Ectopic activities in pulmonary veins initiating atrial fibrillation

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Spontaneous electrical activities originating from the pulmonary vein myocardial sleeves play important roles in the initiation and maintenance of atrial fibrillation, but little is known about the ionic mechanisms of arrhytmogenic activities in the pulmonary veins. We investigated ion channel expression in rabbit and rat pulmonary veins and compared those in the sinoatiral node and atrial muscle. Hyperpolarization-activated channels (HCN1, HCN4) and Cav1.3 L-type Ca channel mRNAs were abundantly expressed in the sinoatrial node but their expression in the pulmonary veins was less than in the atrial muscle. Inward rectifier K channels (Kir2.1, Kir2.2), cardiac type Na channel (Nav1.5) and Ca-handling proteins (ryanodine receptor and SERCA) mRNAs were lower in the pulmonary veins than in atrial muscle. These results suggest that the unique ion channel expression profile in the pulmonary veins may underlie arrhythmogenic substrates such as impaired conduction and intracellular Ca overload.Atrial fibrillation is often associated with atrial dilatation. We investigated the effects of stretch-activated channel (SAC) blockers on the vulnerability of atrial fibrillation in intra-atrial pressure-overloaded rabbit hearts. Ga^<3+> reduced the stretch-induced vulnerability. Synthesized peptides, which are reported to block a subset of SAC, and Cl^-channel blockers have no significant effects on atrial fibrillation propensity during pressure overload. Blockade of SAC might be a novel antiarrhythmic approach to atrial fibrillation under conditions of increased atrial pressure.