Platelet function abnormalities in response to arachidonic acid in the acute phase of myocardial infarction

Academic Article


  • The aggregation of platelets to arachidonic acid was studied serially in patients admitted to the hospital with suspected acute myocardial infarction (MI) and no history of platelet-altering drug ingestion. Of 17 patients studied within the first 48 hours after MI, 16 had a marked decrease in aggregation, to 0.5 mM arachidonic acid (15 ± 12% compared with 64 ±15% for control subjects, p < 0.01). The exception was a patient with documented coronary artery spasm who was receiving nifedipine at the time of MI. He had a delayed but normal final percent aggregation. The aggregation response returned to normal at 2 to 4 days and was slightly above normal at 6 to 10 days (change not statistically significant). Thromboxane B formation correlated with the response of patients' platelets to arachidonic acid (38 ± 15 ng in the low responders versus 161 ± 30 ng/3 × 10 platelets/4 min in the normal responders, p < 0.05). Low responding platelets after washing had normal adenosine diphosphate and adenosine triphosphate contents and aggregated and formed thromboxane B normally with arachidonic acid. The plasma of patients with MI was found to inhibit platelet aggregation and thromboxane B formation to arachidonic acid. © 1983. 2 2 2 8
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    Digital Object Identifier (doi)

    Author List

  • McDaniel HG; Maddox WT; Poon MC; Rogers WJ; Rackley CE
  • Start Page

  • 965
  • End Page

  • 968
  • Volume

  • 52
  • Issue

  • 8