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Comment
. 2021 Jun 14;42(23):2311-2312.
doi: 10.1093/eurheartj/ehaa905.

Because of its association with major bleeding the ADP-binding enzyme creatine kinase should be estimated in studies of patients treated for non-ST-segment elevation acute coronary syndromes (NSTE-ACS)

Lizzy M Brewster  1
Affiliations
Comment

Because of its association with major bleeding the ADP-binding enzyme creatine kinase should be estimated in studies of patients treated for non-ST-segment elevation acute coronary syndromes (NSTE-ACS)

Lizzy M Brewster. Eur Heart J. .
No abstract available

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Figures

Figure 1
Figure 1
Potential inhibitory role of creatine kinase (CK) in platelet aggregation. Central to the development of acute coronary syndromes (ACS) is plaque rupture or erosion resulting in platelet activation, aggregation, and thrombosis. Activated platelets release substances including adenosine diphosphate (ADP) and thromboxane A2 (TXA2) synthesized from arachidonic acid (AA) through prostaglandin (PG) catalyzed by cyclooxygenase-1 (COX1). ADP and TXA2 amplify the response to injury and produce sustained platelet aggregation. ADP is considered to be central to platelet activation.  ,   ADP-stimulation of the P2Y1 receptor activates phospholipase C resulting in weak, transient platelet aggregation, while P2Y12 receptor activation results in the activation of glycoprotein receptors IIb/IIIa [integrin (I)-αIIbβ3] and firm platelet aggregation.  ,   CK strongly binds ADP and reduces platelet aggregation in the presence of phosphocreatine (CrP), in an effect that resembles that of P2Y12 receptor blockers such as clopidogrel.  ,   The enzyme might act in synergy with antithrombotic and fibrinolytic drugs to increase bleeding risk in ACS.  ,   ATP, adenosine triphosphate.
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References

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