Key result
In ACS patients on dual antiplatelet therapy, moderate/severe chronic kidney disease was associated with a higher prevalence of high residual platelet reactivity (21.4% vs 1.7%; OR 15.91, P<0.001).
Why the study?
Conflicting results exist regarding platelet response in CKD patients with stable coronary artery disease, and the impact of CKD on platelet aggregation in ACS patients receiving dual antiplatelet therapy remained unclear.
Does chronic kidney disease increase platelet aggregation and high residual platelet reactivity in patients with acute coronary syndrome receiving dual antiplatelet therapy?
Observational (n=206)
Does chronic kidney disease increase platelet aggregation and high residual platelet reactivity in patients with acute coronary syndrome receiving dual antiplatelet therapy?
Odds Ratio: 15.91 (95% CI 3.71–68.17)
Absolute Event Rate: 21.4% vs 1.7%
p-value: p=<0.001
In patients with acute coronary syndrome on dual antiplatelet therapy, chronic kidney disease is associated with increased platelet aggregation and a higher prevalence of high residual platelet reactivity, which is strongly correlated with clopidogrel use.
CKD-associated high residual platelet reactivity on DAPT in ACS warrants no practice change; leaves open prospective outcome trials.
AIMS: Chronic kidney disease (CKD) is associated with increased thrombotic events and seems to influence platelet reactivity. Conflicting results have been published on platelet response in CKD patients with stable coronary artery disease. The aim of our study was to investigate the impact of CKD on platelet aggregation in acute coronary syndrome (ACS) patients receiving dual antiplatelet therapy, included the more potent P2Y12 inhibitors. METHODS: We enrolled 206 patients with ACS, divided in two groups, according to the presence or the absence of moderate/severe CKD. Platelet aggregation was performed with light transmission aggregometry and results are expressed as percentage of maximum platelet aggregation. High residual platelet reactivity (HRPR) was defined as maximum platelet aggregation more than 59%. RESULTS: Patients with CKD [estimate glomerular filtration rate (eGFR) < 60 ml/min/1.73 m, n = 28] were prevalent older, diabetic, had previous coronary revascularization. In these patients, platelet aggregation was significantly higher than in those with eGFR ≥ 60 ml/min/1.73 m (ADP 10 μmol/l: 28.46 ± 26.19 vs. 16.64 ± 12.79, P < 0.001; ADP 20 μmol/l: 30.07 ± 25.89 vs. 17.46 ± 12.82, P < 0.001). HRPR was observed in 4.4% of patients, with higher prevalence in those with eGFR less than 60 ml/min/1.73 m [21.4 vs. 1.7%, P < 0.001, odds ratio (OR) [95% confidence interval (CI)] = 15.91 (3.71-68.17), P < 0.001]. At multivariate analysis, after correction for baseline confounders, eGFR [adjusted OR (95% CI) = 0.95 (0.91-0.98), P = 0.007], together with the use of clopidogrel [adjusted OR (95% CI) = 23.59 (4.01-138.82), P < 0.001], emerged as determinants of HRPR. CONCLUSION: In patients with ACS receiving dual antiplatelet therapy, CKD is associated with an increasing ADP-induced platelet aggregation and higher prevalence of HRPR, which is mainly correlated to clopidogrel use.
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Ilardi et al. (2020) conducted an observational in Acute coronary syndrome (n=206). Moderate/severe chronic kidney disease (eGFR < 60 ml/min/1.73 m2) vs. Absence of moderate/severe chronic kidney disease (eGFR ≥ 60 ml/min/1.73 m2) was evaluated on High residual platelet reactivity (HRPR) (OR 15.91, 95% CI 3.71-68.17, p=<0.001). In ACS patients on dual antiplatelet therapy, moderate/severe chronic kidney disease was associated with a higher prevalence of high residual platelet reactivity (21.4% vs 1.7%; OR 15.91, P<0.001).
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