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Individually Controlled Aspirin in the Long-Term Treatment of Patients with Chronic Arterial Diseases

Central Institute for Cardiovascular Research, Academy of Sciences of the GDR, Berlin-Buch, East Germany

C. Norden

Central Institute for Cardiovascular Research, Academy of Sciences of the GDR, Berlin-Buch, East Germany

H. Heine

Central Institute for Cardiovascular Research, Academy of Sciences of the GDR, Berlin-Buch, East Germany

A simple method of measuring the biological effect of acetylsalicylic acid (ASA), based on the determination of the disaggregation rate (DR) of plate let aggregation induced by adenosine diphosphate (ADP), is described. The DR was found to correlate with the inhibition of the production of ma londialdehyde (MDA) by platelets (r = 0.66, P < 0.001). Therefore, the DR was used for laboratory monitor ing of the ASA effect. The study in cluded 63 arteriosclerotic patients — patients with ischemic heart disease (IHD), peripheral arterial disease (PAD), or cerebrovascular insuffi ciency (CVI) — who were analyzed before treatment and after receiving ASA in an individually controlled dosage. Before treatment the authors found an increased level of MDA and a longer euglobulin clot lysis time in patients when compared with healthy volunteers (n=16). Extremely differ ent doses of ASA were required to normalize initially elevated MDA lev els in patients. Normalization of the MDA level corresponds to a DR of at least 50% (in comparison with 0-13% without treatment). When judging the ASA dose individually from the 50% DR, the authors demonstrated that there were no differences in the levels of cyclooxygenase- and lipoxy genase-derived eicosanoids between healthy volunteers (n = 16) and arteri osclerotic patients receiving 100-250 mg (n=18), 500 mg (n=17), or 750-1500 mg ASA per day (n=6). Thus, their results support the idea of using individually controlled ASA as the most promising way of resolv ing the "aspirin dilemma" and pro vide a simple and reproducible method of measuring the biological effect of ASA.

Angiology, Vol. 40, No. 5, 464-471 (1989)
DOI: 10.1177/000331978904000507


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