• H Darius, B Beisiegel, R Erbel, H J Rupprecht, G Hafner, T Pop, N Treese, and J Meyer.
• II. Medizinische Klinik und Poliklinik, Johannes Gutenberg-Universität, Mainz.
• Z Kardiol. 1991 Jan 1;80 Suppl 5:65-70.

AbstractIn patients with coronary heart disease platelet activity may be pathologically increased. Administration of platelet inhibitor drugs is an established treatment principle. The interactions between platelet activation, platelet inhibitor drugs like acetylsalicylic acid (ASA) or molsidomine and the endogenous fibrinolysis were studied in three trials. Platelet aggregation and thromboxane synthesis are dose- dependently inhibited after oral intake of ASA (0, 10, 30, 100 or 500 mg/d) Additional intake of the antianginal agent and nitric oxide donator Molsidomine (8 mg) results in a synergistic platelet inhibitor effect characterized by a significantly delayed aggregation response. In a group of patients with coronary artery stenoses platelet activity was markedly enhanced, when compared to healthy individuals. During physical exercise platelet activity was even further enhanced and plasma t-PA-activity was increased by a factor of 2.2. The stimulation of the endogenous fibrinolytic system was markedly reduced when compared to healthy subjects. Following successful coronary angioplasty 393 patients were randomized to receive either molsidomine (2 x 8 mg/d) or ASA (1 x 500 mg/d) plus nifedipine (3 x 20 mg/d). Coronary angiography performed after the 6 month treatment period revealed a restenosis rate of 29% in the molsidomine group and of 33% in patients treated with ASA + nifedipine. This difference was not statistically significant.

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