Platelet function abnormalities in response to arachidonic acid in the acute phase of myocardial infarction.
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 less than 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 B2 formation correlated with the response of patients' platelets to arachidonic acid (38 +/- 15 ng in the low responders versus 161 +/- 30 ng/3 X 10(8) platelets/4 min in the normal responders, p less than 0.05). Low responding platelets after washing had normal adenosine diphosphate and adenosine triphosphate contents and aggregated and formed thromboxane B2 normally with arachidonic acid. The plasma of patients with MI was found to inhibit platelet aggregation and thromboxane B2 formation to arachidonic acid.
D000244:Adenosine Diphosphate / Q000097:blood; D000255:Adenosine Triphosphate / Q000097:blood; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000494:pharmacology*; D001792:Blood Platelets / Q000187:drug effects* / Q000378:metabolism; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D008297:Male; D009203:Myocardial Infarction / Q000097:blood*; D010974:Platelet Aggregation / Q000187:drug effects*; D013929:Thromboxane B2 / Q000096:biosynthesis; D013997:Time Factors
D001095:Arachidonic Acids; D016718:Arachidonic Acid; D013929:Thromboxane B2; D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate