title: Viscosity, hemostasis and inflammation in atherosclerotic heart diseases.
abstract: BACKGROUND
  In atherosclerotic diseases vascular reserve is impaired and pressure gradient is decreased, therefore the reduced blood fluidity can lead to tissue ischemia more rapidly. In previous investigations we demonstrated the deterioration of plasma and whole blood viscosities in patients with acute ischemic coronary syndromes, chronic coronary artery disease, and percutaneous transluminal coronary angioplasty.
  
  
  METHODS
  Hemorheological variables (plasma and whole blood viscosities, hematocrit, red blood cell aggregation), hemostaseological parameters (plasma fibrinogen and von Willebrand factor (vWf)), and platelet aggregation were detected in more recent studies in cardio- and cerebrovascular diseases, and diabetes mellitus. Common risk factors (lipid profile, smoking, glucose level, previous diseases) and medication were also recorded.
  
  
  RESULTS
  High portion of vascular patients were demonstrated to have poor ex vivo platelet inhibition. Effective antiplatelet treatment detected by aggregometry was related to lower plasma fibrinogen concentration and red blood cell aggregation and was also associated with less recurrent vascular events during the follow-up (p < 0.001). Beside the impaired hemorheological characteristics, the diabetic patients showed elevated vWf activity, which turned to correlate with hemoglobin A1c concentration (p < 0.01) rather than the fasting glucose.
  
  
  CONCLUSIONS
  Our studies indicate the active role and interaction of hemorheological and hemostaseological factors in atherosclerotic heart diseases.
authors.affiliation: First Department of Medicine, University of Pécs, Pécs, Hungary. gabor.kesmarky@aok.pte.hu
authors.forename: Gábor
authors.initials: G
authors.lastname: Késmárky
authors.forename: Gergely
authors.initials: G
authors.lastname: Fehér
authors.forename: Katalin
authors.initials: K
authors.lastname: Koltai
authors.forename: Beáta
authors.initials: B
authors.lastname: Horváth
authors.forename: Kálmán
authors.initials: K
authors.lastname: Tóth
mesh_terms: D000368:Aged; D001241:Aspirin / Q000008:administration & dosage; D001809:Blood Viscosity; D002545:Brain Ischemia / Q000097:blood* / Q000188:drug therapy; D000077144:Clopidogrel; D003324:Coronary Artery Disease / Q000503:physiopathology*; D048909:Diabetes Complications / Q000097:blood*; D005260:Female; D005947:Glucose / Q000378:metabolism; D006442:Glycated Hemoglobin / Q000502:physiology; D006487:Hemostasis; D006801:Humans; D007249:Inflammation; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000097:blood* / Q000188:drug therapy; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage; D013988:Ticlopidine / Q000008:administration & dosage / Q000031:analogs & derivatives; D014841:von Willebrand Factor / Q000502:physiology
chemical_list: D001241:Aspirin; D000077144:Clopidogrel; D005947:Glucose; D006442:Glycated Hemoglobin; D010975:Platelet Aggregation Inhibitors; D013988:Ticlopidine; D014841:von Willebrand Factor