Mild hypothermia does not attenuate platelet aggregation and may even increase ADP-stimulated platelet aggregation after
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BioMed Central
Open Access
Original basic research
Mild hypothermia does not attenuate platelet aggregation and may even increase ADP-stimulated platelet aggregation after clopidogrel treatment Carl Högberg, David Erlinge* and Oscar Ö Braun Address: Department of Cardiology, Lund University, Lund, Sweden Email: Carl Högberg - [email protected]; David Erlinge* - [email protected]; Oscar Ö Braun - [email protected] * Corresponding author
Published: 23 February 2009 Thrombosis Journal 2009, 7:2
doi:10.1186/1477-9560-7-2
Received: 19 November 2008 Accepted: 23 February 2009
This article is available from: http://www.thrombosisjournal.com/content/7/1/2 © 2009 Högberg et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract Background: Mild hypothermia is currently standard of care for cardiac arrest patients in many hospitals and a common belief is that hypothermia attenuates platelet aggregation. We wanted to examine the effects of clopidogrel on platelet aggregation during hypothermia. Methods: Platelet reactivity at 37°C and 33°C was evaluated by light transmission aggregometry and vasodilator-stimulated phosphoprotein (VASP) in blood from healthy volunteers before, and 24 hours after, a 600 mg loading dose of clopidogrel. Results: Collagen, 5-HT, epinephrine, U46619 and ADP-induced platelet aggregation was unaltered or even increased by hypothermia. After clopidogrel, there was a significant increase in platelet aggregation for 5 and 20 μM ADP at 33°C compared to 37°C (46 ± 5 vs. 34 ± 5% and 58 ± 4 vs. 47 ± 4%, p < 0.001, n = 8). Hypothermia also increased ADP-induced aggregation after pretreatment with the P2Y1 antagonist MRS2500. The decreased responsiveness to clopidogrel during hypothermia could be overcome by addition of the reversible P2Y12 antagonist AZD6140. ADP-induced inhibition of VASP-phosphorylation was unaffected by hypothermia both in the presence and absence of clopidogrel. A dose-response curve for ADP-induced platelet aggregation revealed increased potency for ADP during hypothermia with no difference in efficacy. Conclusion: Mild hypothermia did not attenuate platelet aggregation, instead it even increased ADP-stimulated platelet aggregation after clopidogrel treatment. Dual platelet inhibition with aspirin and a P2Y12 receptor antagonist is probably needed for patients with acute coronary syndromes treated with mild hypothermia, and it is possible that future ADP blockers could be of benefit.
Introduction Hypothermia is a condition in which many biological reactions are altered. Even a minor change of temperature in a cell can alter the response to stimuli. Mild hypothermia (33–35°C) has been shown to reduce mortality and improve neurological outcome in unconscious patients
with cardiac arrest [1,2], and is recommen
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