NEW YORK (Reuters Health) – The antiplatelet effect of clopidogrel is much reduced in patients undergoing therapeutic hypothermia after cardiac arrest, according to a Norwegian study published online August 19th in Resuscitation.

Dr. Thor Wilhelm Bjelland at the Norwegian University of Science and Technology in Trondheim, and colleagues note that guidelines recommend therapeutic hypothermia for comatose patients after successful resuscitation from cardiac arrest, and that clopidogrel is indicated for the subset of these patients with myocardial infarction.

However, inhibited gastrointestinal function and slowed metabolism during hypothermia might attenuate the effect of clopidogrel. To investigate that possibility, the researchers studied platelet reactivity in 25 patients treated with therapeutic hypothermia and clopidogrel given enterally with a loading dose of 300-600 mg followed by 75 mg/d.

Blood samples collected on day 1 and 3 were analyzed for inhibition by clopidogrel using the VSP phosphorylation method. Mean core temperatures on those two days were 33.2 and 37.5 degrees C, respectively.

An adequate antiplatelet effect was defined as a platelet reactivity index <0.5. Dr. Bjelland and colleagues found that the mean index was 0.77 on day 1 and 0.57 on day 3. “Zero day 1 samples, and five day 3 samples had platelet reactivity index <0.5.” The investigators conclude, “In patients treated with therapeutic hypothermia after cardiac arrest, the effect of clopidogrel on platelets was virtually nonexistent on day 1 after administration, with some improvement on day 3.” They say this is a matter of concern, “in the light of recent studies showing a clear relation between low responsiveness (to clopidogrel) and cardiovascular events” Reference:
Antiplatelet effect of clopidogrel is reduced in patients treated with therapeutic hypothermia after cardiac arrest

Resuscitation 2010.