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Dtsch Med Wochenschr 2006; 131(15): 817-820
DOI: 10.1055/s-2006-939853
Prinzip & Perspektive | Review article
Physiologie/Kardiologie
© Georg Thieme Verlag KG Stuttgart · New York

Pathophysiologie des Renin-Angiotensin-Systems bei Vorhofflimmern

Pathophysiology of the renin-angiotensin-system in atrial fibrillationG. Heusch1 , R. Schulz1
  • 1Institut für Pathophysiologie, Universitätsklinikum Essen
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Publication History

eingereicht: 13.2.2006

akzeptiert: 16.3.2006

Publication Date:
11 April 2006 (online)

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Zusammenfassung

Kardiovaskuläre Erkrankungen, die mit einer Aktivierung des Renin-Angiotensin-Systems einhergehen - Myokardinfarkt, Herzinsuffizienz, Hypertonie - führen häufig zu Vorhofflimmern. An der Auslösung und Aufrechterhaltung von Vorhofflimmern ist nicht nur die mechanische Vorhofdehnung, sondern auch eine verstärkte Expression einzelner Komponenten des Renin-Angiotensin-Systems in den Vorhöfen beteiligt. Diese induziert über eine inflammatorische Signalkaskade und oxidativen Stress eine Myolyse und verstärkte Fibrose. Letztlich ermöglichen eine lokal verlangsamte Erregungsleitung und eine verkürzte Refraktärzeit kreisende Erregungen, die einen grundlegenden Mechanismus von Vorhofflimmern darstellen. Sowohl ACE-Hemmer als auch AT1-Blocker reduzieren in einer Meta-Analyse das relative Risiko von Vorhofflimmern um ca. 30 %; weitere prospektive, randomisierte, klinische Studien sind notwendig, um diesen Effekt endgültig zu belegen.

Pathophysiology of the renin-angiotensin-system in atrial fibrillation

Cardiovascular diseases which are associated with an activation of the renin-angiotensin-system - myocardial infarction, heart failure, hypertension - often induce atrial fibrillation. The initiation and maintenance of atrial fibrillation is not only initiated by mechanical distension of the atria, but also by increased atrial expression of components of the renin-angiotensin-system, which initiate an inflammatory signal cascade and oxidative stress and in consequence myolysis and interstitial fibrosis. Ultimately, locally decreased conduction velocity and abbreviated refractory period facilitate reentry circuit(s) as an underlying pathomechanism of atrial fibrillation. In a meta-analysis, ACE inhibitors and AT1 blockers, both reduce the relative risk of atrial fibrillation by about 30 %. Further prospective randomized clinical studies are required to establish final evidence.

Schlüsselwörter

Vorhofflimmern - Angiotensin - ACE-Hemmer - AT1-Blocker - Inflammation - Oxidativer Stress

Key words

atrial fibrillation - angiotensin - ACE inhibitor - AT1-Blocker - inflammation - oxidative stress

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Prof. Dr. med. Dr. h. c. Gerd Heusch

Direktor des Instituts für Pathophysiologie, Zentrum für Innere Medizin, Universitätsklinikum Essen

Hufelandstraße 55

45122 Essen

Phone: 0201/7234480

Fax: 0201/7234481

Email: gerd.heusch@uni-essen.de

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