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[Modification of thrombocyte function in diagnostic and therapeutic interventions in cardiology]
H Darius1, B Beisiegel, R Erbel
1II. Medizinische Klinik und Poliklinik, Johannes Gutenberg-Universität, Mainz.
Insights
Platelet inhibitor drugs like acetylsalicylic acid and molsidomine reduce platelet activity in coronary heart disease patients. These drugs showed comparable effectiveness in preventing restenosis after coronary angioplasty.
Area of Science:
- Cardiovascular Medicine
- Pharmacology
- Hematology
Background:
- Patients with coronary heart disease often exhibit heightened platelet activity.
- Platelet inhibitor drugs are a cornerstone of treatment for these patients.
- Understanding drug interactions with endogenous fibrinolysis is crucial.
Purpose of the Study:
- To investigate the interactions between platelet activation, acetylsalicylic acid (ASA), molsidomine, and endogenous fibrinolysis.
- To compare the efficacy of molsidomine versus ASA plus nifedipine in preventing restenosis post-coronary angioplasty.
Main Methods:
- Dose-dependent inhibition of platelet aggregation and thromboxane synthesis by ASA was assessed.
- Synergistic antiplatelet effects of molsidomine combined with ASA were evaluated.
- A randomized trial compared molsidomine with ASA plus nifedipine in 393 post-angioplasty patients over six months.
Main Results:
- Acetylsalicylic acid (ASA) demonstrated dose-dependent inhibition of platelet aggregation and thromboxane synthesis.
- Molsidomine (8 mg) combined with ASA showed a synergistic platelet inhibitor effect, delaying aggregation.
- In patients with coronary artery stenoses, platelet activity was significantly enhanced, particularly during exercise, with reduced fibrinolysis.
- After coronary angioplasty, restenosis rates were 29% for molsidomine and 33% for ASA plus nifedipine, a non-significant difference.
Conclusions:
- Both molsidomine and acetylsalicylic acid (ASA) effectively inhibit platelet activity.
- Molsidomine and ASA plus nifedipine exhibit similar efficacy in preventing restenosis after coronary angioplasty.
- Further research may explore optimizing combination therapies for coronary heart disease management.
Abstract:
In 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.