title: Prevalence and biologic profile of aspirin resistance in patients with angiographically proven coronary artery disease.
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.
  
  
  OBJECTIVE
  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.
authors.affiliation: FIDEC, Department of Atherosclesosis and Thrombosis, Gurtubay s/n, 48012, Bilbao, Vizcaya, Spain. nfpirezj@lg.ehu.eh
authors.forename: Idoia
authors.initials: I
authors.lastname: Narvaez
authors.forename: Jose Domingo
authors.initials: JD
authors.lastname: Sagastagoitia
authors.forename: Marta
authors.initials: M
authors.lastname: Vacas
authors.forename: Yolanda
authors.initials: Y
authors.lastname: Saez
authors.forename: Manolo
authors.initials: M
authors.lastname: Lafita
authors.forename: Santos
authors.initials: S
authors.lastname: Monica
authors.forename: Jesus Pablo Saez
authors.initials: JP
authors.lastname: de Lafuente
authors.forename: Enrique
authors.initials: E
authors.lastname: Molinero
authors.forename: Jose Antonio
authors.initials: JA
authors.lastname: Iriarte
mesh_terms: D000368:Aged; D001055:Apolipoproteins B / Q000378:metabolism; D001241:Aspirin / Q000627:therapeutic use*; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism; D003324:Coronary Artery Disease / Q000188:drug therapy / Q000453:epidemiology / Q000473:pathology*; D004351:Drug Resistance; D004837:Epinephrine / Q000627:therapeutic use; D005260:Female; D006487:Hemostasis; D006801:Humans; D007249:Inflammation; D017270:Lipoprotein(a) / Q000737:chemistry; D008297:Male; D008875:Middle Aged; D009389:Neovascularization, Pathologic; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D010979:Platelet Function Tests; D015995:Prevalence
chemical_list: D001055:Apolipoproteins B; D017270:Lipoprotein(a); D010975:Platelet Aggregation Inhibitors; D001241:Aspirin; D004837:Epinephrine