Abstract
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.
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