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Ann Thorac Surg 1996;61:1590-1591
© 1996 The Society of Thoracic Surgeons
Department of Cardiac, Thoracic, and Vascular Surgery and Department of Clinical Chemistry Laboratory Medicine, University of Regensburg, Fran-Josef-Strauss-Allee 11, 93053 Regensburg, Germany
To the Editor:
With interest we read the article by Khuri and associates [1], who found that heparin causes platelet dysfunction and increases fibrinolysis independent of cardiopulmonary bypass (CPB). We would like to add our own findings.
We found a significant effect of heparin on platelet surface antigen expression in vivo and in vitro in patients undergoing aortocoronary bypass grafting. Blood samples were taken in 30 patients after opening the chest before administration of heparin to investigate the in vivo effect of heparin. Platelet-rich plasma was prepared immediately, and the platelet surface expression of glycoprotein (GP) IIb-IIIa, GP Ib, and P-selectin was determined using flow cytometry. The level of GP IIb-IIa, the fibrinogen receptor responsible for platelet aggregation, was unchanged. The level of GP Ib, the von Willebrand receptor on the platelet surface, was significantly reduced (p = 0.001), indicating platelet activation. This was confirmed by a significant increase of P-selectin concentration, a marker of platelet activation (p = 0.004).
The in vitro effect of heparin was investigated by taking blood samples of 40 patients on the day before operation. The surface expression of GP IIb-IIIa and GP Ib was measured with whole-blood flow cytometry before and after in vitro administration of a heparin dose equivalent to in vivo concentrations during CPB. Heparin again induced a significant platelet activation deduced from a significant decrease in GP Ib level (p < 0.001). The level of GP IIb-IIIa was unchanged.
Recent studies have postulated a CPB-independent effect of heparin on platelets [1, 2]. Suppression of platelet activation has been suggested to be one of the possible mechanisms responsible for this effect [1, 2]. Our results refute this hypothesis, because we found a significant platelet activation by heparin in vitro and in vivo before CPB. Moreover, we found a decrease in the expression of GP IIb-IIIa, P-selectin, and GPIb during CPB coinciding with a loss of larger and thus more active platelets [3]. We suggest that platelet activation by heparin promotes the loss of activated platelets during CPB and thus contributes to the resulting platelet function defect [3].
References
Department of Surgery, Brockton West Roxbury VA Medical Center, Brigham and Women's Hospital and Harvard Medical School, 1400 Veterans Of Foreign Wars Parkway, Boston, MA 02132
Naval Blood Research Laboratory, Department of Medicine, Whitaker Cardiovascular Institute, and Evans Department of Medicine, Boston University School of Medicine, Boston MA
Center for Platelet Function Studies, Departments of Pediatrics, and Surgery, University of Massachusetts Medical School, Worcester MA
To the Editor:
Doctor Wahba and his associates observed that heparin produced an increase in platelet P-selectin expression, a decrease in platelet GP Ib level, and no change in platelet GP IIb-IIIa level in platelet-rich plasma obtained before and after heparin administration before cardiopulmonary bypass operation in 30 patients. They reported that heparin in vitro, in concentrations similar to the level present in patients subjected to cardiopulmonary bypass, produced a decrease in platelet GP Ib level and no change in platelet GP IIb-IIIa level when whole blood was evaluated using flow cytometry. However, their letter does not state the quantitative degree of any of these increases and decreases (This is important because a statistically significant increase or decrease in a platelet surface antigen does not necessarily imply biological or clinical significance. For example, heterozygotes for Bernard-Soulier syndrome [an autosomal recessive inherited deficiency of platelet GPIb, GPIX, and GPV] have a normal bleeding time and no hemorrhagic diathesis despite an approximately 50% reduction in platelet surface GPIb, GPIX, and GPV [2].)
Our article [1] did not report platelet surface marker data; only data on bleeding time, shed blood thromboxane B2, plasmin, and D-dimer levels were reported. However, in a previous report by Kestin and associates [3], heparin (6 U/mL) had no effect on platelet P-selectin and GP Ib levels in patients before cardiopulmonary bypass operation. In addition, in the article in press by Upchurch and co-workers [4], heparin had no effect on platelet P-selectin or GP Ib level in baboons infused with heparin ranging from 0 to 13 U/mL. The article by Upchurch and co-workers also provides evidence that the platelet dysfunction observed after heparin administration was due, in part, to the profibrinolytic effect of heparin.
Hence, although our previous article [1] did not report platelet surface marker data, other articles by our group have clearly shown that the administration of heparin in doses equivalent to those administered during cardiopulmonary bypass do not alter the expression of platelet P-selectin nor the expression of platelet GP Ib. These observations, along with our observation [1] that heparin markedly decreases the ability of the platelet to produce thromboxane A2, do not support Wahba and associates' assertion that heparin administration before cardiopulmonary bypass causes increased platelet activation.
References
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  T. M. Dewey and M. J. Mack Myocardial Revascularization Without Cardiopulmonary Bypass Card. Surg. Adult, January 1, 2003; 2(2003): 609 - 625. [Full Text]
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