BACKGROUND: Our aim was to prospectively assess the potential influence of pantoprazole therapy on the antiplatelet effects of acetylsalicylic acid (ASA) and clopidogrel (CLO) in stable angina pectoris (SAP) patients after percutaneous coronary intervention (PCI). METHODS:Forty-four patients with SAP (CCS I-III) and successful PCI with stent implantation were enrolled into the study. The patients were divided into group proton pump inhibitors (PPI): 23 patients with indications for PPI (F/M = 9/14; age = 64 ± 9; standard therapy + 20 mg pantoprazole) and the control group (group C): 21 patients (F/M = 6/15; age = 64 ± 8; standard therapy). The platelet function analysis in whole blood based on impedance aggregometry (ASPI, COL, ADP, TRAP tests) using Multiplate--V2.02.11 was performed 18-24 h after the PCI + CLO loading dose (600 mg) and 30 days after PCI. RESULTS: Both baseline patient characteristics and clinical outcomes were comparable between the study groups. There were no differences in the mean values of the platelets (PTL) tests measured at the 30(th) day after PCI between both groups (PPI vs. C: ASPI: 24.6 ± 10.0 vs. 42.1 ± 14.8 U, COL: 32.9 ± 8.6 vs. 34.0 ± 7.7 U, ADP: 26.8 ± 12.4 vs. 30.4 ± 8.1 U, TRAP: 78.7 ± 16.6 vs. 78.1 ± 22.6 U, p = ns). The mean delta values of the PTL tests (18-24 h post-PCI/30 days post-PCI) were also comparable between the groups. The PTL aggregometry results were related to time (ADP, ASPI, TRAP vs. time, p = 0.001; COL vs. time, p = 0.03)--the baseline values of ADP, ASPI, COL and TRAP tests were smaller than those measured after the one-month observation. CONCLUSION:Pantoprazole treatment does not impair the efficacy of dual antiplatelet therapy in patients with SAP after PCI.
RCT Entities:
BACKGROUND: Our aim was to prospectively assess the potential influence of pantoprazole therapy on the antiplatelet effects of acetylsalicylic acid (ASA) and clopidogrel (CLO) in stable angina pectoris (SAP) patients after percutaneous coronary intervention (PCI). METHODS: Forty-four patients with SAP (CCS I-III) and successful PCI with stent implantation were enrolled into the study. The patients were divided into group proton pump inhibitors (PPI): 23 patients with indications for PPI (F/M = 9/14; age = 64 ± 9; standard therapy + 20 mg pantoprazole) and the control group (group C): 21 patients (F/M = 6/15; age = 64 ± 8; standard therapy). The platelet function analysis in whole blood based on impedance aggregometry (ASPI, COL, ADP, TRAP tests) using Multiplate--V2.02.11 was performed 18-24 h after the PCI + CLO loading dose (600 mg) and 30 days after PCI. RESULTS: Both baseline patient characteristics and clinical outcomes were comparable between the study groups. There were no differences in the mean values of the platelets (PTL) tests measured at the 30(th) day after PCI between both groups (PPI vs. C: ASPI: 24.6 ± 10.0 vs. 42.1 ± 14.8 U, COL: 32.9 ± 8.6 vs. 34.0 ± 7.7 U, ADP: 26.8 ± 12.4 vs. 30.4 ± 8.1 U, TRAP: 78.7 ± 16.6 vs. 78.1 ± 22.6 U, p = ns). The mean delta values of the PTL tests (18-24 h post-PCI/30 days post-PCI) were also comparable between the groups. The PTL aggregometry results were related to time (ADP, ASPI, TRAP vs. time, p = 0.001; COL vs. time, p = 0.03)--the baseline values of ADP, ASPI, COL and TRAP tests were smaller than those measured after the one-month observation. CONCLUSION:Pantoprazole treatment does not impair the efficacy of dual antiplatelet therapy in patients with SAP after PCI.