BACKGROUND: Aspirin protects from cardiovascular events. However, a number of patients who take this drug suffer events, probably due to aspirin resistance. The role of certain biologic variables that may affect resistance is still uncertain. AIM: To determine the prevalence of aspirin resistance in patients taking this drug and to test if resistance is related to haemostatic, inflammatory and lipidic variables. METHODS: Platelet function measured with PFA-100 was studied in 268 patients (185 men) with stable coronary disease who took aspirin (100 to 300 mg/day). Aspirin resistance was defined when epinephrine closure time <174 s. Results of lipoprotein(a) are expressed in median (interquartile range). RESULTS: Aspirin resistance was found in 16% of cases. Patients with aspirin resistance had higher levels of Apolipoprotein B (109.27+/-27.65 vs 100.92+/-23.77 mg/dl; p<0.05), lipoprotein(a) [20.37 (4.83-36.72) vs 10.02 (1.88-25.41); p<0.01], Platelet Count (241.42+/-75.35 vs 213.94+/-56.74 mm(3); p<0.05) and fibrinogen (388.93+/-107.27 vs 354.33+/-89.35 mg/dl; p<0.05). We used the logistic regression analysis to detect the independent predictors of aspirin resistance. Lipoprotein(a) was found to be the only independent risk factor to identify aspirin resistance (p<0.05; OR: 1.302; CI 95%: 1.003-1.688). CONCLUSIONS: Although the potential mechanisms of aspirin resistance still remains uncertain, we found that platelet responsiveness to aspirin is reduced in patients with high levels of Apolipoprotein B and lipoprotein(a). Our work demonstrate that lipoprotein(a) is an independent risk factor for aspirin resistance possibly due to the interaction of Apolipoprotein(a) with human platelets.
BACKGROUND:Aspirin protects from cardiovascular events. However, a number of patients who take this drug suffer events, probably due to aspirin resistance. The role of certain biologic variables that may affect resistance is still uncertain. AIM: To determine the prevalence of aspirin resistance in patients taking this drug and to test if resistance is related to haemostatic, inflammatory and lipidic variables. METHODS: Platelet function measured with PFA-100 was studied in 268 patients (185 men) with stable coronary disease who took aspirin (100 to 300 mg/day). Aspirin resistance was defined when epinephrine closure time <174 s. Results of lipoprotein(a) are expressed in median (interquartile range). RESULTS:Aspirin resistance was found in 16% of cases. Patients with aspirin resistance had higher levels of Apolipoprotein B (109.27+/-27.65 vs 100.92+/-23.77 mg/dl; p<0.05), lipoprotein(a) [20.37 (4.83-36.72) vs 10.02 (1.88-25.41); p<0.01], Platelet Count (241.42+/-75.35 vs 213.94+/-56.74 mm(3); p<0.05) and fibrinogen (388.93+/-107.27 vs 354.33+/-89.35 mg/dl; p<0.05). We used the logistic regression analysis to detect the independent predictors of aspirin resistance. Lipoprotein(a) was found to be the only independent risk factor to identify aspirin resistance (p<0.05; OR: 1.302; CI 95%: 1.003-1.688). CONCLUSIONS: Although the potential mechanisms of aspirin resistance still remains uncertain, we found that platelet responsiveness to aspirin is reduced in patients with high levels of Apolipoprotein B and lipoprotein(a). Our work demonstrate that lipoprotein(a) is an independent risk factor for aspirin resistance possibly due to the interaction of Apolipoprotein(a) with human platelets.