Biomedical Engineering Reference
In-Depth Information
Fig. 7
Inl uence of ACE-Inhibitors and ARB on pathophysiology of AF.
Atrial i brillation (AF)
causes structural remodeling and inl ammation (Curved arrows on the right). Upregulation of
adhesion molecules among other predisposing factors leads to thrombus formation. Angiotensin
receptor blockers (ARB) and angiotensin converting enzyme (ACE) inhibitors positively inl uence
remodeling and inl ammation. Further studies are warranted to show a clinically signii cant impact
of ACE-inhibitors and ARB on thrombus generation.
stimulus to cause frequent collisions of platelets and injury of endothelial cells
leading to platelet activity and thrombus formation.
THERAPEUTIC IMPLICATIONS
h e impact of ARB therapy on systemic adhesion molecule levels has been shown
in patients with atherosclerosis and heart failure (Tsutamoto
et al.
2000). Figure
7 summarizes the points of action of ARB therapy on AF-related processes and
myocardial changes. In our recent AF-studies we were able to demonstrate
the direct impact of ARB treatment on adhesion molecule expression.
Our
ex vivo
experiments using organotypic human atrial tissue cultures and
in vivo
experiments showed that ARB treatment reduces adhesion molecule expression
in atrial tissue during rapid pacing. h us, rapid atrial stimulation inl uences
prothrombotic endocardial remodeling via the AT1R. In support of this view we
