|
Irregular Heart Beat: Support for Controversial
Theory
Reported June 19, 2009
(Ivanhoe Newswire) -- Atrial fibrillation, the most common form of
human heart beat irregularity, can be fatal if left untreated. Some
clinicians believe it is caused, in part, by calcium leaking from a cellular
store in heart cells, potentially through the RyR2 channel, although this
mechanism remains controversial.
Now, a team of researchers at Baylor College of Medicine, Houston, and
Dresden University of Technology, Germany, has provided support for this
hypothesis by showing that the protein CaMKII can enhance RyR2-mediated
calcium leak, promoting atrial fibrillation in mice.
The team, led by Xander Wehrens and Dobromir Dobrev, studied mice engineered
to express a mutant form of RyR2 associated with calcium leak. Although they
did not spontaneously develop atrial fibrillation, these mice were more
likely to develop atrial fibrillation than normal mice if their heart rate
was forced up.
The development of atrial fibrillation in these mice was related to the
functional interaction of CaMKII with RyR2. Blocking CaMKII function in
these mice prevented them from developing atrial fibrillation when their
heart rate was forced up.
As a functional link between CaMKII and RyR2 was observed in heart biopsies
from patients with chronic atrial fibrillation, the authors suggest that
enhanced CaMKII function might increase calcium leakage via RyR2 and
initiate clinical atrial fibrillation.
SOURCE: Journal of Clinical Investigation, June 15, 2009 |
