BACKGROUND: Current evidence supports the preventive role of statins on platelet aggregation in patients with coronary heart disease. AIM: Our aim was to determine the effects of aggressive statin therapy on platelet function in patients with coronary heart disease. MATERIAL AND METHODS: A total of 178 consecutive patients (37-68 years old, 35.9% women) with stable coronary artery disease (CAD) was enrolled in the study. Platelet function assays were realized by the Platelet Function Analyzer (PFA)-100 with collagen and epinephrine (Col/Epi) and collagen and ADP (Col/ADP) cartridges. Aspirin resistance was defined as having a closure time (CT) of <186 s with Col/Epi cartridges despite regular aspirin therapy. A statin therapy protocol applied to the patients with aspirin resistance for 3 months. RESULTS: We determined that 20 (11.2%) of patients had aspirin resistance by the PFA-100. Mean closure time measured with the Col/ADP cartridges was 83 +/- 18 s (53-162 s). Of the patients 12 were not on a statin therapy and eight were taking 10 mg daily atorvastatin. After 3 months of 40 mg daily atorvastatin therapy 13 subjects with aspirin resistance became aspirin sensitive by PFA-100 (P < 0.0001). There was also a significant decrease in total and LDL cholesterol levels and an increase in HDL cholesterol at the third month of statin therapy (P < 0.0001 for all). CONCLUSION: Statin therapy reduced the in vitro aspirin resistance in 65% of the patients after a therapy of 3 months. Further studies are needed to elucidate the mechanism of statins' effects on platelet reactivity.
BACKGROUND: Current evidence supports the preventive role of statins on platelet aggregation in patients with coronary heart disease. AIM: Our aim was to determine the effects of aggressive statin therapy on platelet function in patients with coronary heart disease. MATERIAL AND METHODS: A total of 178 consecutive patients (37-68 years old, 35.9% women) with stable coronary artery disease (CAD) was enrolled in the study. Platelet function assays were realized by the Platelet Function Analyzer (PFA)-100 with collagen and epinephrine (Col/Epi) and collagen and ADP (Col/ADP) cartridges. Aspirin resistance was defined as having a closure time (CT) of <186 s with Col/Epi cartridges despite regular aspirin therapy. A statin therapy protocol applied to the patients with aspirin resistance for 3 months. RESULTS: We determined that 20 (11.2%) of patients had aspirin resistance by the PFA-100. Mean closure time measured with the Col/ADP cartridges was 83 +/- 18 s (53-162 s). Of the patients 12 were not on a statin therapy and eight were taking 10 mg daily atorvastatin. After 3 months of 40 mg daily atorvastatin therapy 13 subjects with aspirin resistance became aspirin sensitive by PFA-100 (P < 0.0001). There was also a significant decrease in total and LDL cholesterol levels and an increase in HDL cholesterol at the third month of statin therapy (P < 0.0001 for all). CONCLUSION: Statin therapy reduced the in vitro aspirin resistance in 65% of the patients after a therapy of 3 months. Further studies are needed to elucidate the mechanism of statins' effects on platelet reactivity.
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