Key result
Elevated prostacyclin (PGI2) degradation was directly related to intravascular platelet activation, suggesting it may be a risk factor for thromboembolic events in cerebrovascular disorders.
Why the study?
Is elevated velocity of prostacyclin degradation in blood associated with intravascular platelet activation in patients with cerebrovascular disorders?
Observational (n=280)
Is elevated velocity of prostacyclin degradation in blood associated with intravascular platelet activation in patients with cerebrovascular disorders?
Elevated prostacyclin degradation in blood may serve as a risk factor for thromboembolic events in patients with cerebrovascular disorders.
May warrant biomarker validation; leaves open causal role in thromboembolic risk pending prospective studies.
Blood and plasma from 193 patients at risk of cerebrovascular disorders and 87 patients with brain infarction were tested to study prostacyclin (PGI2) degradation. It has been reported that patients at risk for cerebrovascular disorders and especially with brain infarction have an enhanced velocity of PGI2 degradation. The increase in velocity was more marked in blood than in plasma. A direct relation between this enhancement and the manifestation of intravascular platelet activation was observed. These data suggest that elevated PGI2 degradation might be a risk factor for thromboembolic events in patients with cerebrovascular disorders.
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Akopov et al. (2008) conducted an observational in Cerebrovascular disorders and brain infarction (n=280). Elevated prostacyclin (PGI2) degradation was evaluated on Intravascular platelet activation. Elevated prostacyclin (PGI2) degradation was directly related to intravascular platelet activation, suggesting it may be a risk factor for thromboembolic events in cerebrovascular disorders.
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