[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 AT (1) blockers, both reduce the relative risk of atrial fibrillation by about 30 %. Further prospective randomized clinical studies are required to establish final evidence.
Heusch
G
G
Institut für Pathophysiologie, Universitätsklinikum Essen. gerd.heusch@uni-essen.de
Schulz
R
R
D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D000818:Animals; D001281:Atrial Fibrillation / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology*; D002320:Cardiovascular Physiological Phenomena; D020022:Genetic Predisposition to Disease; D006439:Hemodynamics; D006801:Humans; D000451:Mineralocorticoid Receptor Antagonists / Q000627:therapeutic use; D016032:Randomized Controlled Trials as Topic; D012084:Renin-Angiotensin System / Q000235:genetics / Q000502:physiology
D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000451:Mineralocorticoid Receptor Antagonists