title: Erythrocyte deformability and white blood cell count are associated with aspirin resistance in high-risk vascular patients.
abstract: Recently the phenomenon of aspirin resistance has been object of several studies, but no data are available on the possible role of the haemorheologic parameters in affecting platelet function and resistance to antiplatelet agents. Aim of our study was to evaluate platelet function and haemorheology in patients with acute coronary syndromes (ACS), receiving double antiplatelet therapy with aspirin and clopidogrel. The study population included 301 (231M/70F; age: 66 +/- 13 yrs) consecutive adult patients admitted to the Coronary Care Unit of the Azienda Ospedaliero-Universitaria Careggi, with diagnosis of acute myocardial infarction or unstable angina. We assessed: whole blood viscosity (WBV) at shear rates of 0.512 s(-1) and 94.5 s(-1), plasma viscosity (PLV) at 94.5 s(-1) shear rate, erythrocyte deformability index (DI) and PFA-100 closure times with ADP (PFA/ADP) and epinephrine (PFA/EPI). We considered any PFA-100-EPI result < 203 sec (95th percentile of control distribution) to be indicative of aspirin resistance. 104/301 patients (34.5%) had PFA/EPI CTs in the reference range (group 1) whereas the remaining had values higher than 203 sec (group 2). WBV at 94.5 sec (-1) s.r. was similar in group 1 and 2 (WBV: 4.43 +/- 0.25 vs 4.45 +/- 0.61 mPa.sec, respectively). PLV and WBV at 0.512 sec (-1) s.r. were slightly higher, but not significantly, in group 1 than in group 2 (PLV: 1.47+/-0.13 vs 1.44 +/- 0.15 mPa.sec; p = 0.08 and WBV: 23.37 +/- 4.6 vs 22.54 +/- 3.90 mPa.sec; p = 0.07). DI was significantly lower in group 1 with respect to group 2 (4.05 +/- 2.93 vs 5.71 +/- 3.30, p < 0.0001). White blood count (WBC) was significantly higher in group 1 than in group 2 (11464 +/- 3504 vs 7867 +/- 2162, p < 0.0001). In conclusion, these results demonstrate that in patients with acute coronary syndromes the antiaggregant effect of aspirin is modulated not only by the direct action on platelets, but also by erythrocyte deformability and white blood cell count.
authors.affiliation: Department of Medical and Surgical Critical Care, Thrombosis Centre, University of Florence, Azienda Ospedaliera Universitaria Careggi, Florence, Italy.
authors.forename: Lucia
authors.initials: L
authors.lastname: Mannini
authors.forename: Rossella
authors.initials: R
authors.lastname: Marcucci
authors.forename: Rita
authors.initials: R
authors.lastname: Paniccia
authors.forename: Emilia
authors.initials: E
authors.lastname: Antonucci
authors.forename: Cristina
authors.initials: C
authors.lastname: Giglioli
authors.forename: Serafina
authors.initials: S
authors.lastname: Valente
authors.forename: Anna Maria
authors.initials: AM
authors.lastname: Gori
authors.forename: Domenico
authors.initials: D
authors.lastname: Prisco
authors.forename: Gian Franco
authors.initials: GF
authors.lastname: Gensini
authors.forename: Rosanna
authors.initials: R
authors.lastname: Abbate
mesh_terms: D000368:Aged; D000789:Angina, Unstable / Q000097:blood* / Q000188:drug therapy; D001241:Aspirin / Q000494:pharmacology*; D001760:Bleeding Time / Q000379:methods; D001809:Blood Viscosity / Q000187:drug effects; D000077144:Clopidogrel; D004351:Drug Resistance; D004907:Erythrocyte Deformability / Q000187:drug effects*; D005260:Female; D018056:Hemorheology / Q000187:drug effects; D006801:Humans; D007958:Leukocyte Count; D007962:Leukocytes / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000188:drug therapy; D010974:Platelet Aggregation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology*; D013927:Thrombosis / Q000503:physiopathology; D013988:Ticlopidine / Q000031:analogs & derivatives* / Q000494:pharmacology
chemical_list: D010975:Platelet Aggregation Inhibitors; D000077144:Clopidogrel; D013988:Ticlopidine; D001241:Aspirin