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  • Title: Hemorheological background of acetylsalicylic acid resistance.
    Author: Feher G, Koltai K, Kesmarky G, Toth K.
    Journal: Clin Hemorheol Microcirc; 2008; 38(3):143-52. PubMed ID: 18239256.
    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. OBJECTIVES: 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. CONCLUSION: 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.
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