OBJECTIVE: To investigate the occurrence of aspirin resistance in coronary heart disease (CHD) patients and its influence on myonecrosis among patients undergoing non-emergent percutaneous coronary intervention (PCI). METHODS: 256 CHD patients who have been on aspirin (100 mg/d) for at least 7 days were recruited based on aspirin responsiveness determination. All the patients were divided into two groups: aspirin-resistant group and aspirin-sensitive group. For all patients scheduled for non-emergent PCI, a loading dose of 300 mg of clopidogrel was given at least 12 h before PCI and a 75 mg maintenance dose was given every morning before and after PCI. The incidence of myonecrosis was evaluated by the levels of creatine kinase-myocardial band (CK-MB) and troponin I (TnI) before and after PCI. RESULTS: Aspirin resistance was found in 67 (26.2%) patients and 189 (73.8%) patients were aspirin-sensitive. There was a significantly higher proportion of female subjects in the aspirin-resistant group. The incidence of any CK-MB elevation was 38 (56.7%) in aspirin-resistant group and 42 (22.2%) in aspirin-sensitive group (P < 0.01). The elevation of TnI was observed in 41 (61.2%) of the aspirin-resistant group and in 67 (35.4%) of the aspirin-sensitive group (P < 0.05). Multivariate analysis revealed that aspirin resistance was an independent predictor for CK-MB elevation after PCI (OR = 2.5; 95% CI 1.5 to 6.5; P < 0.05). CONCLUSION: Aspirin resistance exists in some CHD patients, which increases the risk of myonecrosis following non-emergent PCI.
OBJECTIVE: To investigate the occurrence of aspirin resistance in coronary heart disease (CHD) patients and its influence on myonecrosis among patients undergoing non-emergent percutaneous coronary intervention (PCI). METHODS: 256 CHD patients who have been on aspirin (100 mg/d) for at least 7 days were recruited based on aspirin responsiveness determination. All the patients were divided into two groups: aspirin-resistant group and aspirin-sensitive group. For all patients scheduled for non-emergent PCI, a loading dose of 300 mg of clopidogrel was given at least 12 h before PCI and a 75 mg maintenance dose was given every morning before and after PCI. The incidence of myonecrosis was evaluated by the levels of creatine kinase-myocardial band (CK-MB) and troponin I (TnI) before and after PCI. RESULTS:Aspirin resistance was found in 67 (26.2%) patients and 189 (73.8%) patients were aspirin-sensitive. There was a significantly higher proportion of female subjects in the aspirin-resistant group. The incidence of any CK-MB elevation was 38 (56.7%) in aspirin-resistant group and 42 (22.2%) in aspirin-sensitive group (P < 0.01). The elevation of TnI was observed in 41 (61.2%) of the aspirin-resistant group and in 67 (35.4%) of the aspirin-sensitive group (P < 0.05). Multivariate analysis revealed that aspirin resistance was an independent predictor for CK-MB elevation after PCI (OR = 2.5; 95% CI 1.5 to 6.5; P < 0.05). CONCLUSION:Aspirin resistance exists in some CHD patients, which increases the risk of myonecrosis following non-emergent PCI.