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Summary Background Recent studies have suggested that ticagrelor 90 mg twice daily provides stronger platelet inhibition than prasugrel 10 mg once daily in acute coronary syndrome patients undergoing percutaneous coronary intervention. Objectives To compare the effects of ticagrelor 90 mg twice daily and prasugrel 10 mg once daily on platelet reactivity in patients with ST-segment elevation myocardial infarction (STEMI), using: the VerifyNow ® P2Y 12 (VN-P2Y 12 ) assay, expressed in P2Y 12 reaction units (PRU); measurement of the vasodilator-stimulated phosphoprotein platelet reactivity index (VASP-PRI; %); and light transmission aggregometry (LTA), expressed as residual platelet aggregation (RPA; %). Methods Platelet reactivity was evaluated prospectively using the three assays 30 days after primary PCI in 118 patients with STEMI on a maintenance dose of prasugrel 10 mg once daily ( n = 60) or ticagrelor 90 mg twice daily ( n = 58). Results On-treatment platelet reactivity, assessed by the VN-P2Y 12 assay, was lower for ticagrelor compared with prasugrel (20.91 ± 4.59 PRU vs. 43.50 ± 6.98 PRU; P = 0.008) but was not significantly different when using the more specific VASP-PRI assay (13.05 ± 1.61% vs. 17.44 ± 1.97%; P = 0.09) or RPA assessed by LTA (10.49 ± 1.44% vs. 7.20 ± 1.27%; P = 0.09). Conclusions The difference in platelet reactivity between ticagrelor and prasugrel varies according to the platelet function test in patients with STEMI. The differences observed may be related more to the tests than to the drugs used.

Objectives: This study sought to determine whether red blood cell (RBC) transfusion increases in vivo platelet aggregation and inflammation in coronary and noncoronary patients.Background: RBC tran...

Objectives: This study sought to determine whether the pharmacokinetic (PK) and pharmacodynamic (PD) responses to high or standard clopidogrel loading doses (LDs) differ according to CYP2C19*2 alle...

SummaryThe FXIII-A Leu34 genetic variant increases and accelerates fibrin stabilisation; however, its association with premature coronary artery disease (CAD) and thrombotic events remains controversial. FXIII Val34Leu genotype was determined in 242 young individuals (

Aim To explore platelet reactivity on dual antiplatelet therapy (DAPT) of acute coronary syndrome (ACS) patients infected with HIV. Methods and results Acute coronary syndrome patients infected with HIV ( n = 80) were matched to ACS patients without HIV ( n = 160) on age, sex, diabetes, and DAPT (aspirin 100%, clopidogrel 68%, prasugrel 31%, ticagrelor 1%). Platelet reactivity was evaluated after ACS (>30 days) by measuring residual platelet aggregation (RPA) to aspirin and to P2Y12 inhibitors with light transmission aggregometry (LTA), VerifyNow aspirin assay (ARU), and P2Y12 assay (PRU) and with the VASP platelet reactivity index (VASP-PRI). Proportion of patients with high residual platelet reactivity (HPR) was evaluated. HIV-infected ACS patients had higher levels of platelet reactivity in response to P2Y12 inhibitors (RPA: 23.8 ± 2.7% vs. 15.3 ± 1.3%; P = 0.001; PRU: 132 ± 10 vs. 107.4 ± 6.6; P = 0.04; and VASP-PRI: 45.2 ± 2.6% vs. 32.0 ± 2.0%; P

ObjectivesThis study evaluated the ability of the bedside test Hemochron Jr. Hemonox (International Technidyne Corporation, Edison, New Jersey) to identify patients with insufficient anti-Xa activity level in the catheterization laboratory.BackgroundInadequate anticoagulation in patients undergoing percutaneous coronary intervention (PCI) is associated with increased periprocedural ischemic events.MethodsIn 296 unselected patients undergoing catheterization and/or PCI, whole blood Hemonox clotting time (CT) and activated partial thromboplastin time (aPTT) were measured at baseline (T1) and 10 min after the intravenous administration of enoxaparin (T2) in patients receiving additional enoxaparin and compared with plasma chromogenic anti-Xa activity level.ResultsMedian values were 0.1 IU/ml (interquartile range [IQR]: 0.1 to 0.1 IU/ml) and 0.87 IU/ml (IQR: 0.74 to 1.03 IU/ml) for anti-Xa; 74 s (IQR: 70 to 81 s) and 143 s (IQR: 114 to 206 s) for Hemonox CT; and 44 s (IQR: 39 to 50 s) and 72 s (IQR: 58 to 93 s) for aPTT at T1 and T2, respectively. When using Hemonox CT to discriminate patients with anti-Xa level

High on-treatment platelet reactivity is an independent risk factor of major adverse cardiovascular events following percutaneous coronary intervention or Acute Coronary Syndrome (ACS). HIV-infected patients have a higher risk of recurrent events after ACS than HIV uninfected patients. We

BackgroundInadequate anticoagulation in patients undergoing percutaneous coronary Intervention (PCI) is associated with more frequent periprocedural ischemic events.MethodsWe evaluated the ability of the bedside Hemonox test to identify patients with an anti-Xa activity level out of the therapeutic range in 296 unselected patients undergoing catheterization and/or PCI. Bedside measure of whole blood Hemonox Clotting Time (CT) and activated Partial Prothrombin Time (aPTT) were measured at baseline (T1) and 10’ after the IV administration of enoxaparin (T2) in patients receiving additional enoxaparin and compared to differed plasma chromogenic anti-Xa (AXA) activity measurement.ResultsMedian [IQR] values were 0.1 [0.1-0.1] and 0.87 [0.74-1.03] IU/mL for AXA; 74 [70-81] and 143 [114-206] sec for Hemonox CT, and 44 [39-50] and 72 [58-93] sec for aPTT at T1 and T2 time points, respectively. Hemonox CT strongly correlated with Anti-Xa level spearman r=0.81 (95% CI 0.77-0.84, p