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Discusses the role of angiotensin-receptor blockers in the prevention of atrial fibrillation and the underlying mechanisms of atrial remodeling.
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.14 These adaptations include ionic and genomic alterations over the short term and cellular changes over the medium term; fortunately, these effects may be reversible.24 Apoptosis and interstitial fibrosis develop over the longer term and are usually irreversible. . . .
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Anne M. Gillis (2009) studied this question.
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