title: Hemorheological background of acetylsalicylic acid resistance.
abstract: BACKGROUND
  Pathologic hemorheological parameters and increased platelet aggregation in association with other risk factors significantly increase the possibility of the development of ischemia. Acetylsalicylic acid (ASA) is an effective antithrombotic agent, which prevents a variety of cardiovascular diseases.
  
  
  OBJECTIVE
  The aim of our present study was to compare the hemorheological parameters of patients with effective platelet inhibition by ASA to those with ineffective one.
  
  
  METHODS
  2045 patients taking 100 mg ASA daily were involved in our study (1255 males, mean age: 63+/-11 yrs, 790 females, mean age: 63+/-12 yrs). To exclude the effect of risk profile, previous diseases and medication, 323 patients (197 males, mean age 60+/-13 yrs and 126 females, mean age 60+/-12 yrs) were selected from the examined group with matching parameters. Blood was taken after an overnight fast between 8:00 and 9:00 a.m. Platelet aggregation was measured in Carat TX-4 optical platelet aggregometer. Blood hematocrit was measured by Heraeus microhematocrit centrifuge and red blood cell aggregation was detected by Myrenne aggregometer. Plasma fibrinogen was measured by Clauss' method. Plasma and whole blood viscosities were measured in Hevimet 40 capillary viscosimeter.
  
  
  RESULTS
  Patients with effective ASA inhibition had significantly lower plasma fibrinogen level (p<0.05) and red blood cell aggregation values both in the heterogenous and the selected populations (p<0.01). The other hemorheological parameters were not statistically different in the two groups.
  
  
  CONCLUSIONS
  The background of ineffective ASA medication has not yet been fully elucidated. Higher fibrinogen concentration increases red blood cell aggregation and can also result in increased platelet aggregation. Thus, increased plasma fibrinogen level may play an important role in the in vitro and in vivo platelet resistance to ASA.
authors.affiliation: 1st Department of Medicine, University of Pecs, Medical School, Pecs, Hungary. gerely.feher@aok.pte.hu
authors.forename: Gergely
authors.initials: G
authors.lastname: Feher
authors.forename: Katalin
authors.initials: K
authors.lastname: Koltai
authors.forename: Gabor
authors.initials: G
authors.lastname: Kesmarky
authors.forename: Kalman
authors.initials: K
authors.lastname: Toth
mesh_terms: D000368:Aged; D000925:Anticoagulants / Q000627:therapeutic use; D001241:Aspirin / Q000009:adverse effects* / Q000494:pharmacology* / Q000627:therapeutic use; D001809:Blood Viscosity / Q000187:drug effects; D002561:Cerebrovascular Disorders / Q000188:drug therapy / Q000503:physiopathology; D004903:Erythrocyte Aggregation / Q000187:drug effects; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D006331:Heart Diseases / Q000188:drug therapy / Q000503:physiopathology; D006400:Hematocrit; D018056:Hemorheology; D006801:Humans; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D018570:Risk Assessment
chemical_list: D000925:Anticoagulants; D010975:Platelet Aggregation Inhibitors; D005340:Fibrinogen; D001241:Aspirin