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The ebb and flow of atrial fibrillation

ESC Congress 2010

Atrial Fibrillation


This symposium reviewed a number of emerging mechanisms that may promote the new-onset or persistence of atrial fibrillation (AF).

Intriguing findings on cellular “structural” remodelling of left atrial myocytes in a sheep model of heart failure were presented by Dr Kathryn Dibb. Left ventricular failure and mitral valve regurgitation were associated with a loss of T-tubules and profound alterations in calcium handling in atrial myocytes, brought about by dyssynchronous intracellular EC coupling. The functional consequences of these cellular structural changes and their relevance to the AF substrate in the presence of heart failure are the focus of ongoing investigations.

It is increasingly difficult to imagine how we managed to make sense of myocardial signalling, growth and EC coupling before we knew of the importance of Calmodulin kinase and, more specifically, of CamKId. Over the last few years CamKId -signalling has been implicated in the dysregulation of EC coupling in experimental and human heart failure and AF. In a series of elegant experiments, Dr Dobrev illustrated the role of CamKId in the regulation of phospholamban and RyR phosphorylation in human atrial myocytes from patients with AF and in genetically modified mouse models. Availability of small molecules able to modulate CamKId activity will soon test the potential of this signalling pathway as a therapeutic target.

As illustrated by the new ESC guidelines on the management of AF, restoring sinus rhythm in patients with AF and atrial structural remodelling remains a significant clinical problem. Dr Schotten presented new and exciting data on the qualitative and quantitative differences in atrial fibrosis induced by AV block or long-term AF and their impact on AF organisation and reversibility. Finally, Dr Hatem illustrated a number of new mechanisms that may underlie ion currents remodelling in AF, including modulation of transcription, trafficking and post-translational modifications of ion channels.

Taken together these talks have highlighted a number of promising new targets in the “upstream” treatment of AF.

References


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The ebb and flow of atrial fibrillation
The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.