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J Thorac Cardiovasc Surg 2001;122:405
© 2001 The American Association for Thoracic Surgery

Letters to the Editor

Aprotinin administration in the pericardial cavity does not prevent platelet activation

R. Clive Landis, Kenneth M. Taylor

Imperial College School of Medicine, Hammersmith Hospital, London W12 0NN, United Kingdom

To the Editor:

To better understand the hemostatic and platelet-preserving properties of aprotinin and to address the continuing controversy whether aprotinin may be prothrombotic when given to patients undergoing cardiopulmonary bypass, one must elucidate its mechanism of action on platelets in greater detail. The article by Maquelin and associatesGo 1 provides clinical support for a subtle mechanism that we have proposed on the basis of our in vitro platelet studies: this states that aprotinin is simultaneously "hemostatic yet antithrombotic."Go 2 Aprotinin achieves these two apparently disparate properties by selectively targeting the two major categories of agonistic receptors expressed by platelets: those that require proteolytic cleavage to transduce a platelet-activating signal (the "protease-activated" thrombin receptors, PAR1 and PAR4) versus those that are proteolysis-independent (the receptors for collagen, adenosine diphosphate [ADP], or epinephrine). This dualistic mechanism of action was most clearly observed in a simple platelet aggregation experiment, in which aprotinin prevented thrombin-induced platelet aggregation (by inhibiting the proteolytic activation of PAR1) but permitted aggregation to proceed in response to the nonproteolytic agonists collagen or ADP.Go 2 Because collagen and ADP are both expressed at wound and suture sites throughout the pericardial cavity, aprotinin would not be expected to prevent platelet activation when administered directly to the pericardial cavity. This expectation has now been borne out by the studies of Maquelin and associates.Go 1 However, when administered systemically, it would be expected to inhibit platelet activation as a result of thrombin generation in the bypass circuit. Systemic aprotinin may therefore prevent the unwanted participation of platelets in the coagulation cascade (exerting a net antithrombotic effect) but preserve the hemostatic capacity of platelets in surgical wounds.

12/8/115696

References

  1. Maquelin KM, Nieuwland R, Lentjes EGWM, Böing AN, Mochtar B, Eijsman L, et al. Aprotinin administration in the pericardial cavity does not prevent platelet activation. J Thorac Cardiovasc Surg. 2000;120:552-7.[Abstract/Free Full Text]
  2. Poullis M, Manning R, Laffan M, Haskard DO, Taylor KM, Landis RC. The antithrombotic effect of aprotinin: actions mediated via the protease-activated receptor 1. J Thorac Cardiovasc Surg. 2000;120:370-8.[Abstract/Free Full Text]



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