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Mitochondrial dysfunction and redox signaling in atrial tachyarrhythmia
Date:4/23/2008

al implications. Atrial ischemia produces an increase in cellular calcium load and oxidative stress in the atria. Thereby, atrial ischemia provides a specific substrate for AF. Recent experimental and clinical data showed that calcium channel blockers have a specific efficacy to prevent AF in this specific situation. Thus, our data provide more information about the potential pathophysiologic mechanism explaining why calcium channel blockers are effective and useful to attenuate atrial cellular remodelling especially under conditions of increased cellular calcium load and oxidative stress. The authors say the use of ex vivo human atrial tissue from patients with and without AF as well as the rapid pacing of atrial tissue slices to mimic AF ex vivo is a valuable approach to identify molecular and cellular effects that are solely due to the AF excluding the effects of concomitant cardiac diseases.

Dr. Steven R. Goodman, Editor-in-Chief of Experimental Biology and Medicine said Professor Lendeckel, Professor Goette and colleagues have demonstrated that inward calcium current via L-type calcium channels contributes to oxidative stress and increased expression of oxidative stress markers and adhesion molecules during cardiac tachyarrhythmia.. He further stated These observations are important to the understanding of the molecular mechanisms by which calcium overload and resulting mitochondrial dysfunction and resulting oxidative stress impact atrial remodelling during atrial fibrillation.


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Contact: Dr. Uwe Lendeckel
uwe.lendeckel@med.ovgu.de
49-391-671-4454
Society for Experimental Biology and Medicine
Source:Eurekalert

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