What does this research mean for the field?

Chronic kidney disease independently causes high residual platelet reactivity under standard clopidogrel therapy, increasing mortality risk, but this biological resistance can be effectively overcome with newer P2Y12 antagonists like ticagrelor. Novelty: ClaimNovelty.SYNTHESIS. Consensus alignment: ConsensusAlignment.NEUTRAL.

March 8, 2013Nephrology Dialysis TransplantationOpen Access

Impaired platelet P2Y12 inhibition by thienopyridines in chronic kidney disease: mechanisms, clinical relevance and pharmacological options

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Population

Patients with chronic kidney disease undergoing percutaneous coronary intervention or treated for acute…

Design

Review

Authors

OMOlivier MorelInterventional / Structural Cardiology CMC. MüllerEM Strasbourg Business School

Laurence JeselElectrophysiology

Discussion

Member takes

Implication

Supports exploring ticagrelor in CKD-ACS/PCI; hypothesis-generating pending dedicated RCTs.

Structured PICO

Population

Patients with chronic kidney disease (CKD) undergoing percutaneous coronary intervention (PCI) or treated for acute coronary syndrome (ACS)

Intervention

Anti-platelet therapy including thienopyridines (clopidogrel, prasugrel), ticagrelor, and cilostazol

In CKD patients with ACS or undergoing PCI, impaired platelet inhibition by standard thienopyridines is common, suggesting that newer agents like ticagrelor may be preferred to overcome biological resistance and reduce ischemic events.

Cite This Study

Morel et al. (2013) studied this question.

synapsesocial.com/papers/6a1df12ccd67cee373350bb3 https://doi.org/10.1093/ndt/gft027

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