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Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Influence of Chronic Kidney Disease on Platelet Reactivity Response to Clopidogrel and Ticagrelor
André Franci1,2, Roberto Giraldez1, Carlos Barbosa3
1Instituto do Coracao (InCor), Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo CEP 05403-000, Brazil.
Insights
Chronic kidney disease (CKD) impairs clopidogrel effectiveness, increasing high platelet reactivity (HPR). Ticagrelor maintains low platelet reactivity in CKD patients, offering a significant advantage over clopidogrel for managing ischemic risk.
Area of Science:
- Cardiology
- Pharmacology
- Nephrology
Background:
- High platelet reactivity (HPR) in patients with coronary artery disease (CAD) on P2Y12 inhibitors is linked to increased ischemic risk.
- Chronic kidney disease (CKD) is recognized as a factor contributing to HPR, particularly with clopidogrel therapy.
Purpose of the Study:
- To investigate the impact of CKD on platelet reactivity (PR) in patients treated with either clopidogrel or ticagrelor.
- To compare the efficacy of clopidogrel versus ticagrelor in managing PR in patients with and without CKD.
Main Methods:
- A double-blind, double-dummy study involving 106 stable patients post-acute coronary syndrome.
- Patients were randomized to receive either clopidogrel or ticagrelor and were stratified based on the presence or absence of CKD.
- Platelet reactivity was assessed using the VerifyNow™ P2Y12 assay, with HPR defined as P2Y12 reaction units (PRU) ≥ 208.
Main Results:
- Ticagrelor demonstrated consistent low PR in both non-CKD (36 PRU) and CKD (35 PRU) groups.
- Clopidogrel showed a trend towards higher PR in CKD patients (209 PRU) compared to non-CKD patients (180 PRU).
- High platelet reactivity was significantly more prevalent with clopidogrel in CKD patients (adjusted OR 4.42, p=0.01).
Conclusions:
- CKD significantly reduces responsiveness to clopidogrel, leading to higher PR and increased HPR.
- Ticagrelor effectively controls PR irrespective of CKD status, suggesting a superior therapeutic option for CKD patients.
- The findings highlight a greater relative benefit of ticagrelor over clopidogrel in patients with CKD and CAD on P2Y12 inhibitors.
Abstract:
High platelet reactivity (HPR) in patients with coronary artery disease receiving P2Y12 inhibitors increases ischemic risk. Chronic kidney disease (CKD) is an established contributor to HPR during clopidogrel therapy. The objective of the study was to assess whether CKD influences platelet reactivity (PR) in patients treated with clopidogrel or ticagrelor. This double-blind, double-dummy study enrolled 106 stable patients more than one year after an acute coronary syndrome, with or without CKD. Participants were matched by age and sex and randomized to clopidogrel or ticagrelor. PR was measured using the VerifyNow™ P2Y12 assay, and HPR was defined as P2Y12 reaction units (PRU) ≥ 208. Median glomerular filtration rates were 80 mL/min/1.73 m2 in non-CKD patients and 41 mL/min/1.73 m2 in CKD patients (p < 0.01). Ticagrelor produced similarly low PR in both groups (36 vs. 35 PRU; p = 0.61). Clopidogrel resulted in a numerically higher PR in CKD patients (209 vs. 180 PRU; p = 0.07). The magnitude of PR reduction with ticagrelor relative to clopidogrel was greater in CKD patients (p-interaction = 0.09). HPR was markedly more common with clopidogrel, particularly in CKD (difference 37%; adjusted OR 4.42; p = 0.01). In conclusion, CKD significantly impairs clopidogrel responsiveness but does not affect ticagrelor, resulting in a greater relative advantage of ticagrelor in patients with CKD.
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