title: Temperature effects on haemostasis in whole blood from ticagrelor- and aspirin-treated patients with acute coronary syndrome.
abstract: BACKGROUND
  Comatose survivors after cardiac arrest are treated with mild induced hypothermia and potent platelet- inhibiting drugs after coronary stenting. Previous studies have shown an increased incidence of stent thrombosis during clopidogrel and aspirin treatment in conjunction with induced hypothermia. The aim of this study was to investigate the in vitro effect of induced hypo- and hyperthermia on blood from patients undergoing ticagrelor- and aspirin-mediated platelet inhibition.
  
  
  METHODS
  Whole blood from 15 patients with acute coronary syndrome who were treated with ticagrelor and aspirin and from eight healthy volunteers was incubated for 1 hour at 28, 33, 37, and 39°C.
  
  
  RESULTS
  In blood from patients with acute coronary syndrome, the activated clotting time (Sonoclot) was prolonged in mild hypothermic (33°C) compared to normothermic (37°C) samples. Sonoclot, clotting rate and platelet function were decreased in hypothermic compared to normothermic samples. Platelet-induced activation and aggregation (Multiplate) was unchanged in mild hypothermic compared to normothermic samples. In contrast, mild hypothermia supported increased platelet activation as measured with flow cytometry with up-regulation of PAC-1 and P-selectin on the platelet surface.
  
  
  CONCLUSIONS
  In acute coronary syndrome patients treated with ticagrelor and aspirin, in vitro hypothermia to 33°C markedly increased platelet activity measured with flow cytometry, whereas viscoelastic coagulation test (Sonoclot) revealed a hypocoagulative response. Prospective clinical trials studying platelet inhibition at different temperatures and correlating changes in platelet function to bleeding or stent occlusion are needed.
authors.affiliation: Department of Intensive and Perioperative Care, Skåne University Hospital , Lund , Sweden.
authors.forename: Thomas
authors.initials: T
authors.lastname: Kander
authors.forename: Jens
authors.initials: J
authors.lastname: Brokopp
authors.forename: David
authors.initials: D
authors.lastname: Erlinge
authors.forename: Christian
authors.initials: C
authors.lastname: Lood
authors.forename: Ulf
authors.initials: U
authors.lastname: Schött
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood* / Q000188:drug therapy; D000241:Adenosine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D000368:Aged; D000369:Aged, 80 and over; D001241:Aspirin / Q000627:therapeutic use*; D016022:Case-Control Studies; D003131:Combined Modality Therapy; D005260:Female; D006487:Hemostasis; D006706:Homeostasis; D006801:Humans; D007036:Hypothermia, Induced; D008297:Male; D008875:Middle Aged; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D000077486:Ticagrelor; D016896:Treatment Outcome
chemical_list: D010975:Platelet Aggregation Inhibitors; D000077486:Ticagrelor; D000241:Adenosine; D001241:Aspirin
keywords: Induced hypothermia; antiplatelet drugs; blood coagulation; flow cytometry; platelet aggregation; platelet function tests