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Previous Volume 360:1669-1671 April 16, 2009 Number 16 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Atrial fibrillation is the most common sustained arrhythmia and is associated with substantial morbidity and mortality.¹ Antiarrhythmic drug therapy is often ineffective and may cause serious adverse effects, including ventricular proarrhythmia. In the past decade, we have learned much about the electrical, mechanical, and structural remodeling that occurs as a result of atrial fibrillation and that leads to more atrial fibrillation.^1,2,3,4 These adaptations include ionic and genomic alterations over the short term and cellular changes over the medium term; fortunately, these effects may be reversible.^2,3,4 Apoptosis and interstitial fibrosis develop over the longer term and are usually irreversible.^2,3,4

There is . . . [Full Text of this Article]

Source Information

From the Department of Cardiac Sciences, the University of Calgary and Calgary Health Region, and the Libin Cardiovascular Institute of Alberta, Calgary, AB, Canada.

This article has been cited by other articles:

• (2009). An Angiotensin-Receptor Blocker Fails to Prevent Atrial Fibrillation Recurrence. Journal Watch Cardiology 2009: 1-1 [Full Text]