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Atrial fibrillation (AF) is one of the most prevalent and vexing cardiovascular conditions. Available treatments for AF based on ion channel blockade are only poorly effective. The fundamental mechanisms that underlie AF are still not clearly understood, and likely vary depending on the etiology of AF. In older individuals with senile AF, likely mechanisms include abnormal calcium cycling, oxidant stress, and deleterious inflammatory responses. Clinical and experimental evidence is provided to support the role of oxidant and inflammatory mechanisms in AF. On the basis of these studies, the prospects of manipulating oxidant and inflammatory pathways as targets for therapeutic intervention are discussed.