Atrial fibrillation (AF) is the most common cardiac arrhythmia seen in clinical practice and can induce cardiac dysfunction and strokes. Mechanisms of AF involve a triggering mechanism from thoracic vein and/or a substrate mechanism in the atria. Studies showed that elimination of ectopic focus from pulmonary vein (PV) or non-PVs by catheter ablation could cure AF. As noted, PVs are the most important focus in the initiation of paroxysmal AF. The mechanisms of AF are quite complex because of the fact that AF results from a variety of clinical conditions, autonomic tone modulation, and the self-perpetuation phenomenon " AF begets AF." Likewise, there is a wide range of changes in the function and expression of ion channels (electrical remodeling). Ion channels involved in AF triggers include those mediating calcium homeostasis and non-calcium ion channels. Abnormal calcium homeostasis and heterogeneous expression of potassium channels, pacemaker channels, and stretch- and swelling-activated chloride channels may promote the electrical activity of PV and consequently the occurrence of AF. Shortening of action potential duration in response to decreases in inward currents and/or increases in outward currents can facilitate the genesis and maintenance of AF. Additionally, different underlying diseases may yield different patterns of electrical remodeling. This review summarizes the recent findings in this area of research.
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