Pronounced platelet hyperfunction in patients with cardiac arrest achieving restoration of spontaneous circulation.
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.
Spiel
Alexander O
AO
Departments of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria.
Frossard
Martin
M
Mayr
Florian B
FB
Kliegel
Andreas
A
Janata
Andreas
A
Uray
Thomas
T
Wandaller
Cosima
C
Sterz
Fritz
F
Jilma
Bernd
B
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