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Acetylsalicylsäure im Kardiovaskulären System pp 62–88Cite as

Acetylsalicylsäure im Vergleich zu anderen Thrombozytenfunktionshemmern — Wirkungsmechanismen

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Zusammenfassung

Acetylsalicylsäure ist der „Gold-Standard“ zur Thrombozytenhemmung für die Verhinderung bzw. Prognoseverbesserung akuter arterieller thrombotischer Ereignisse. Die Substanz wird der kleinen Gruppe von Medikamenten zugerechnet, deren lebensverlängernde Wirkung in der sekundären und — weniger anerkannt — auch in der primären Gefäßprävention bewiesen ist. Daher fällt es schwer, das Prinzip der Cyclooxygenasehemmung gegen andere, neuere Konzepte der Thrombozytenhemmung zu profilieren. Thrombozytenhemmung kann nicht mehr ausschließlich als antithrombogenes Prinzip verstanden werden. Vielmehr sind Thrombozyten durch die von ihnen gebildeten bzw. aus dem Megakaryozytenkompartiment transportierten und bei Aktivierung auch ohne Thrombusbildung sezernierten Mediatoren an der Steuerung des lokalen Vasotonus, dem lokalen Gefaßwandmodeling sowie der Ko-Aktivierung anderer korpuskularer Blutbestandteile beteiligt. Die Bewertung des Effektes von Thrombozytenfunktionshemmern auf den Verlauf degenerativer Gefäßkrankheiten erfordert daher eine differenziertere Betrachtung. Unter diesen molekularen Aspekten der Thrombozytenaktivierung muß bei der Anwendung von Acetylsalicylsäure zwischen akuten und langfristigen, aber insbesondere auch zwischen direkten und indirekten Wirkungen unterschieden werden. Neben der substanzimmanenten Reduktion des Wirkspektrums auf den Thromboxansignalweg werden so Wirkungsdefizite bei kurzfristiger Anwendung, wie andererseits aber auch neue Effekte im Gesamtspektrum der Thrombozytenfunktionen, insbesondere die mögliche Beeinflußbarkeit der Leukozyteninteraktion, sichtbar. Zu den neueren Thrombozytenfunktionshemmern gehören Ticlopidin, Prostacyclinmimetika, insbesondere aber auch antiadhäsive Substanzen wie Fibrinogenrezeptorblocker, die die molekulare Quervernetzung, d.h. die funktionelle Endstrecke aktivierter Thrombozyten, blockieren. Diese hochpotenten Substanzen werden das breite Konzept der Cyclooxygenasehemmung nicht ablösen. Vielmehr bestätigen die heute verfügbaren Daten, daß wie mit Fibrinolytika auch, eine Kombination antithrombozytärer Konzepte zu einer Verbesserung der gewünschten klinischen Effektivität führen kann.

Summary

Acetylsalicylic acid is the „golden standard“ to reduce the incidence and to improve the outcome of acute thrombotic events in arteries. Acetylsalicylic acid belongs to the small group of drugs with established beneficial effects in life-expectancy in secondary prevention. Similar, though less well established conclusions have also been drawn for primary prevention. This makes it difficult to design other, eventually more contemporary concepts of drug-induced inhibition of platelet function versus the concept of inhibition of cyclooxygenase. Inhibition of platelet function is more than inhibition of thrombogenesis and also involves local vasomotor control, vascular remodeling and activation of additional blood cells, induced by platelet-derived mediators. The evaluation of efficacy of inhibitors of platelet function, therefore, has also to consider these facts.

This is also true for acetylsalicylic acid where short-term effects have to be separated from long-term effects as well as direct actions from indirect actions. The action profile is focussed on the thromboxane signal and, therefore, limited in short-term use. On the other hand, any change in cyclooxygenase metabolites by acetylsalicylic acid may allow for additional effects, such as modulation of white cell function. More recently developed inhibitors of platelet function involve ticlopidine, prostacyclin mimetics and antiadhesive compounds, such as fibrinogen receptor antagonists. Fibrinogen receptor antagonists block platelet aggregate formation, i.e. the final common pathway of activated platelets. These highly potent compounds will not replace the more general concept of cyclooxygenase inhibition. However, available data suggest that, similar to fibrinolytics, a combination of different antiplatelet strategies may result in an improved clinical efficacy.

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  1. Arbeitsgruppe „Zelluläre Hämostase und Klinische Angiologie“, Diabetes-Forschungsinstitut an der Heinrich-Heine-Universiät, Auf’m Hennekamp 65, D-40225, Düsseldorf, Germany

    D. Tschoepe & B. Schwippert

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  1. Institutes für Pharmakologie, Heinrich-Heine-Universität Düsseldorf, Universitätsstr. 1, D-40225, Düsseldorf, Deutschland

    K. Schrör (Direktor) (Direktor)

  2. International Institute of Thrombosis and Vascular Diseases, Ferdinand-Schrey-Weg 6, D-60598, Frankfurt am Main, Deutschland

    H. K. Breddin

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Tschoepe, D., Schwippert, B. (1996). Acetylsalicylsäure im Vergleich zu anderen Thrombozytenfunktionshemmern — Wirkungsmechanismen. In: Schrör, K., Breddin, H.K. (eds) Acetylsalicylsäure im Kardiovaskulären System. Birkhäuser Basel. https://doi.org/10.1007/978-3-0348-7574-5_4

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