Key result
Unfractionated heparin drives a ~7% absolute increase in platelet-monocyte aggregation via P-selectin.
Why the study?
Does unfractionated heparin increase platelet-monocyte aggregation compared to fractionated heparins or direct thrombin inhibitors in healthy volunteers and PCI patients?
Population
18 healthy volunteers and 28 patients scheduled for elective percutaneous coronary intervention
Comparison
Unfractionated heparin vs Enoxaparin, lepirudin, bivalirudin, and controls
Design
Other
Authors
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May explain differential PCI outcomes with heparins; hypothesis-generating for P-selectin modulation in anticoagulation.
Does unfractionated heparin increase platelet-monocyte aggregation compared to fractionated heparins or direct thrombin inhibitors in healthy volunteers and PCI patients?
Absolute Event Rate: 20.1% vs 16.2%
p-value: p=<0.001
Unfractionated heparin promotes proinflammatory platelet-monocyte aggregation via a P-selectin-dependent mechanism, providing a potential mechanistic explanation for the superior cardiovascular outcomes associated with fractionated heparins and direct thrombin inhibitors.
Harding et al. (2006) studied Scheduled for elective PCI (n=46). Unfractionated heparin vs. Controls (in vitro) and bivalirudin (in vivo) was evaluated on Platelet-monocyte aggregates (in vitro) (p=<0.001). Unfractionated heparin significantly increased platelet-monocyte aggregation both in vitro (20.1% vs 16.2%, P<0.001) and in vivo (absolute increase 7.1%, P<0.01) via a P-selectin mechanism.
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