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Herz-Kreislauf-Erkrankungen und Störungen von Blutgerinnungs- und Fibrinolysevorgängen

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Tabakabhängigkeit

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Abstract

•Die Störungen im komplexen Geschehen von Blutgerinnungs- und Fibrinolysevorgängen werden vor allem durch zahlreiche Inhaltsstoffe des Tabakrauchs und weniger durch das Nikotin ausgelöst. Tabakrauchen bewirkt einen präthrombotischen Zustand, indem die Aggregation der Thrombozyten auch über eine Zunahme der Glykoproteine IIb/IIIa gesteigert und die Ausschüttung von Plättchenfaktor 4 und β-Thromboglobulin in den Thrombozytengranula erhöht wird. Im Zuge der Wechselwirkungen zwischen Endothelzellen und den Reaktionen der Thrombozyten erhöhen sich neben dem Thrombomodulin als „Thrombinrezeptor“ auch der Von-Willebrand-Faktor und Adhäsionsmoleküle (z. B. PECAM- 1).

•Bei der plasmatischen Blutgerinnung kommt es durch das Rauchen zu einer Erhöhung von Faktor XIIa und Faktor VIII sowie zu einer gesteigerten Thrombinbildung mit Zunahme der Prothrombinfragmente F1+2 und des Thrombin- Antithrombin-Komplexes. Die Fibrinogenspiegel sind bei Rauchern in jedem Lebensalter im Vergleich zu Nichtrauchern erhöht. Ebenso ist durch das Rauchen die Fibrinbildung gesteigert, was sich anhand der D-Dimere untersuchen lässt. Die erhöhte Gerinnbarkeit des Blutes wird noch durch die bei Rauchern verminderten Plasminogenspiegel unterstützt.

•Schwere Herz-Kreislauf-Ereignisse, wie Myokardinfarkte, apoplektische Insulte etc., können bei Rauchern auch durch genetisch veränderte Blutgerinnungsfaktoren ausgelöst werden (z. B. durch Polymorphismen am Glykoprotein IIIa, Thrombomodulin oder Faktor V), wie in klinisch-epidemiologischen Studien nachzuweisen war.

•Mit den in Abb. 7.13 dargestellten Zusammenhängen werden diese Vorstellungen noch einmal verdeutlicht. Der Raucher ist nur selten bereit, seine erhöhte Gesundheitsgefährdung im Hinblick auf einen Myokardinfarkt oder ein Bronchialkarzinom zu realisieren. Beispielsweise traf dies nur auf 39 bzw. 49% der Befragten einer umfassenden Studie für beide Erkrankungen zu, wobei der Bildungsgrad einen deutlichen Einfluss hatte [314]. Trotz einer umfassenden Analyse über die Wirkungen von Nikotin auf die Ausbildung einer Arteriosklerose gibt es immer wieder gegenteilige Befunde. Tierversuche lassen vermuten, dass Nikotin die Arterioskleroseprogression beschleunigt (Aktivierung des Fettsäuremetabolismus bei herabgesetztem HDL-Turnover). Andererseits gibt es keine Befunde, die für eine Zunahme der Hypertonie oder eine Aktivierung der Plättchenaggregation sprechen [315].

•Kurzzeitmaßnahmen mit mehrwöchigen Interventionsprogrammen (physische Belastung, vorübergehender Rauchstopp) führen bei Erwachsenen mit einem erhöhten Koronarrisiko nicht zu einer Verbesserung der Endothelfunktion [316].

•Darüber hinaus ist die Aufklärungssituation in einigen Ländern sicherlich beklagenswert, weil selbst Raucher nach einem überstandenen frischen Myokardinfarkt eine nur unzureichende Aufklärung von ihren behandelnden Ärzten erfahren. Einer in Israel durchgeführten Studie zufolge waren dies dort nur 62% [169].

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(2008). Herz-Kreislauf-Erkrankungen und Störungen von Blutgerinnungs- und Fibrinolysevorgängen. In: Haustein, KO. (eds) Tabakabhängigkeit. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-73309-6_7

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