Key result
Intravenous administration of unfractionated heparin significantly enhanced platelet aggregation and increased platelet volume, indicating in vivo platelet activation.
Why the study?
Does intravenous administration of unfractionated heparin cause in vivo platelet activation in healthy volunteers?
Does intravenous administration of unfractionated heparin cause in vivo platelet activation in healthy volunteers?
Intravenous administration of unfractionated heparin induces in vivo platelet activation in healthy volunteers, providing mechanistic insight into heparin-associated platelet effects.
May warrant caution with IV heparin in at-risk patients; hypothesis-generating and requires validation in cardiovascular cohorts.
In view of the evidence that unfractionated heparins (UH) cause thrombocytopenia in vivo and platelet activation in vitro, we investigated the effect of UH administration on platelet indices likely to reflect in vivo activation. Our experiments, in healthy volunteers, show that following the intravenous administration of UH: (1) platelet aggregation in whole blood is significantly enhanced; (2) platelet counts in platelet rich plasma (PRP), prepared using citrate as anticoagulant, are significantly diminished; this effect is not observed in PRP prepared from blood anticoagulated with EDTA or in the whole blood itself and (3) the modal and median platelet volume increases significantly. We conclude that some degree of platelet activation occurs after the intravenous injection of UH.
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Mikhailidis et al. (1990) studied Healthy volunteers. Intravenous unfractionated heparin (UH) was evaluated on Platelet indices reflecting in vivo activation (platelet aggregation, platelet counts, and platelet volume). Intravenous administration of unfractionated heparin significantly enhanced platelet aggregation and increased platelet volume, indicating in vivo platelet activation.