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The ratio of concentrations of aminocaproic acid and tranexamic acid that prevent plasmin activation of platelets does not provide equivalent inhibition of plasmatic fibrinolysis

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Abstract

Aminocaproic acid (EACA) availability has recently been decreased whereas tranexamic acid (TXA) is still available as an antifibrinolytic agent to decrease blood loss associated with procedures involving cardiopulmonary bypass (CPB) by inhibiting plasmin mediated platelet activation. Given that the clinical inclination is to substitute TXA for EACA, we sought to compare the antifibrinolytic efficacy of the two agents using the clinically accepted molar ratio of EACA:TXA (7.9:1) that prevents platelet activation in a viscoelastic based system under a variety of conditions in human plasma; 25–50% therapeutic concentration (EACA 32.5–65 µg/ml, TXA 5–10 µg/ml) in the presence of 1500–3000 IU tissue-type plasminogen activator, with 0–50% dilution of plasma with buffer. In all equipotent concentrations, TXA provided superior antifibrinolytic action compared to EACA. It is hoped that this work will serve as a rationale to further investigate these and other similar agents, especially now in a time of unpredictable unavailability of key medications needed to optimize patient care. It is also our wish that these data assist perfusionists, anesthesiologists and cardiothoracic surgeons with their consideration of using an antifibrinolytic agent when managing complex patients with hypercoagulable states (e.g., ventricular assist device explant, infective endocarditis) undergoing CPB.

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Funding

This investigation was supported by the Department of Anesthesiology, College of Medicine, at the University of Arizona.

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Correspondence to Vance G. Nielsen.

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Both authors declare that they have no conflict of interest.

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This was an in vitro investigation and did not involve any living subjects.

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Nielsen, V.G., Ford, P.M. The ratio of concentrations of aminocaproic acid and tranexamic acid that prevent plasmin activation of platelets does not provide equivalent inhibition of plasmatic fibrinolysis. J Thromb Thrombolysis 46, 365–370 (2018). https://doi.org/10.1007/s11239-018-1705-3

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  • DOI: https://doi.org/10.1007/s11239-018-1705-3

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