mentioned; systemic heparinization may artifactually lower platelet counts with some anticoagulants [3]. Previous studies have shown that during cardiopulmonary bypass a preferential loss of activated platelets occurs [3, 7]. Therefore, reducing heparin dosage would possibly have a platelet-sparing effect by decreasing platelet stimulation. We tested this hypothesis by studying platelet counts in ethylenediaminetetraacetic acid anticoagulated blood after incremental heparin administration before cardiopulmonary bypass. We found that the platelet count (mean ± standard deviation) 185 ± 32 x 109/L was unaffected by 30 U/kg of heparin and remained at 186 ± 30 x 109/L (p = 1.0; n = 18; Friedman analysis of variance). However, after additional heparin, thus reaching a dose of 300 U/kg, the platelet count decreased significantly to 173 ± 42 x 108/L (p = 0.01 versus 30 U/kg heparin; p = 0.009 versus 0 U/kg heparin: n = 18). This decrease in the platelet count in ethylenediaminetetraacetic acid anticoagulated blood, which occurred after heparinization but before the start of extracorporeal circulation, supports the hypothesis that heparin contributes to the loss of platelets from the circulation during cardiopulmonary bypass. However, as the additional heparin was administered 5 minutes after the initial dose, we cannot exclude the possibility that delayed effects of the earlier low dose also affected the final counts.
References
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