Die Rolle der Gefäßwand in der Pathophysiologie des akuten Koronarsyndroms

Zusammenfassung

Das Endothel ist in der Entstehung des akuten Koronarsyndroms von entscheidender Bedeutung. Als endo-/parakrines Organ nimmt das Endothel eine Schlüsselfunktion in der Regulation der vaskulären Homöostase ein. Die endotheliale Integrität und vor allem die Bioverfügbarkeit von Stickstoffmonoxid (NO) sind essenziell für die korrekte Funktion des Endothels. Kardiale Risikofaktoren können eine Endotheldysfunktion mit einem resultierenden Ungleichgewicht der vaskulären Homöostase verursachen. Im inflammatorischen oder prothrombotischen Zustand zeigt das Endothel oxidativen Stress, vermehrte Expression von Zelladhäsionsmolekülen, eine Aktivierung von Zell-Signalsystemen (Renin-Angiotensin-System, CD40/CD40L-System) und insbesondere einen NO-Verlust. Diese entzündungsbedingten Kaskaden führen oft über Jahre zur Koronarsklerose oder binnen kurzer Zeit zum akuten Koronarsyndrom, das durch Endothelerosion oder die Ruptur einer instabilen Plaque ausgelöst wird. Durch die Kenntnis der pathophysiologischen Vorgänge in der Gefäßwand beim akuten Koronarsyndrom lassen sich sowohl Hochrisikopatienten identifizieren als auch gezielte therapeutische Maßnahmen entwickeln.

Summary

The endothelium is of important significance in the development of the acute coronary syndrome. As an endo-/paracrine organ, the endothelium plays a key role in the regulation of the vascular homeostasis. The endothelial integrity and above all the bioavailability of nitric oxide (NO) are essential for the correct function of the endothelium. Cardiac risk factors may lead to an endothelial dysfunction with a consecutive imbalance of the vascular homeostasis. In an inflammatory or prothrombotic state the endothelium shows a number of abnormalities such as oxidative stress, expression of cell adhesion molecules, activation of cell signal- systems (renin-angiotensin-system, CD40/CD40L-system) and especially the loss of NO. The inflammatory cascades lead to coronary atherosclerosis over years or, more instantly, to the acute coronary syndrome caused by endothelial erosion or the rupture of an instable plaque. The knowledge of the pathophysiological processes in the arterial wall during the acute coronary syndrome may lead to the identification of high risk patients and the development of more targeted therapies.

Schlüsselwörter

Akutes Koronarsyndrom - Endotheldysfunktion - Stickstoffmonoxid - Atherosklerose

Keywords

Acute coronary syndrome - endothelial dysfunction - nitric oxide - atherosclerosis

• References

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