title: Pronounced platelet hyperfunction in patients with cardiac arrest achieving restoration of spontaneous circulation.
abstract: OBJECTIVE
  Markers of platelet activation are increased in patients undergoing cardiopulmonary resuscitation. Hyperfunctional platelets may contribute to impairment of microcirculatory function and overall poor outcome despite restoration of spontaneous circulation (ROSC). Patients with myocardial infarction have hyperfunctional platelets, which predict the degree of myocardial necrosis. Thus, we hypothesized that platelets may be even more activated in patients whose myocardial infarction leads to cardiac arrest and compared them with patients whose cardiac arrest was due to a noncardiac origin.
  
  
  METHODS
  Prospective observational study.
  
  
  METHODS
  Emergency department of a tertiary care hospital.
  
  
  METHODS
  One hundred four patients with witnessed cardiac arrest who achieved ROSC.
  
  
  METHODS
  Blood sampling.
  
  
  RESULTS
  We assessed collagen adenosine diphosphate closure time with the platelet function analyzer-100, and measured plasma levels of von Willebrand factor: ristocetin cofactor activity levels by turbidometry. Independent physicians diagnosed the origin of cardiac arrest. The majority of cardiac arrests were caused by myocardial ischemia. Invariably, collagen adenosine diphosphate closure time values (55 seconds; 95% confidence interval: 52-58 seconds) were much shorter in these patients compared with patients with other causes of cardiac arrest (110 seconds; 95% confidence interval: 84-135 seconds, p < 0.001). von Willebrand factor: ristocetin cofactor activity plasma levels were more than three-fold above normal values in both groups.
  
  
  CONCLUSIONS
  Patients with myocardial ischemia-triggered cardiac arrest had the highest degree of platelet hyperfunction under high shear rates, which was not solely due to increased von Willebrand factor. Future trials are necessary to clarify whether rapid, more aggressive antiplatelet therapy improves outcome after cardiac arrest.
authors.affiliation: Departments of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria.
authors.forename: Alexander O
authors.initials: AO
authors.lastname: Spiel
authors.forename: Martin
authors.initials: M
authors.lastname: Frossard
authors.forename: Florian B
authors.initials: FB
authors.lastname: Mayr
authors.forename: Andreas
authors.initials: A
authors.lastname: Kliegel
authors.forename: Andreas
authors.initials: A
authors.lastname: Janata
authors.forename: Thomas
authors.initials: T
authors.lastname: Uray
authors.forename: Cosima
authors.initials: C
authors.lastname: Wandaller
authors.forename: Fritz
authors.initials: F
authors.lastname: Sterz
authors.forename: Bernd
authors.initials: B
authors.lastname: Jilma
mesh_terms: D000328:Adult; D003326:Coronary Circulation; D005260:Female; D006323:Heart Arrest / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications; D015539:Platelet Activation; D011446:Prospective Studies